Pharmacological Inhibition or Silencing of TREM1 Restrains HCC Cell Metastasis by Inactivating TLR/PI3K/AKT Signaling.

Hepatocellular carcinoma (HCC), a widely prevalent malignancy strongly linked to inflammation, remains a significant public health concern. Triggering receptor expressed on myeloid cells 1 (TREM1), a modulator of inflammatory responses identified in recent years, has emerged as a crucial facilitator in cancer progression. Despite its significance, the precise regulatory mechanism of TREM1 in HCC metastasis remains unanswered. In the present investigation, we observed aberrant upregulation of TREM1 in HCC tissues, which was significantly linked to poorer overall survival. Inhibition of TREM1 expression resulted in a significant reduction in HCC Huh-7 and MHCC-97H cell proliferation, invasion, and epithelial-mesenchymal transition (EMT) process. Furthermore, inhibiting TREM1 decreased protein expressions of toll-like receptor 2/4 (TLR2/4) and major myeloid differentiation response gene 88 (MyD88), leading to the inactivation of phosphatidylinositol 3-kinase (PI3K) and protein kinase B (AKT) in HCC cells. Notably, these effects were reversed by treatment with TLR2-specific agonist (CU-T12-9), indicating a potential crosstalk between TREM1 and TLR2/4. Mechanistic studies revealed a direct interaction between TREM1 and both TLR2 and TLR4. In vivo studies demonstrated that inhibition of TREM1 suppressed the growth of HCC cells in the orthotopic implant model and its metastatic potential in the experimental lung metastasis model. Overall, our findings underscore the role of TREM1 inhibition in regulating EMT and metastasis of HCC cells by inactivating the TLR/PI3K/AKT signaling pathway, thereby providing deeper mechanistic insights into how TREM1 regulates metastasis during HCC progression.

Demystify esophageal submucosal tumor: angiomas.

A 51-year-old man presented to the gastroenterology department with a history of abdominal discomfort. Computed tomography was unremarkable. Upper gastrointestinal endoscopy showed a submucosal mass lesion at the esophagus, with a 36cm distance from the incisors. The esophageal submucosal mass lesion with mixed echo was confirmed by endoscopic ultrasound (EUS). Endoscopic submucosal dissection (ESD) was performed, and the mass lesion was resected in a whole piece. Histopathological examination showed lymphatic and blood vessels, which demonstrated an esophageal vascular tumor. Further immunohistochemistry revealed tumor cells that stained positive for CD34 and D2-40.

Forecasting oil consumption with attention-based IndRNN optimized by adaptive differential evolution.

Accurate prediction of oil consumption plays a dominant role in oil supply chain management. However, because of the effects of the coronavirus disease 2019 (COVID-19) pandemic, oil consumption has exhibited an uncertain and volatile trend, which leads to a huge challenge to accurate predictions. The rapid development of the Internet provides countless online information (e.g., online news) that can benefit predict oil consumption. This study adopts a novel news-based oil consumption prediction methodology-convolutional neural network (CNN) to fetch online news information automatically, thereby illustrating the contribution of text features for oil consumption prediction. This study also proposes a new approach called attention-based JADE-IndRNN that combines adaptive differential evolution (adaptive differential evolution with optional external archive, JADE) with an attention-based independent recurrent neural network (IndRNN) to forecast monthly oil consumption. Experimental results further indicate that the proposed news-based oil consumption prediction methodology improves on the traditional techniques without online oil news significantly, as the news might contain some explanations of the relevant confinement or reopen policies during the COVID-19 period.

Solute Carrier Family 35 Member F2 Regulates Cisplatin Resistance and Promotes Malignant Progression of Pancreatic Cancer by Regulating RNA Binding Motif Protein 14.

We aimed to explore the role of Solute Carrier Family 35 Member F2 (SLC35F2) in pancreatic cancer (PCa) and to further study whether SLC35F2 regulates cisplatin resistance of PCa cells through the modulation of RNA binding motif protein 14 (RBM14) expression. SLC35F2 expression in 60 pairs of PCa tissues and adjacent ones was studied by RT-PCR analysis. Meanwhile, SLC35F2 expression levels in PCa cell lines were also evaluated by qPCR assay. In addition, SLC35F2 knockdown models were constructed in PCa cisplatin-resistant cells. Furthermore, we determined the interaction between SLC35F2 and RBM14 via luciferase assay. The findings of the present study demonstrated that SLC35F2 was significantly upregulated in PCa tissues. High level of SLC35F2 indicated higher incidence of metastasis and shorter survival rates. In vitro cell experiments revealed that knockdown of SLC35F2 suppressed cell invasion and metastasis capacity of cisplatin-resistant PCa cell lines PANC-1/DDP and CFPAC-1/DDP. It was also suggested that the key protein RBM14 in the SLC35F2 knockdown group was remarkably reduced. SLC35F2 can bind to RBM14 specifically. Overexpression of RBM14 partially reversed the effects of knockdown of SLC35F2 on the development of PCa. SLC35F2 expression in PCa tissues and cell lines is remarkably increased. In addition, it was also suggested that SLC35F2 may regulate cisplatin resistance of PCa cells through modulating RBM14 expression. In conclusion, it is conceivable from the study that SLC35F2 was remarkably upregulated in PCa and promoted the malignancy of PCa via regulating RBM14.

Interferon regulatory factor 5­induced upregulation of zinc­finger protein 217 promotes pancreatic carcinoma progression.

The aim of the present study was to investigate the molecular mechanisms of zinc­finger protein 217 (ZNF217) in pancreatic carcinoma (PC) progression. ZNF217­associated expression and survival data from patients with PC were retrieved from the Gene Expression Profiling Interactive Analysis server. The mRNA expression level of ZNF217 was detected by reverse transcription­quantitative PCR. Cell Counting Kit­8, colony formation, wound­healing and Transwell assays were conducted to assess cellular proliferation, migratory and invasive abilities. Proliferation was also examined by immunofluorescence detection of Ki67 expression, and chromatin immunoprecipitation (ChIP) and luciferase reporter assays were performed to detect the interaction between ZNF217 and interferon regulatory factor 5 (IRF5). ZNF217 was found to be significantly upregulated in tumor tissues and cancer cell lines, which was associated with a poor survival rate in patients with PC. ZNF217 silencing markedly suppressed cellular proliferation and migratory and invasive abilities, as well as decreased the expression of Ki67. IRF5 was also upregulated in PC tumor tissues and was shown to positively regulate the activity of the ZNF217 promoter and its mRNA expression levels. Furthermore, ChIP assays demonstrated that IRF5 bound to the promoter region of ZNF217 in vitro. In conclusion, ZNF217 silencing exerted notable inhibitory effects on the progression of PC. Thus, ZNF217 may serve as a potential target for developing novel therapeutic strategies for PC.

ASPM facilitates colorectal cancer cells migration and invasion by enhancing ß-catenin expression and nuclear translocation.

Increased abnormal spindle-like microcephaly (ASPM) expression has been linked to clinical stage and poor prognosis in cancers, but the molecular mechanisms by which ASPM promotes cell metastasis in colorectal cancer (CRC) has not been identified. This study showed that the abilities of cell migration, invasion, and epithelial-mesenchymal transition (EMT) were attenuated in ASPM-deficient CRC cell lines. Furthermore, we reported that attenuation of ASPM expression inhibited CRC cell metastasis in vivo. Additionally, the expression of ASPM was positively correlated with ß-catenin level in CRC tissues. Mechanistically, ASPM can upregulate ß-catenin transcription by stimulating the ß-catenin promoter and enhancing the nuclear translocation of ß-catenin in CRC cells, which leads to the activation of the Wnt/ß-catenin pathway. Finally, we showed that ASPM effectively induced CRC cell migration and invasion in a ß-catenin-dependent manner.

Clinical study of submucosal tunneling endoscopic resection and endoscopic submucosal dissection in the treatment of submucosal tumor originating from the muscularis propria layer of the esophagus.

Herein, we aimed to evaluate the clinical value and safety of transendoscopic submucosal tunnel tumor resection (STER) and endoscopic submucosal dissection (ESD) for the resection of esophageal submucosal intrinsic muscle tumors. We retrospectively analyzed the clinical data of 68 patients with esophageal submucosal intrinsic muscle tumors treated with STER (STER group, n = 38, March 2018 to January 2020) or ESD (ESD group, n = 30, January 2017 to January 2020) at the First People's Hospital of Lianyungang to compare the treatment efficacy, hospitalization time and costs, and postoperative complications between the 2 groups. All 68 cases were of single lesions. The mean operative duration was shorter in the STER group (53.39 ±â€…11.57 min) than in the ESD group (68.33 ±â€…18.52 min, P < .05). The postoperative hospital stay duration was significantly shorter in the STER group (5.86 ±â€…1.01 days; P < .05) than in the ESD group (8.2 ±â€…3.4 days, P < .05). The mean hospitalization cost was significantly lower in the STER group than in the ESD group (12,468.8 + 4966.8 yuan vs 17,033.3 ±â€…4547.2 yuan; P < .05). Only 1 case of intraoperative perforation occurred in ESD group. There were no other complications in both groups. The wound healed in both groups, and no residual or recurrent tumors were detected during the follow-up period. Both STER and ESD can be used for the treatment of esophageal intrinsic muscular layer (MP) tumors, and STER is safer and more efficient for lesions with a diameter <3.5 cm.

Mechanism of methyltransferase like 3 in epithelial-mesenchymal transition process, invasion, and metastasis in esophageal cancer.

Methyltransferase like 3 (METTL3) has been identified to serve as a definitive inducer in cancer progression. This study sought to analyze the regulatory mechanism of METTL3 in epithelial-mesenchymal transition (EMT), invasion, and metastasis in esophageal cancer (ESCA). The METTL3 expressions in cancer tissues and cells were detected with extensive analysis of its correlation with clinical baseline data. The cells were transfected with sh-RNA-METTL3 and microRNA (miR)-20a-5p mimic, followed by evaluation of invasion, migration, and EMT. The N6-methyladenosine (m6A) level and enrichment of DiGeorge Critical Region 8 (DGCR8) and m6A were observed. The binding relationship between miR-20a-5p and Nuclear Factor I-C (NFIC) was verified, followed by Pearson correlation analysis. A subcutaneous tumor formation assay was conducted prior to observation of lung metastases. Our results revealed that METTL3 was highly expressed in ESCA patients and associated with severe lymph node involvement and distant metastasis. METTL3 downregulation radically inhibited the invasiveness, migration, and EMT. METTL3 elevated the miR-20a-5p expression via improving m6A modification. METTL3 inhibition downregulated the miR-20a-5p expression. Moreover, miR-20a-5p upregulation facilitated ESCA cell invasiveness and migration by targeting NFIC transcription. METTL3 inhibition suppressed tumor growth and lung metastasis in vivo. Overall, METTL3 promoted m6A modification and the binding of DGCR8 to miR-20a-5p to further elevate the miR-20a-5p expression and inhibit NFIC transcription, thus promoting EMT, invasion and migration.

MiR-200b Suppresses Gastric Cancer Cell Migration and Invasion by Inhibiting NRG1 through ERBB2/ERBB3 Signaling.

PURPOSE: Accumulating evidence indicates that miRNAs (miRs) play crucial roles in the modulation of tumors development. However, the accurately mechanisms have not been entirely clarified. In this study, we aimed to explore the role of miR-200b in the development of gastric cancer (GC). METHODS: Western blot and RT-PCR were applied to detect epithelial-mesenchymal transition (EMT) marker expression and mRNA expression. Transwell assay was used for measuring the metastasis and invasiveness of GC cells. TargetScan system, luciferase reporter assay, and rescue experiments were applied for validating the direct target of miR-200b. RESULTS: MiR-200b was prominently decreased in GC tissues and cells, and its downregulation was an indicator of poor prognosis of GC patients. Reexpression of miR-200b suppressed EMT along with GC cell migration and invasion. Neuregulin 1 (NRG1) was validated as the target of miR-200b, and it rescued miR-200b inhibitory effect on GC progression. In GC tissues, the correlation of miR-200b with NRG1 was inverse. CONCLUSION: MiR-200b suppressed EMT-related migration and invasion of GC through the ERBB2/ERBB3 signaling pathway via targeting NRG1.

LCN2 Mediated by IL-17 Affects the Proliferation, Migration, Invasion and Cell Cycle of Gastric Cancer Cells by Targeting SLPI.

INTRODUCTION: Gastric cancer occurred in China and even the whole East Asia with high incidence. The objective of this study was to investigate the role of IL-17 in gastric cancer cells mediated by LCN2 binding to SLPI. METHODS: The expression of LCN2 and SPLI in gastric cancer cells and transfection effects were confirmed by RT-qPCR analysis. The proliferation, clone formation ability, invasion, migration, apoptosis, and cell cycle of gastric cancer cells were in turn detected by CCK-8 assay, clone formation assay, transwell assay, wound healing assay, and flow cytometry analysis. The combination between LCN2 and SLPI was determined by co-immunoprecipitation assay. The expression of Caspase-3, Bcl-2, cyclinB1, cyclinD1, MMP9, and SLPI in gastric cancer cells was detected by Western blot analysis. RESULTS: LCN2 and SPLI exhibited the highest levels in AGS cells, and thus AGS cells were selected for the next experiments. Down-regulation of LCN2 suppressed the proliferation and clone formation ability of AGS cells treated with IL-17. IL-17 promoted the invasion and migration of AGS cells, which was partially reversed by the down-regulation of LCN2. Down-regulation of LCN2 mediated by IL-17 promoted apoptosis and suppressed the cell cycle of AGS cells. DISCUSSION: Down-regulation of LCN2 mediated by IL-17 suppressed the proliferation and suppressed the migration and invasion and cell cycle of gastric cancer cells by targeting SLPI.

LINC00662 promotes cell viability and metastasis in esophageal squamous cell carcinoma by sponging miR-340-5p and upregulating HOXB2.

BACKGROUND: Previous studies have shown that lncRNA LINC00662 plays an important role in pathogenesis of malignancies. The purpose of this study was to elucidate the regulatory mechanism of LINC00662 in esophageal squamous cell carcinoma (ESCC). METHODS: In this study, the regulatory mechanism of LINC00662 was investigated by RT-qPCR. MTT, transwell and dual luciferase reporter assays. RESULTS: Upregulation of LINC00662 was found in ESCC and associated with worse clinical outcomes in ESCC patients. More importantly, knockdown of LINC00662 restrained cell proliferation, migration and invasion in ESCC. In addition, LINC00662 acts as a molecular sponge for miR-340-5p in ESCC, and miR-340-5p directly targets HOXB2. HOXB2 expression can be positively regulated by LINC00662 in ESCC. Furthermore, HOXB2 downregulation or miR-340-5p overexpression weakened the carcinogenesis of LINC00662 in ESCC. CONCLUSIONS: LncRNA LINC00662 promotes the progression of ESCC by upregulating HOXB2 by sponging miR-340-5p.

Association between the miR-146a Polymorphisms and the Risk of Gastric Cancer: a Meta-Analysis.

BACKGROUND: Published data regarding associations between the microRNA-146a polymorphism and the risk of gastric cancer are inconclusive. This study aims at evaluating the genetic risk of microRNA-146a polymorphism in gastric cancer. METHODS: A systematic literature search was carried out in Pubmed, Medline (Ovid), Embase, CBM, CNKI, Weipu, and Wanfang databases, covering all available publications (last search was performed on Apr 15th, 2019). Statistical analysis was performed using Revman 5.2 and STATA 10.1 software. RESULTS: A total of 5,017 cases and 4,869 controls in 14 case-control studies were included in this meta-analysis. No significant association between microRNA-146a polymorphism and gastric cancer risk was observed in all kinds of genetic models (homozygote genetic model CC vs. GG: OR = 0.96, 95% CI = 0.81 - 1.15, p = 0.66; the heterozygote genetic model CG vs. GG: OR = 0.94, 95% CI = 0.86 - 1.02, p = 0.15; the recessive genetic model CC vs. CG + GG: OR = 0.98, 95% CI = 0.91 - 1.05; the dominant genetic model CC + CG vs. GG: OR = 0.94, 95% CI = 0.86 - 1.01, p = 0.1, p = 0.55; and the allele genetic model C vs. G: OR = 0.98, 95% CI = 0.89 - 1.06, p = 0.58). In subgroup analysis, the C allele may be a protective factor for gastric cancer development in the analysis of the dominant genetic model (CC + CG vs. GG) in HCC studies (OR = 0.90, 95% CI = 0.83 - 0.98, p = 0.02) but a risk factor in Japanese when calculated with the recessive genetic model (CC vs. CG + GG) (OR = 1.19, 95% CI = 1.02 - 1.40, p = 0.03). CONCLUSIONS: Based on our meta-analysis, the microRNA-146a polymorphism is unlikely to be a risk factor for gastric cancer in overall population.

Role of gastroscopic biopsy of gastric ulcer margins and healed sites in the diagnosis of early gastric cancer: A clinical controlled study of 513 cases.

The present case study aimed to evaluate the effect of gastroscopic biopsy of gastric ulcer margins and healed sites in the diagnosis of early gastric cancer. A total of 513 patients who were diagnosed with gastric ulcers using gastroscopy between January 1999 and December 2013 were included in the present study and were divided into either the experimental or the control group. In the control group, samples were only taken from the ulcer margin, whereas in the experimental group samples were taken from the ulcer margin and from the ulcer base. In the experimental group, a routine biopsy of the ulcer margin was performed on first examination, and recheck by gastroscopy was performed from the second week. For ulcers that remained unhealed, a biopsy of the ulcer margin was subsequently conducted; however, for healed or almost healed ulcers, a biopsy of the ulcer base was conducted. The duration of follow-up by gastroscopy ranged between 1 week and 24 months. For the control group, a biopsy of the ulcer margin was conducted using the conventional method. The detection rate of the experimental group was 3.88% (9/232), with 4 cases of gastric cancer confirmed from examinations of the ulcer base. The detection rate of the control group was 1.07% (3/281), which was significantly decreased compared with that of the experimental group (P=0.0345). Overall, patients who underwent regular follow-up gastroscopy following treatment exhibited a markedly increased detection rate of early gastric cancer, suggesting that early cancer may occur in healed gastric ulcer sites.

Isovitexin (IV) induces apoptosis and autophagy in liver cancer cells through endoplasmic reticulum stress.

Liver cancer is a leading cause of cancer death worldwide, and novel chemotherapeutic drugs to suppress liver cancer are urgently required. Isovitexin (IV), a glycosylflavonoid, is extracted from rice hulls of Oryza sativa, and has various biological activities. However, the anti-tumor effect of IV against liver cancer has not yet been demonstrated in vitro or in vivo. In the present study, we showed that IV significantly suppressed the growth of liver cancer cells. Mechanistic studies indicated that IV induced apoptosis by the mitochondrial apoptotic pathway, as evidenced by the increase of Bax, cleaved Caspase-3, poly (ADP-ribose) polymerase (PARP), and cytoplasm Cyto-c released from mitochondria. In addition, IV resulted in autophagy in liver cancer cells, supported by the enhancement of LC3II, autophagy-related protein (Atg) 3, Atg5 and Beclin1. Suppressing autophagy using bafilomycin A1 (BFA) or siRNA Atg-5 reduced apoptotic cells in IV-treated cells, demonstrating that autophagy induction regulated apoptosis. Moreover, IV was found to cause endoplasmic reticulum (ER) stress in liver cancer cells, along with the promotion of ER stress-related molecules, including inositol-requiring enzyme 1α (IRE1α), X-box-binding protein-1s (XBP-1s), C/EBP homologous protein (CHOP) and glucose-regulated protein (GRP)-78. Of note, inhibition of ER stress by use of its inhibitor, tauroursodeoxycholate (TUDCA), significantly reversed IV-induced apoptosis and autophagy. In vivo, IV treatment showed significant tumor growth inhibition compared to the non-treated group. IV could therefore be a strong candidate for liver cancer prevention.

The effect of JAK2 knockout on inhibition of liver tumor growth by inducing apoptosis, autophagy and anti-proliferation via STATs and PI3K/AKT signaling pathways.

Liver cancer is a leading cause of cancer death, making it as the second most common cause for death from cancer globally. Though many studies before have explored a lot for liver cancer prevention and treatment, there are still a lot far from to know based on the molecular mechanisms. Janus kinase 2 (JAK2) has been reported to play an essential role in the progression of apoptosis, autophagy and proliferation for cells. Therefore, we were aimed to investigate the underlying mechanisms by which JAK2 performed its role in ameliorating liver cancer. JAK2 knockout liver cancer cell lines were involved for our experiments in vitro and in vivo. Western blotting, quantitative RT-PCR (qRT-PCR), ELISA, Immunohistochemistry, and flow-cytometric analysis were used to determine the key signaling pathway regulated by JAK2 for liver cancer progression. Data here indicated that JAK2, indeed, expressed highly in cancer cell lines compared to the normal liver cells. And apoptosis and autophagy were found in JAK2 knockout liver cancer cells through activating Caspase-3, Cyclin-D1 and mTOR regulated by STAT3/5 and PI3K/AKT signaling pathway. And also, the liver cancer cells proliferation was inhibited. In addition, tumor size and weight were reduced by knockout of JAK2 in vivo experiments. These findings demonstrated that JAK2 and its down-streaming signaling pathways play a direct role in the progression of liver cancer possibly. To our knowledge, it was the first time to evaluate the role of JAK2 knockout in improving liver cancer from apoptosis, autophagy and proliferation, which could be a potential target for future therapeutic approach clinically.

Protective effect of histamine microinjected into the cerebellar fastigial nucleus on stress-induced gastric mucosal damage in rats.

AIMS: We investigated the effffects and the possible mechanism of microinjection of histamine into cerebellar fastigial nucleus (FN) on stress-induced gastric mucosal damage (SGMD) in rats. The effect of microinjection of histamine into FN on SGMD was observed. METHODS: The model of SGMD was established by restraint and water (21 ± 1°C)-immersion (RWI) for 3 h in rats. The gastric mucosal damage index indicated the severity of SGMD. Western blotting was performed to assess gastric mucosal cell apoptosis and proliferation. RESULTS: We observed that histamine microinjection into the FN markedly attenuated SGMD in a dose-dependent manner, and was prevented by pre-treatment with the ranitidine (a selective histamine H2 receptor antagonist) into the FN. The effect of histamine was abolished by pre-treatment with 3-MPA (a glutamic acid decarboxylase antagonist) into the FN. There was a decrease in the discharge frequency of greater splanchnic nerve, and an increase in gastric mucosal blood flow after histamine injection into the FN. Additionally, anti-apoptotic and anti-oxidative factors of gastric mucosa might be involved in this process. CONCLUSION: The exogenous histamine in FN participates in the regulation of SGMD, and our results may help to provide new ideas on the treatment of gastroenterological diseases.

Reduction of fibrosis in dibutyltin dichloride-induced chronic pancreatitis using rat umbilical mesenchymal stem cells from Wharton's jelly.

OBJECTIVES: The objective of this study was to investigate the effects of rat umbilical cord mesenchymal stem cells (UCMSCs) from Wharton's jelly on dibutyltin dichloride (DBTC)-induced chronic pancreatitis (CP) and subsequent pancreatic fibrosis in rats. METHODS: A rat model of CP induced by DBTC was used. Male Sprague-Dawley rats were randomly divided into 4 groups: the control, DBTC, DBTC + UCMSCs, and control + UCMSC groups. Umbilical cord mesenchymal stem cells were administered intravenously on day 5 after the administration of DBTC. On days 14 and 28, the rats were evaluated morphologically and biochemically. The expression levels of inflammatory cytokines and chemokines in the pancreatic tissues of different groups were evaluated using quantitative real-time polymerase chain reaction. The activation of pancreatic stellate cells was estimated by immunochemistry and Western blot analysis of α-smooth muscle actin. RESULTS: Umbilical cord mesenchymal stem cells were detected in inflamed pancreatic tissues. Umbilical cord mesenchymal stem cell treatment improved the histological scores and alleviated the fibrosis of pancreas samples, The expression of cytokines in the DBTC + UCMSC group was significantly lower than that in the DBTC group. Also, pancreatic stellate cell activation was inhibited by UCMSC treatment. CONCLUSIONS: Xenogeneic transplantation of UCMSCs is a novel approach for the treatment of CP and subsequent fibrosis. Umbilical cord mesenchymal stem cells may be a promising therapeutic intervention for human CP in the future.

Expression of R132H mutational IDH1 in human U87 glioblastoma cells affects the SREBP1a pathway and induces cellular proliferation.

Sterol regulatory element-binding protein-1a (SREBP1a) is a member of the SREBP family of transcription factors, which mainly controls homeostasis of lipids. SREBP1a can also activate the transcription of isocitrate dehydrogenase 1 (IDH1) by binding to its promoter region. IDH1 mutations, especially R132H mutation of IDH1, are a common feature of a major subset of human gliomas. There are few data available on the relationship between mutational IDH1 expression and SREBP1a pathway. In this study, we investigated cellular effects and SREBP1a pathway alterations caused by R132H mutational IDH1 expression in U87 cells. Two glioma cell lines, stably expressing mutational (U87/R132H) or wild type (U87/wt) IDH1, were established. A cell line, stably transfected with pcDNA3.1(+) (U87/vector), was generated as a control. Click-iT EdU assay, sulforhodamine B assay, and wound healing assay respectively showed that the expression of R132H induced cellular proliferation, cell growth, and cell migration. Western blot revealed that SREBP1 was increased in U87/R132H compared with that in U87/wt. Elevated SREBP1a and several its target genes, but not SREBP1c, were detected by real-time polymerase chain reaction in U87/R132H. All these findings indicated that R132H mutational IDH1 is involved in the regulation of proliferation, growth, and migration of glioma cells. These effects may partially be mediated by SREBP1a pathway.

Biopsy from the base and edge of gastric ulcer healing or complete healing may lead to detection of gastric cancer earlier: an 8 years endoscopic follow-up study.

BACKGROUND/AIMS: To assess the incidence of gastric cancer development in gastric benign ulcer patients and to evaluate the value of biopsy by taking specimens from both the base and edges of ulcers in contrast to the traditional biopsy which takes specimens from the edges of ulcers only. METHODOLOGY: An endoscopic followup of more than 1 year was conducted on 456 gastric ulcer patients in our hospital for a duration over 8 years. We collected clinical, endoscopic and pathological data and obtained at least 6 biopsies from both the edges and the bases of ulcers healing or complete healing, respectively and assessed H. pylori infection. RESULTS: Gastric cancers developed in 11 (2.41%) of 456 GU patients. In the experimental group, 3 cases that were diagnosed by histology showed adenocarcinoma with specimens taken from the ulcer bases and in the other 5 cases the specimens were taken from the ulcer edges. The detection rate of gastric cancer from gastric ulcer between experimental group and control group was statistically significant (4.57% vs. 1.07%, p<0.05). CONCLUSIONS: Gastric ulcer may develop into gastric cancer over a certain period of time in patients infected with H. pylori. Biopsies from ulcer bases and edges at the second or subsequent endoscopies may lead to defection of gastric cancer earlier and more effectively than the biopsies which take specimens from the edges of ulcers only.

Biopsy from the base of gastric ulcer may find gastric cancer earlier.

Gastric cancer is one of the most common malignancies in the world; however, its exact mechanism of development which may be relevant to many factors is still unclear, such as age, diet, Helicobacter pylori infection, smoking, polyps, chronic gastric ulcer and so on. Chronic gastric ulcer is considered as precancerous lesion of gastric cancer. The above-mentioned diseases are usually diagnosed by endoscopy and biopsy. In general, biopsy specimens are usually taken from the edges of lesions, seldom from the base. In patients with chronic gastric ulcer, especially healing or healed benign ulcer, we took the biopsy specimens from both the edges and the base of ulcers in the follow-up. Malignant lesions were found in several cases of chronic gastric ulcer, in which specimens were taken from the base of lesions. Therefore, we hypothesize that biopsy from the base of healing or healed chronic gastric ulcer in the second or third endoscopy may find gastric cancer earlier than traditional biopsy.