Ribosomal protein RPS15A augments proliferation of colorectal cancer RKO cells via regulation of BIRC3, p38 MAPK and Chk1.

OBJECTIVE: Ribosomal protein S15A (RPS15A) has been implicated in tumorigenesis, but its role in colorectal cancer (CRC) is not fully studied. The objective of this study was to investigate the role of RPS15A in CRC carcinogenesis. PATIENTS AND METHODS: RBSP15A expression was detected in 120 colorectal adenocarcinoma biopsies by immunohistological staining, and we examined the association of RSP15A expression with clinicopathological outcomes. We generated RPS15A stable knockdown CRC cell lines using shRNAs and assessed cell proliferation by MTT assays, clonogenicity by colony formation assays, and apoptosis and cell cycle arrest by flow cytometric analyses. A mouse tumor xenograft model was used to confirm the influence of RPS15A expression on CRC in vivo. RESULTS: RPS15A expression was predictive for poor disease-free survival. Knockdown of RPS15A expression significantly inhibited cell proliferation and colony formation and augmented apoptosis in both the RKO and SW620 CRC cell lines. Moreover, RPS15A knockdown arrested RKO cells at the G2/M phase and SW620 cells at the G0/G1 phase. KEGG pathway analysis of 785 genes differentially expressed between wild-type and shRPS15A RKO cells showed enrichment for the pathway in cancer and MAPK signaling pathway KEGG terms. RPS15A knockdown induced apoptosis via regulation of BIRC3, p38 MAPK, and Chk1. Consistently, RPS15A knockdown significantly impaired the growth of subcutaneous CRC xenografts in nude mice. CONCLUSIONS: These results indicate that RPS15A is a novel, potentially oncogenic gene involved in colorectal carcinogenesis. RPS15A knockdown may be an attractive strategy for treating CRC with gene therapy.

The influence of oncolytic reovirus on the biological activities of umbilical cord-derived mesenchymal stem cells.

OBJECTIVE: To investigate the influence of oncolytic reovirus on the biological activities of human umbilical cord-derived mesenchymal stem cells (hUC-MSCs) as a novel virotherapy strategy. MATERIALS AND METHODS: The Cell Counting Kit-8 assay was used to detect the viability of hUC-MSCs infected with different multiplicities of infection (MOIs) of reoviruses. The biological activities (proliferation, marker expression, multipotency, and migration) of hUC-MSCs were verified by assaying osteogenic and adipogenic differentiation potential, flow cytometry, and electrical cell-substrate impedance sensing, respectively. RESULTS: The viability of hUC-MSCs slightly decreased by infection with low titers of reoviruses. A MOI of 1 had no effect on the viability of hUC-MSCs within 96 h. The biological activities (proliferation, marker expression, multipotency, and migration) of hUC-MSCs were not affected by reovirus infection at a MOI of 1. CONCLUSIONS: Reovirus at a MOI of 1 had no effect on the biological activities of hUC-MSCs.

Circ_001680 aggravates the malignant process of gastric carcinoma by targeting MAP2.

OBJECTIVE: This study aims to explore the expression pattern and clinical significance of circ_001680 in gastric carcinoma (GC) process. PATIENTS AND METHODS: Circ_001680 levels in 40 pairs of GC and paracancerous ones were detected by quantitative real-time polymerase chain reaction (qRT-PCR). The relationship between circ_001680 and GC clinicopathological parameters was analyzed. AGS and SGC-7901 cells were used for constructing circ_001680 knockdown models by shRNA transfection. Proliferative and metastatic abilities in GC cells with circ_001680 knockdown were examined by cell counting kit-8 (CCK-8) and transwell assay, respectively. Dual-Luciferase reporter assay was conducted to clarify the interaction between circ_001680 and MAP2. Their co-regulation on GC process was detected through rescue experiments. RESULTS: Circ_001680 was highly expressed in GC tissues and cell lines. High level of circ_001680 predicted high incidences of lymphatic and distant metastasis, and poor prognosis in GC patients. Knockdown of circ_001680 suppressed proliferative and metastatic abilities in AGS and SGC-7901 cells. MAP2 was the target gene binding circ_001680, which was lowly expressed in GC. In addition, MAP2 was negatively correlated to circ_001680. Knockdown of MAP2 could abolish the suppressed proliferative and metastatic abilities in GC cells with circ_001680 knockdown. CONCLUSIONS: Circ_001680 is highly expressed in GC tissues and closely related to metastasis and prognosis in GC patients, which promotes the proliferative and metastatic abilities in GC cells by negatively interacting with MAP2.

MiR-185-3p downregulates advanced glycosylation end product receptor expression and improves renal function in diabetic nephropathy mice.

OBJECTIVE: To investigate the effects of the downregulation of AGER by miRNA-185-3p on renal function in diabetic nephropathy (DN) mice. MATERIALS AND METHODS: Mice were divided into normal, model, NC, miR-185-3p mimic, si-AGER, and miR-185-3p mimic + si-AGER groups. Eight weeks following the establishment of the model, various indicators were assessed. RESULTS: Compared to control groups, miR-185-3p expression, body weight, superoxide dismutase (SOD) content, catalase (CAT) content, proliferation, S-phase ratios, and proliferating cell nuclear antigen (PCNA) expression were significantly lower in all experimental groups, whilst AGER expression, water intake, food intake, urine volume, urine protein content, serum creatinine (Scr), Blood Urea Nitrogen (BUN), MDA content, G0/G1 status, and rates of apoptosis were significantly higher (all p<0.05). Compared to the model group, miR-185-3p mimics, si-AGER, and miR-185-3p mimic + si-AGER groups had a significantly higher SOD content, CAT content, proliferation, S phase ratios, PCNA expression and lower AGER expression, water intake, food intake, urine output, urine protein, Scr, BUN, MDA content, G0/G1 ratios, and apoptosis rates (all p<0.05). In addition, the effects of the miR-185-3p mimics + si-AGER were superior to miR-185-3p mimics and si-AGER monotherapy groups (both p<0.05). CONCLUSIONS: MiR-185-3p inhibits AGER, downregulates AGER expression, and improves renal function in DN mice.

MSCs transplantation may be a potential therapeutic strategy for COVID-19 treatment.

At present, SARS-Cov-2 is spread all over the world, becoming a serious threat to people's health. SARS-Cov-2 has a strong infection, and the mortality rate of severe patients after infection is high, but there is no effective treatment. Mesenchymal stem cells (MSCs) have anti-inflammatory and immunomodulatory functions, which can reduce the occurrence of cytokine storm syndrome and acute respiratory distress syndrome. At the same time, MSCs can reduce the level of pulmonary fibrosis and enhance tissue injury repair. In this short report, combined with the progress of preclinical and clinical research, we comment the efficacy of MSCs in the treatment of COVID-19.

Linc00702 inhibits cell growth and metastasis through regulating PTEN in colorectal cancer.

OBJECTIVE: To elucidate the expression and influence of Linc00702 on the development and progression of colorectal cancer (CRC). PATIENTS AND METHODS: The expression of Linc00702 was evaluated using quantitative Real Time-Polymerase Chain Reaction (qRT-PCR) in 91 paired CRC tissue samples and adjacent normal tissue samples, as well as in CRC cell lines. Cell proliferation in Caco2 and SW620 cells was detected using colony formation assay and 5-Ethynyl-2'-deoxyuridine (EdU) assay. Wound-healing assay and transwell analysis were utilized to assess the abilities of cell migration and invasion. Western blot analysis was employed to further explore the underlying mechanism of Linc00702 in CRC. RESULTS: Linc00702 was lowly expressed in CRC tissues and cells. Over-expression of Linc00702 reduced cell proliferation, migration, and invasion of Caco2 cells, while knockdown of Linc00702 promoted cell growth and metastasis of SW620 cells comparing to control group, relatively. PTEN was verified as the target for Linc00702 in CRC, and Linc00702 promoted PTEN expression to inhibit the PI3K/AKT pathway. CONCLUSIONS: Linc00702 was downregulated in CRC and inhibited cell proliferation, migration, and invasion by repressing the PI3K/AKT pathway via promoting PTEN expression. This might provide a new target for the biological treatment for CRC.

Deep thought of COVID-19 based on Diamond Princess's quarantine and home quarantine.

Not Available.

LncRNA ROR1-AS1 promotes colon cancer cell proliferation by suppressing the expression of DUSP5/CDKN1A.

OBJECTIVE: The purpose of this study was to explore the possible role of ROR1-AS1 in the pathogenesis of colon cancer and the underlying mechanism. PATIENTS AND METHODS: The expression levels of ROR1-AS1 in 75 colon cancer tissue samples and adjacent ones, as well as in cell lines were examined by quantitative Polymerase Chain Reaction (qPCR). Then, ROR1-AS1 overexpression plasmid and siRNA were transfected into colon cancer cells using liposome method. After that, Cell Counting Kit-8 (CCK-8) and plate colony formation assays were conducted to analyze cell proliferation, while flow cytometry was applied for the analysis of cell cycle and apoptosis. At last, the mechanism of action of ROR1-AS1 was further explored by nuclear separation, RNA binding protein immunoprecipitation (RIP) and chromatin immunoprecipitation (CHIP) assays. RESULTS: ROR1-AS1 level in colon cancer tissues was remarkably higher than that in normal tissues, and the expression in tumors of stage III and IV was remarkably higher than those of stage I and II. Meanwhile, tumors with diameters more than 5 cm had a higher ROR1-AS1 expression than those less than 5 cm. After transfection with ROR1-AS1 overexpression plasmid, the cell proliferation ability was enhanced, the G0/G1 phase time of cell cycle was shortened, and the apoptosis was suppressed. However, the opposite result was observed after ROR1-AS1 was downregulated. Furthermore, RIP showed that ROR1-AS1 can bind to enhancer of zeste homolog 2 (EZH2) and inhibit the expression of DUSP5, and thus be engaged in the proliferation and apoptosis of colon cancer cells. CONCLUSIONS: ROR1-AS1 is highly expressed either in colon cancer tissues or in cell lines, which is able to enhance cell proliferation, accelerate cell cycle, and inhibit cell apoptosis. The mechanism of ROR1-AS1 to participate in the development of colon cancer may be the downregulation of DUSP5 via combination with EZH2.

Cost-effectiveness analysis of capecitabine plus bevacizumab versus capecitabine alone in elderly patients with previously untreated metastatic colorectal cancer from Chinese societal perspective.

PURPOSE: The aim of the study was to evaluate the cost-effectiveness of capecitabine plus bevacizumab compared with capecitabine alone in elderly patients with metastatic colorectal cancer (CRC) from a Chinese societal perspective. METHODS: A decision-analytic Markov model was conducted to simulate the process of metastatic CRC. Three distinct health states: progression-free survival (PFS), progressive disease and death were included. Clinical data were derived from the AVEX trial. Health effectiveness was denoted in quality-adjusted life years (QALYs) and health utilities were derived from previously published studies. Incremental cost-effectiveness ratio (ICER) was regarded as the primary endpoint and willingness-to-pay (WTP) threshold was set at $26,753.37/QALY (3 × per capita GDP of China, 2017). One-way sensitivity analyses and probabilistic sensitivity analysis were also performed to explore the parameters uncertainty in the study. RESULTS: Over a 10-year life horizon, capecitabine plus bevacizumab gained 1.14 QALYs at an average cost of $21,609.48, while the effectiveness and cost of capecitabine group were 0.99 QALYs and $7274.83, respectively. The ICER between the two groups was $95,564.33/QALY. Parameters that mostly influenced the results of the model were utility of PFS state, duration of PFS state for capecitabine plus bevacizumab, total cost of PFS state for capecitabine plus bevacizumab and price of bevacizumab. The probabilities of capecitabine plus bevacizumab and capecitabine as the dominant option were 0% and 100% at the WTP threshold of $26,753.37/QALY. CONCLUSIONS: The results of the study showed that capecitabine plus bevacizumab is unlikely to be a cost-effective treatment option for elderly patients with metastatic CRC.

LINC01605 promotes the proliferation of laryngeal squamous cell carcinoma through targeting miR-493-3p.

OBJECTIVE: The purpose of this study was to elucidate the potential influence of LINC01605 on the progression of laryngeal squamous cell carcinoma (LSCC) and the underlying mechanism. PATIENTS AND METHODS: LINC01605 and microRNA-493-3p (miR-493-3p) levels in normal laryngeal tissues, LSCC tissues, and paired paracancerous tissues were detected. Regulatory effects of LINC01605 on proliferative ability and apoptosis in HEp-2 and AMC-HN-8 cells were assessed. Besides, the interaction between LINC01605 and miR-493-3p was evaluated by Dual-Luciferase reporter gene assay and Spearman's rank correlation analysis. Finally, rescue experiments were conducted to clarify the role of LINC01605/miR-493-3p axis in the progression of LSCC. RESULTS: LINC01605 was upregulated and miR-493-3p was downregulated in LSCC tissues. Knockdown of LINC01605 inhibited proliferative ability, and stimulated apoptosis in HEp-2 and AMC-HN-8 cells. Moreover, LINC01605 directly bound to miR-493-3p, and the former negatively regulated the level of the latter. In addition, miR-493-3p was able to reverse the regulatory effect of LINC01605 on proliferative ability in LSCC. CONCLUSIONS: LINC01605 is upregulated in LSCC tissues, and it promotes the malignant progression of LSCC via targeting miR-493-3p.

Meta-analysis of the association between primary tumour location and prognosis after surgical resection of colorectal liver metastases.

BACKGROUND: Primary tumour location is emerging as an important prognostic factor in localized and metastatic colorectal cancers. However, its prognostic role in colorectal liver metastasis (CRLM) after hepatectomy remains controversial. A systematic review and meta-analysis was undertaken to evaluate its prognostic value. METHODS: References were identified through searches of PubMed, Embase, Web of Science and the Cochrane Library comparing overall or disease-free survival after hepatic resection between patients with CRLM originating from right- or left-sided colorectal cancers. Data were pooled using hazard ratios (HRs) and 95 per cent confidence intervals according to a random-effects model. Meta-regression and subgroup analyses were conducted to assess the effect of underlying confounding factors on HR estimates and to adjust for this. RESULTS: The final analysis included 21 953 patients from 45 study cohorts. Compared with left-sided primary tumour location, right-sided location was associated with worse overall survival (HR 1·39, 95 per cent c.i. 1·28 to 1·51; P < 0·001; prediction interval 1·00 to 1·93), and also tended to have a negative impact on disease-free survival (HR 1·18, 1·06 to 1·32; P = 0·004; prediction interval 0·79 to 1·75). Subgroup analysis showed that the negative effect of right-sided primary tumour location on overall survival was more prominent in the non-Asian population (HR 1·47, 1·33 to 1·62) than the Asian population (HR 1·18, 1·05 to 1·32) (P for interaction <0·01). CONCLUSION: This study demonstrated a prognostic role for primary tumour location in patients with CRLM receiving hepatectomy, especially regarding overall survival. Adding primary tumour location may provide important optimization of prognosis prediction models for CRLM in current use.

ANTECEDENTES: La ubicación del tumor primario (primary tumor location, PTL) ha surgido como un factor pronóstico importante en los cánceres colorrectales (colorectal cancers, CRCs) localizados y metastásicos. Sin embargo, todavía se discute su relevancia como factor pronóstico tras la resección de metástasis hepáticas de cáncer colorrectal (colorectal liver metastases, CRLM). Se realizó una revisión sistemática y un metaanálisis para determinar su valor pronóstico. MÉTODOS: En PubMed, EMBASE, Web of Science y la Biblioteca Cochrane se identificaron los trabajos que compararon la supervivencia global (overall survival, OS) y la supervivencia libre de enfermedad (disease-free survival, DFS) tras la resección hepática de CRLM cuyo CRCs estuviese situado en el lado derecho o izquierdo. Los datos se expresaron en forma del cociente de riesgos instantáneos (hazard ratio, HR) e intervalos de confianza del 95% (i.c. del 95%) de acuerdo con un modelo de efectos aleatorios. Se efectuaron análisis de metarregresión y de subgrupos para evaluar el efecto de los factors de confusión existentes en las estimaciones de HR, ajustando por los mismos. RESULTADOS: El análisis final incluyó 21.953 pacientes de cohortes de 45 estudios. La PTL en el lado derecho en comparación con el lado izquierdo se asoció con una peor supervivencia global (HR 1,39; i.c. del 95% 1,28-1,51; P < 0,001; intervalo de predicción 1,00-1,93) y una tendencia a un impacto negativo en la DFS (HR 1,18; i.c. del 95% 1,06-1,32; P = 0,004; intervalo de predicción 0,79-1,75). El análisis de subgrupos mostró que el efecto negativo de la PTL del lado derecho en la OS fue más prominente en la población no asiática (HR 1,47; i.c. del 95% 1,33-1,62) que en la asiática (HR 1,18; i.c. del 95% 1,05-1,32; Pinteracción < 0,01). CONCLUSIÓN: Este estudio demostró que la PTL tiene un papel pronóstico tras la hepatectomía de las CRLM, especialmente respecto a la OS. La adición de la PTL proporcionaría una optimización importante en los modelos actuales de predicción pronóstica de CRLM.

The efficacy of simendan in the treatment of acute heart failure and its impact on NT-proBNP.

OBJECTIVE: Simendan is a calcium sensitizer that enhances myocardial contractility but does not affect ventricular diastole. Simendan also has a vasodilatation effect, which causes coronary artery resistance and venous volume blood vessel relax, thereby improving coronary blood supply. This study adopted simendan on the basis of conventional anti-heart failure treatment to explore a new approach for the treatment of heart failure. PATIENTS AND METHODS: Eighty patients with heart failure were randomly and equally divided into an observation group and control group according to the digital table method. The control group was given a conventional anti-heart failure treatment. The observation group was treated with simendan on the basis of the control group. The left ventricular ejection fraction (LEVF), stroke volume (SV), NT-proBNP, K+, and Ca2+ were measured before and after the treatment. The clinical efficacy and adverse reactions after treatment were compared. The 6-minute walking distance (6MWT) was recorded on the 60th day after treatment. RESULTS: There were no significant differences in LVEF and SV between the two groups before the treatment. They were significantly increased after treatment and were significantly higher in the observation group than that in the control group (p < 0.05). The total effective rate in the observation group (92.50%) was significantly higher than that in the control group (67.50%). There was no statistical difference in the occurrence of adverse reactions between the two groups (p > 0.05). The 6MWT in the observation group was 452.63±86.51 meters, which was significantly higher than that in the control group (366.85±70.46 meters) (p < 0.05). There was no significant difference in plasma NT-proBNP levels between the two groups (p > 0.05). The plasma NT-proBNP level was significantly lower in the observation group than that in the control group after treatment (p < 0.05). Serum K+ and Ca2+ were not significantly changed after treatment in the control group (p > 0.05). Serum K+, but not Ca2+, was significantly elevated in the observation group. CONCLUSIONS: Simendan can significantly reduce plasma NT-proBNP level; thus, it is relatively safe and effective for the treatment of acute heart failure (AHF).

The JAK2/STAT3 signaling pathway is required for inflammation and cell death induced by cerulein in AR42J cells.

OBJECTIVE: The study was designed to investigate the JAK2/STAT3 signaling pathway in pancreatitis and its association with inflammation and cell death to provide a potential treatment method for pancreatitis. MATERIALS AND METHODS: The rat pancreatic acinar AR42J cells were used for the study, and they were transfected with JAK2 and STAT3 siRNAs to mimic knockdown condition. Cerulein was used to treat AR42J cells. Western blot and ELISA were employed to detect the expression of related proteins. Flow cytometry was done to analysis the necrosis of AR42J cells. RESULTS: In this study, we found that cell death and the secretion of IL-6 and TGF-ß1 were significantly increased, and the JAK2/STAT3 signaling pathway was activated in cerulein-induced AP. To determine the role of JAK2 and STAT3, JAK2 siRNA and STAT3 siRNA were used to block JAK2 and STAT3, respectively. The levels of IL-6 and TGF-ß1 levels in the medium were lower in JAK2 siRNA and STAT3 siRNA-treated cells compared with controls. Flow cytometry analysis showed that the level of cell death, expression of cleaved caspase-3, and the release of LDH were decreased following JAK2 siRNA and STAT3 siRNA treatment. CONCLUSIONS: These findings point to a novel role for the JAK2/STAT3 signaling pathway in the progression of cerulein-induced AP.

Cytochrome C suppresses renal accumulation and nephrotoxicity of polymyxin B.

The receptor megalin plays an important role in the accumulation of polymyxin B (PMB) in renal cells in vitro. This study aimed to examine the effects of cytochrome c (cyto c), a typical megalin ligand, on renal accumulation and nephrotoxicity of PMB in vivo. Thirty Sprague-Dawley rats were randomly divided into the vehicle control group, PMB group, PMB + cyto c 50, 100, or 200 mg/kg group, respectively, and were treated with intravenous cyto c 30 min before the administration of PMB 4.0 mg/kg once a day for consecutive 5 days. On the 4th day after administration, 24 h urine was collected to determine N-acetyl-ß-D-glucosaminidase excretion. Six hours after the last injection on the 5th day, kidneys were harvested to assay PMB concentration and observe pathological alterations, and blood samples were collected to assay serum creatinine (SCr), blood urea nitrogen (BUN), and blood ß2-microglobulin (ß2-MG) levels. Cyto c 50, 100, and 200 mg/kg decreased the accumulation of PMB in the kidney by 18.5%, 39.1% ( p < 0.01), and 36.8% ( p < 0.01), respectively, and reduced 24 h N-acetyl-ß-D- glucosaminidase excretion by 22.5% ( p < 0.05), 40.4% ( p < 0.01), and 40.4% ( p < 0.01), respectively. Kidney pathological damage induced by PMB was markedly reduced by cyto c 100 mg/kg and 200 mg/kg. However, there were no significant differences in SCr, BUN, and blood ß2-MG levels among the groups. These results indicated that cyto c may inhibit the renal accumulation and nephrotoxicity of PMB in a rat model, further proving the role of megalin in the accumulation of PMB.

TGF-ß1 promotes proliferation and invasion of hepatocellular carcinoma cell line HepG2 by activating GLI-1 signaling.

OBJECTIVE: To investigate the role of GLI-1 signaling pathway on TGF-ß1 induced proliferation and invasion in hepatocellular carcinoma (HCC) cell line HepG2. MATERIALS AND METHODS: Cultured HepG2 cells were treated with various concentration of TGF-ß1 for 24 h and the effect of TGF-ß1 on invasion ability of HepG2 was detected with transwell assay. Next, cultured HepG2 cells were treated with various concentration of TGF-ß1 for 12, 24 and 48 h; then, the proliferation rate was detected by MTT. The mRNA and protein expression levels of GLI-1 were detected by RT-PCR and Western blot. Furthermore, GLI-1 siRNA was used to investigate the role of GLI-1 on TGF-ß1 induced proliferation and invasion. RESULTS: The results demonstrated that TGF-ß1 could promote HepG2 cells proliferation and invasion. The mRNA and protein level of GLI-1 were upregulated by TGF-ß1 treatment, whereas GLI-1 siRNA could block these processes. CONCLUSIONS: TGF-ß1 promotes HCC cell line HepG2 proliferation and invasion by activating GLI-1 signaling pathway.

TGF-ß1 upregulates the expression of lncRNA UCA1 and its downstream HXK2 to promote the growth of hepatocellular carcinoma.

OBJECTIVE: TGF-ß1 plays pivotal roles in the development of various malignancies such as hepatocellular carcinoma, while the mechanism of the TGF-ß1 function in hepatocellular carcinoma remains unclear. Our study aimed to investigate the molecular mechanisms of the TGF-ß1 function in hepatocellular carcinoma. PATIENTS AND METHODS: Tumor tissues and adjacent healthy tissues were collected from hepatocellular carcinoma. Blood samples were collected from both hepatocellular carcinoma patients and healthy controls. Expression of TGF-ß1, long non-coding RNA (lncRNA) UCA1 and hexokinase 2 (HXK2) in those tissues was detected by qRT-PCR. All patients were followed up for 5 years, and prognostic values of serum HOTAIR for hepatocellular carcinoma were investigated by survival curve analysis. TGF-ß1, UCA1, and HXK2 overexpression hepatocellular carcinoma cell lines were established, and the effects on cell proliferation were detected by the CCK-8 assay. Interactions between TGF-ß1, UCA1, and HXK2 were explored by Western blot. Effects of TGF-ß1 on lactate production, glucose uptake, and ATP production were detected by lactate assay, glucose uptake assay, and ATP assay. RESULTS: TGF-ß1, UCA1, and HXK2 expression levels were upregulated in tumor tissues comparing with adjacent healthy tissues. Serum levels of TGF-ß1, UCA1, and HXK2 increased with the increases of primary tumor stage. Patients that have high serum levels of TGF-ß1, UCA1, and HXK2 showed lower overall survival rate compared with patients with low serum levels of TGF-ß1, UCA1, and HXK2. TGF-ß1, UCA1, and HXK2 overexpression promoted proliferation of hepatocellular carcinoma cell. TGF-ß1 is a positive upstream regulator of UCA1, which is a positive upstream regulator of HXK2. TGF-ß1 overexpression increased lactate production, glucose uptake and ATP production in hepatocellular carcinoma. CONCLUSIONS: TGF-ß1 may accelerate cancer cell energy metabolism to promote the growth of hepatocellular carcinoma by upregulating UCA1 and its downstream HXK2.

Comparison of total curative effect between total hip arthroplasty and hip arthrodesis in treating coxotuberculosis.

OBJECTIVE: The purpose of this study was to investigate the clinical effect of total hip arthroplasty (THA) and hip arthrodesis (HA) in treating coxotuberculosis. PATIENTS AND METHODS: 40 patients with coxotuberculosis treated in the Orthopedic Department in our hospital from February 2011 to February 2016 were retrospectively analyzed. Comparison of total curative effect between THA and HA in treating coxotuberculosis was analyzed. The operation time, intraoperative blood loss, postoperative drainage volume, visual analogue scale (VAS) score, Harris hip function score (HHS), erythrocyte sedimentation rate (ESR), C reactive protein, postoperative hip pain time (PHPT), postoperative start walking time(PSWT), postoperative start weight bearing time(PSWBT) and postoperative complications were observed and compared. RESULTS: All patients successfully underwent successful THA or HA without major complications. The operation time, intraoperative blood loss and postoperative drainage volume in patients who underwent HA were better than those of patients who underwent THA (p<0.001, p=0.010, p<0.001, respectively). During the postoperative evaluation, VAS, HHS, ESR, CRP in patients who underwent THA were better than those of patients who underwent HA, and the differences were statistically significant. About the recovery, PHPT, PSWT, PSWBT in patients who underwent THA were shorter than those in patients who underwent HA (p=0.021, p=0.044, p<0.001, respectively). There was no fracture, infection, dislocation, neurological or vascular complications in THA group. No patient had subsidence, loosening or heterotopic ossification. 1 patient in HA group had a fracture of the steel plate, and 1 patient had delayed union in HA group. CONCLUSIONS: THA is an effective treatment for advanced tuberculous arthritis. THA is superior to HA in the treatment of coxotuberculosis.

Research on correlation between GALNT3 gene and osteoporosis.

OBJECTIVE: The aim of this study was to explore the correlation between GALNT3 gene and osteoporosis. PATIENTS AND METHODS: In this study, 184 cases of osteoporosis that were treated at our hospital from 2013 to 2014 were selected as research subjects in the observation group. In addition, 84 healthy people were selected as the control group from 2013 to 2014. The bone mineral density of the observation and control groups were detected by x-rays and the expression levels and differences of mRNA of the GALNT3 gene and protein in their body was detected using fluorescence quantitative polymerase chain reaction (qPCR), enzyme-linked immunoassay, and Western blotting. RESULTS: X-ray results suggest that when compared to the healthy group, bone mineral density of patients in the observation group was significantly lower than that of research subjects in the control group, with significant differences. The fluorescence qPCR results suggest that the expression levels of mRNA of the GALNT3 gene in patients with osteoporosis were significantly lower than that in the healthy group (p<0.05). Enzyme-linked immunosorbent assay (ELISA) results suggest that the expression levels of the GALNT3 gene in patients with osteoporosis (1.26±0.32) µg/L was significantly lower than that in the healthy group (12.41±0.28) µg/L, with significant differences (p<0.05). The Western blotting results agreed with the ELISA results. We also found in our research that the bone mineral density of patients with osteoporosis significantly correlated with the expression levels of the GALNT3 gene (r=0.95). CONCLUSIONS: Therefore, the GALNT3 gene significantly correlated with osteoporosis and the low expression of GALNT3 gene can promote the occurrence and deterioration of osteoporosis.

G-quadruplex antibody attenuates human gastric cancer cell proliferation and promotes apoptosis through hTERT/telomerase pathway.

OBJECTIVE: To investigate the expression of G-quadruplex antibody BG4 in human gastric cancer AGS cells and assess its functions in attenuating proliferation and promoting apoptosis in gastric cancer. MATERIALS AND METHODS: BG4 high-expression gastric cancer AGS cell line was established by pEGFP-N1-BG4 transient transfection. AGS cells transfected with pEGFP-N1 plasmids were included into the pEGFP-N1 group and those not transfected with plasmids were included into the negative control group. Cell counting kit-8 (CCK8) assay was performed to examine the AGS cell proliferation ability, while flow cytometry was used to detect the cell cycle distribution and cell apoptosis. Cell migration was measured using Transwell migration and wound healing assay. Then the expression levels of cell apoptosis associated factors were determined. The mRNA and protein expressions of human telomerase reverse transcriptase (hTERT), B-cell lymphoma 2 (Bcl-2), Bcl-2 associated X (Bax) were examined with real-time quantitative polymerase chain reaction (PCR) and Western blotting, respectively. RESULTS: The results revealed that pEGFP-N1-BG4 group exhibited reduced proliferation and migration, induction of apoptosis. hTERT and Bcl-2 mRNA and protein levels in pEGFP-N1-BG4 group were down-regulated compared with those in the pEGFP-N1 group and control group, but there were no significant differences in Bax mRNA and protein levels compared with those in the pEGFP-N1 group and control group. CONCLUSIONS: We showed that the expression of BG4 in the gastric cancer cell line AGS inhibits cell proliferation and promotes apoptosis though inducing telomere to form G-quadruplex structure and attenuating telomerase activity, thus resulting in reduced expression of hTERT and Bcl-2.

Ptprj-as1 mediates inflammatory injury after intracerebral hemorrhage by activating NF-κB pathway.

OBJECTIVE: We aimed at investigating the expression of long non-coding RNA (lncRNA) Ptprj-as1 and the role of lncRNAPtprj-as1 in inflammatory cells after intracerebral hemorrhage and its potential mechanism. MATERIALS AND METHODS: The rat model of intracerebral hemorrhage was established. Expressions of Ptprj-as1 and inflammatory cytokines in inflammatory cells were detected by quantitative Real-time PCR (qRT-PCR). After BV2 cells were transfected with lentivirus, cell proliferation, migrative ability and apoptosis were detected by cell counting kit-8 (CCK-8) assay, transwell chamber and flow cytometry, respectively. Immunofluorescence was used to explore the ratio of M1 and M2 glial cells. The detection of tumor necrosis factor alpha (TNF-α) expression was performed using enzyme-linked immunosorbent assay (ELISA). Moreover, the expressions of key genes in NF-κB pathway were evaluated using Western blot. RESULTS: Ptprj-as1 was highly expressed in inflammatory tissues caused by intracerebral hemorrhage (ICH). Overexpressed Ptprj-as1 promoted the migration of BV2 cells and expression levels of inflammatory cytokines such as TNF-α, interleukin-1ß (IL-1ß), interleukin-6 (IL-6), iNOS and NO. Meanwhile, Ptprj-as1 enhanced the proportion of M1 glial cells, the mechanism of which might be related to the activation of NF-κB pathway. CONCLUSIONS: Ptprj-as1 activates NF-κB pathway in microglia and promotes the secretion of inflammatory cytokines, which is involved in inflammatory injury caused by intracerebral hemorrhage.