Percutaneous vertebral augmentation for osteoporotic vertebral compression fractures will increase the number of subsequent fractures at adjacent vertebral levels: a systematic review and meta-analysis.

OBJECTIVE: This study aimed to investigate whether percutaneous vertebral augmentation (PVA) was associated with clinical and radiological subsequent adjacent fractures in patients with osteoporotic vertebral compression fractures. MATERIALS AND METHODS: The systematic review was performed following PRISMA guidelines. Data were retrieved from PubMed, EMBASE, Cochrane Library, Google Scholar, Web of Science, and ClinicalTrial.gov, from database inception to March 2020. Eligible studies were those that assessed subsequent adjacent fractures after PVA in comparison with conservative treatment (CT). The number of patients with adjacent secondary vertebral fractures was calculated, and the pooled risk ratio (RR) with its 95% confidence intervals (95% CI) was used. Moreover, heterogeneity, sensitivity, and publication bias analyses were performed. RESULTS: Twenty-four studies were included finally. Moreover, 20/421 (4.75%) patients from the PVA group and 25/359 (6.96%) patients from the CT group had clinical subsequent adjacent fractures, and 46/440 (10.45%) patients from the PVA group and 36/444 (8.10%) patients from the CT group had radiological subsequent adjacent fractures. Both had no significant difference between the two groups (RR = 0.67, 95% CI [0.38, 1.19], p = 0.17)/(RR = 1.13, 95% CI [0.75, 1.70], p = 0.576). However, the number of fractured vertebrae was higher in the PVA group than in the CT group (RR = 1.41, 95% CI [1.03, 1.93], p = 0.03). A sensitivity analysis did not identify specific trials that seriously deflected. No obvious publication bias was identified. CONCLUSIONS: The systematic review revealed that PVA did not increase the incidence for subsequent adjacent fractures regardless of whether they were clinical or radiological fractures. However, PVA can increase the number of subsequent fractures at adjacent vertebral levels.

Polyoxometalate SbW9 regulates proliferation and apoptosis of NSCLC cells via PTEN-dependent AKT signaling pathway.

The article "Polyoxometalate SbW9 regulates proliferation and apoptosis of NSCLC cells via PTEN-dependent AKT signaling pathway, by H.-B. Sun, L. Xu, Z.-X. Wang, Y. Zheng, Y. Zhao, Y.-Y. Yin, X.-L. Han, Z.-N. Xu, published in Eur Rev Med Pharmacol Sci 2019; 23 (18): 7959-7967-PMID: 31599421" has been withdrawn from the authors due to some technical reasons (there are some evident errors and incorrect data). The Publisher apologizes for any inconvenience this may cause. https://www.europeanreview.org/article/19012.

MicroRNA-218 regulates the epithelial-to-mesenchymal transition and the PI3K/Akt signaling pathway to suppress lung adenocarcinoma progression by directly targeting BMI-1.

The article "MicroRNA-218 regulates the epithelial-to-mesenchymal transition and the PI3K/Akt signaling pathway to suppress lung adenocarcinoma progression by directly targeting BMI-1, by L. Xu, H.-B. Sun, Z.-N. Xu, X.-L. Han, Y.-Y. Yin, Y. Zheng, Y. Zhao, Z.-X. Wang, published in Eur Rev Med Pharmacol Sci 2019; 23 (18): 7978-7988-DOI: 10.26355/eurrev_201909_19014-PMID: 31599423" has been withdrawn from the authors due to some technical reasons (there are some errors and  incorrect data). The Publisher apologizes for any inconvenience this may cause. https://www.europeanreview.org/article/19014.

LINC01093 promotes proliferation and invasion of non-small cell lung cancer cells via targeting akt signaling pathway.

The article "LINC01093 promotes proliferation and invasion of non-small cell lung cancer cells via targeting akt signaling pathway, by Z.-X. Wang, Z.-N. Xu, H.-B. Sun, Y. Wang, Z.-F. Han, Y. Yu, X.-L. Han, Y.-Y. Yin, L. Xu, published in Eur Rev Med Pharmacol Sci 2020; 24 (1): 222-229- DOI: 10.26355/eurrev_202001_19914-PMID: 31957835" has been withdrawn from the authors due to some technical reasons (there are some errors and incorrect data). The Publisher apologizes for any inconvenience this may cause. https://www.europeanreview.org/article/19914.

Long noncoding RNA SNHG14 exerts oncogenic functions in lung adenocarcinoma through acting as a sponge to miR-613.

Since this article has been suspected of research misconduct and the corresponding authors did not respond to our request to prove originality of data and figures, "Long noncoding RNA SNHG14 exerts oncogenic functions in lung adenocarcinoma through acting as a sponge to miR-613, by Z.-N. Xu, Z.-X. Wang, L. Xu, H.-X. Yu, K. Chao, L.-L. Yang, X.-L. Han, H.-B. Sun, published in Eur Rev Med Pharmacol Sci 2019; 23 (24): 10810-10817-DOI: 10.26355/eurrev_201912_19784-PMID: 31858549" has been withdrawn. The Publisher apologizes for any inconvenience this may cause. https://www.europeanreview.org/article/19784.

Linc00703 suppresses non-small cell lung cancer progression by modulating CyclinD1/CDK4 expression.

OBJECTIVE: The aim of this study was to detect the expression of linc00703 in non-small cell lung cancer (NSCLC), and to explore the biological function and potential molecular mechanism of linc00703 in NSCLC using in vitro experiments. PATIENTS AND METHODS: The carcinoma tissues and para-carcinoma tissues were collected from 32 patients diagnosed with NSCLC, from which the RNA was extracted. The relative expression of linc00703 in NSCLC tissues was detected via quantitative reverse transcription-polymerase chain reaction (qRT-PCR). The NSCLC cells and normal human bronchial epithelial cells were selected, in which the relative expression of linc00703 was determined via qRT-PCR. Next, the linc00703 overexpression plasmids were designed and synthesized, and then transiently transfected into NSCLC cells. After 48 h, the overexpression efficiency was detected. Finally, the changes in cell proliferation, apoptosis, cycle distribution and expressions of downstream molecular markers were determined using cell counting kit-8 (CCK8) assay, colony formation assay, flow cytometry and Western blotting, respectively, after overexpression of linc00703 in NSCLC cells. RESULTS: The results of qRT-PCR revealed that the expression of linc00703 was down-regulated by 5.14 times on average in 29 out of 32 cases of NSCLC tissues, and it was also down-regulated in NSCLC cells. Besides, it was found through CCK-8 assay, colony formation assay and flow cytometry that after overexpression of linc00703 in NSCLC cells, the cell proliferation was inhibited, the apoptosis was enhanced, and the cell cycle was arrested in G1/G0 phase. Furthermore, the results of Western blotting showed that after overexpression of linc00703, the protein expressions of cyclinD1 and cyclin-dependent kinase 4 (CDK4) declined, while those of cyclinE1 and CDK2 did not change. CONCLUSIONS: The expression of linc00703 is down-regulated in NSCLC, and it suppresses the occurrence and development of NSCLC via mediating the expression of cyclinD1/CDK4.

LINC01093 promotes proliferation and invasion of non-small cell lung cancer cells via targeting akt signaling pathway.

OBJECTIVE: To explore the expression of LINC01093, a long non-coding ribonucleic acid (lncRNA) in non-small cell lung cancer (NSCLC) tissues, and cells and its regulatory role in NSCLC cell proliferation and invasion. PATIENTS AND METHODS: The expression of LINC01093 in NSCLC tissues and cells was detected via quantitative Reverse Transcription-Polymerase Chain Reaction (qRT-PCR) experiment. The specific sequences interfering in LINC01093 were designed and transiently transfected into A549 and SPCA-1 cells using LipofectamineTM 2000, and 48 later, the transfection efficiency was detected. Moreover, the impacts of small interfering (si)-LINC01093 on NSCLC cell proliferation were observed via methyl thiazolyl tetrazolium (MTT) and colony forming assays, the influence of LINC01093 on the cycle distribution of NSCLC cells was determined through flow cytometry, and the changes in the invasion and migration abilities of NSCLC cells were evaluated via transwell assay after interfering in the expression of LINC01093. Finally, the expression changes of the molecular markers in the protein kinase B (Akt) signaling pathway in the downstream of LINC01093 were detected via Western blotting. RESULTS: According to the results of qRT-PCR, the relative expression level of LINC01093 was up-regulated in NSCLC tissues and cells. After interfering in the expression of LINC01093, the results of MTT and colony forming assays revealed that the proliferation ability of NSCLC cells was weakened, according to the findings in the flow cytometry, the cells were arrested in G1/0 phase, the transwell assay results manifested that the cell migration and invasion abilities were weakened, and the results of the Western blotting suggested the changes in the expressions of molecular markers in the Akt signaling pathway. CONCLUSIONS: The expression of LINC01093 is upregulated in NSCLC tissues and cells, and it facilitates the proliferation, invasion, and metastasis of NSCLC cells via the Akt signaling pathway.

Long noncoding RNA SNHG14 exerts oncogenic functions in lung adenocarcinoma through acting as a sponge to miR-613.

OBJECTIVE: Lung adenocarcinoma is one of the most ordinary malignant tumors. Recent researches have proved that long noncoding RNAs (lncRNAs) are vital factors in many diseases. In this work, lncRNA SNHG14 was studied to identify its function in the development of lung adenocarcinoma. PATIENTS AND METHODS: Real Time-quantitative Polymerase Chain Reaction (RT-qPCR) was utilized to detect SNHG14 expression in paired lung adenocarcinoma patients' tissue samples and cells. Then, the function of SNHG14 was detected through MTT (3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide) assay, colony formation assay, and transwell assay in vitro. Besides, mechanism assays and the interaction between SNHG14 and miR-613 were conducted. RESULTS: SNHG14 was remarkably higher-expressed in lung adenocarcinoma tissues than in adjacent samples. Moreover, cell proliferation and invasion of lung adenocarcinoma were promoted via overexpression of SNHG14, while cell proliferation and invasion of lung adenocarcinoma were inhibited via silence of SNHG14. Moreover, RT-qPCR results revealed that miR-613 was downregulated via overexpression of SNHG14, while miR-613 was upregulated via knockdown of SNHG14. Further experiments showed that miR-613 was also a direct target of SNHG14 in lung adenocarcinoma. CONCLUSIONS: Our study suggests that SNHG14 enhances lung adenocarcinoma cell proliferation and invasion via targeting miR-613, which indicates that SNHG14 may be a potential therapeutic target in lung adenocarcinoma.

MicroRNA-218 regulates the epithelial-to-mesenchymal transition and the PI3K/Akt signaling pathway to suppress lung adenocarcinoma progression by directly targeting BMI-1.

OBJECTIVE: To investigate the role of miR-218 in the development of lung adenocarcinoma (LA) and its underlying mechanism. PATIENTS AND METHODS: Fifty-two pairs of human LA samples and adjacent para-carcinoma tissue samples were collected from our hospital between June 2015 and March 2017. Meanwhile, one normal human pulmonary epithelial cell line BEAS-2B and four human LA cell lines (H1299, PC-9, A549, and SPC-A1) were cultured. The cells' ability of proliferation and migration was detected by MTT assays and Transwell assays, respectively. The target gene was clarified by dual-luciferase reporter assay. The related protein and mRNA expression levels were detected by immunohistochemistry (IHC), Western blot and quantitative real-time polymerase chain reaction (qRT-PCR), respectively. At last, the tumor xenograft model was made for further exploring the mechanism. RESULTS: MiR218 expressions were notably reduced in LA tissues in comparison with controls. In addition, the declined miR218 expressions were correlated with the poor OS and worse clinicopathological parameters of LA patients. Furthermore, miR218 overexpression could suppress the proliferation, migration and invasion capacities of LA cells via regulation of PI3K/Akt signaling pathway and epithelial-mesenchymal transition (EMT) respectively. Results in the current study also revealed that miR-218 upregulation could suppress the tumor growth rate and tumor size of LA mice. B-lymphoma Moloney murine leukemia virus insertion region-1 (BMI-1) was confirmed to be a direct target for miR-218 and upregulated in LA tissues, which indicated the poor prognosis of LA patients. CONCLUSIONS: MiR-218 exerted anti-tumor functions in LA partially via the regulation of BMI-1, suggesting that BMI-1/miR-218 axis may provide a novel insight into tumorigenesis and the basis for the development of miRNA-targeting therapies against LA.

Polyoxometalate SbW9 regulates proliferation and apoptosis of NSCLC cells via PTEN-dependent AKT signaling pathway.

OBJECTIVE: To explore the influence of polyoxometalate SbW9 on proliferation and apoptosis of non-small cell lung cancer (NSCLC) cells and its mechanism. MATERIALS AND METHODS: NSCLC cell lines A549 and PC9 were treated with 50 µM polyoxometalate. Then, the proliferation of NSCLC cells was detected via 2,3-bis(2-methoxy-4-nitro-5-sulfophenyl)-5-[(phenylamino)carbonyl]-2H-t tetrazolium hydroxide (XTT) assay and colony formation assay; the apoptosis of NSCLC cells was detected via flow cytometry and terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL); and the expression of apoptosis-related proteins, B-cell lymphoma-2 (Bcl-2), and Bcl-2 associated X protein (Bax), was detected via Western blotting. Moreover, the protein expression levels of phosphatase and tensin homolog deleted on chromosome ten (PTEN), phosphorylated-protein kinase B (P-AKT) and total AKT (T-AKT) were detected via Western blotting. RESULTS: The polyoxometalate inhibited the proliferation of A549 and PC9 cells in a concentration-dependent manner (5-100 µM) (p<0.05), and it (50 µM) also inhibited the proliferation of both cells in a time-dependent manner (0-72 h) (p<0.05). The results of colony formation assay revealed that the polyoxometalate (50 µM) could significantly inhibit the colony formation of A549 and PC9 cells (p<0.05). The results of flow cytometry and TUNEL staining showed that the polyoxometalate (50 µM) significantly induced the apoptosis of A549 and PC9 cells (p<0.05). According to further studies, the polyoxometalate (50 µM) inhibited the expression of anti-apoptotic gene Bcl-2 and promoted the expression of pro-apoptotic gene Bax. Besides, the Western blotting results manifested that the polyoxometalate could activate the expression of PTEN and inhibit the phosphorylation of downstream AKT (p<0.05). CONCLUSIONS: The polyoxometalate can activate the expression of PTEN to inhibit the phosphorylation of AKT, ultimately inhibiting the proliferation and inducing the apoptosis of NSCLC cells. Therefore, the polyoxometalate is expected to become a novel drug for the clinical treatment of NSCLC.

MiR-601 inhibits the proliferation and metastasis of esophageal squamous cell carcinoma (ESCC) by targeting HDAC6.

OBJECTIVE: The aim of this study was to explore the role of microRNA-601 (miR-601) in the proliferation and invasion of esophageal squamous cell carcinoma (ESCC) cells, thereby providing new thoughts for prognosis evaluation and targeted therapy of ESCC. PATIENTS AND METHODS: 23 pairs of ESCC tissue samples and adjacent normal tissues were collected, and the expression level of miR-601 was detected. Biological information analysis and Luciferase report gene assay were used to verify the potential target genes of miR-601. Then, three groups were established in ESCC cell line (TE-1) to perform similar experiments, including the miR-NC group, the miR-601 mimics group and the mimics + HDAC6 group. Cell counting kit-8 (CCK-8) assay was used to detect cell proliferation ability. Meanwhile, transwell assay and scratch-wound assay were applied to observe the effect of miR-601 on cell invasion and migration. Quantitative reverse transcription Polymerase Chain Reaction (qPCR) and Western blot assay were applied to determine the mRNA and protein expression changes after transfection. RESULTS: Compared with normal adjacent tissues and normal esophageal epithelial cells, the expression of miR-601 was significantly decreased in ESCC tissues and cells. HDAC6 was identified as a target gene of miR-601. The expression of HDAC6 in esophageal carcinoma cells transfected with miR-601 mimics was significantly down-regulated. The negative correlation between miR-601 and HDAC6 expression was assessed by qPCR and Western blot (WB) assay. Furthermore, miR-601 remarkably suppressed the proliferation of ESCC cells. Meanwhile, cell invasion and migration were also found markedly restricted after transfection of miR-601 mimics. However, the overexpression of HDAC6 significantly counteracted the effects of miR-601. CONCLUSIONS: MiR-601 suppressed the proliferation, invasion and migration of esophagus carcinoma cells by down-regulating HDAC6 expression.

Randomized phase III trial of prophylactic cranial irradiation versus observation in patients with fully resected stage IIIA-N2 nonsmall-cell lung cancer and high risk of cerebral metastases after adjuvant chemotherapy.

BACKGROUND: This study compared prophylactic cranial irradiation (PCI) with observation in patients with resected stage IIIA-N2 non-small-cell lung cancer (NSCLC) and high risk of cerebral metastases after adjuvant chemotherapy. PATIENTS AND METHODS: In this open-label, randomized, phase III trial, patients with fully resected postoperative pathologically confirmed stage IIIA-N2 NSCLC and high cerebral metastases risk without recurrence after postoperative adjuvant chemotherapy were randomly assigned to receive PCI (30 Gy in 10 fractions) or observation. The primary end point was disease-free survival (DFS). The secondary end points included the incidence of brain metastases, overall survival (OS), toxicity and quality of life. RESULTS: This trial was terminated early after the random assignment of 156 patients (81 to PCI group and 75 to control group). The PCI group had significantly lengthened DFS compared with the control group, with a median DFS of 28.5 months versus 21.2 months [hazard ratio (HR), 0.67; 95% confidence interval (CI) 0.46-0.98; P = 0.037]. PCI was associated with a decrease in risk of brain metastases (the actuarial 5-year brain metastases rate, 20.3% versus 49.9%; HR, 0.28; 95% CI 0.14-0.57; P < 0.001). The median OS was 31.2 months in the PCI group and 27.4 months in the control group (HR, 0.81; 95% CI 0.56-1.16; P = 0.310). While main toxicities were headache, nausea/vomiting and fatigue in the PCI group, they were generally mild. CONCLUSION: In patients with fully resected postoperative pathologically confirmed stage IIIA-N2 NSCLC and high risk of cerebral metastases after adjuvant chemotherapy, PCI prolongs DFS and decreases the incidence of brain metastases.

Survivin silencing enhances radiosensitivity in oral squamous cell carcinoma cell.

OBJECTIVE: Survivin is a member of the inhibitor of apoptosis protein (IAP) family. It is overexpressed in most cancer tissues and induces resistance to radiation therapy. In this study, we investigated whether knockdown of survivin by siRNA could induce apoptosis and enhance radiosensitivity in oral squamous cell carcinoma cells (OSCC). MATERIALS AND METHODS: Oral squamous cell carcinoma cell lines KB was subjected to radiotherapy, small interfering RNA (siRNA) targeting survivin was transfected into KB cells in vitro, then subjected to radiotherapy. After irradiation or/and siRNA transfection, viable and dead cells were counted to determine radiation sensitivity by MTT assay, proliferation by colony-forming ability and apoptosis was analyzed by flow cytometry. Tumor-bearing mice were irradiated with 6 Gy of 60 Co-γ radiator. RESULTS: The results showed knockdown of survivin in KB cells showed reduced cell proliferation and increased number of radiation-induced apoptosis. Apoptosis was increased by survivin silencing alone and increased further in combination with irradiation. Colony formation was significantly reduced by survivin silencing in combination with irradiation. CONCLUSIONS: Survivin silencing sensitizes KB cells toward irradiation. Survivin silencing in combination with radiation inhibits cell proliferation and colony formation significantly and increases apoptosis more than each single treatment alone. In addition, survivin silencing significantly enhanced inhibition of tumor growth and potentiated cell apoptosis by irradiation in KB xenografts. In conclusion, survivin silencing could enhance sensitivity of human KB cells to radiotherapy in vitro and in vivo.

Association of de novo human leukocyte antigen and major histocompatibility complex class I chain-related gene-A antibodies and proteinuria with graft survival 5 years after renal transplantation.

BACKGROUND: Association of de novo human leukocyte antigen (HLA) and major histocompatibility complex class I chain-related gene-A (MICA) antibodies and proteinuria with graft survival 5 years after renal transplantation. De novo presence of HLA and MICA antibodies after renal transplantation is associated with poor graft survival. Proteinuria after transplantation is also considered a risk factor for premature graft loss. In this study, we investigated the association of de novo HLA and MICA antibodies on proteinuria after renal transplantation and the association of proteinuria and de novo antibodies with graft survival. METHODS: We enrolled 275 patients without preexisting HLA and MICA antibodies followed for >5 years after renal transplantation. All donor organs were from living-related donors or from an organ donation program. HLA and MICA antibodies were detected by the Luminex method. Patients with proteinuria (>150 mg/d) underwent intermittent 24-hour proteinuria examination. RESULTS: The frequencies of de novo HLA and MICA antibody 5 years after transplantation were 25.8% and 12%, respectively. In total, 26.5% of patients had proteinuria at the 5-year follow-up. De novo HLA antibody was associated with increased proteinuria after transplantation (relative risk, 3.12). HLA antibody and proteinuria were both associated with poor 5-year graft survival (P = .027 and P = .006, respectively). CONCLUSION: De novo HLA and MICA antibodies and proteinuria after renal transplantation are all associated with poor graft survival. De novo HLA antibody is independent risk factor for posttransplant proteinuria, and proteinuria affects the association of de novo antibodies with decreased graft survival after transplantation.

Highly flexible and efficient top-emitting organic light-emitting devices with ultrasmooth Ag anode.

We demonstrate highly flexible and efficient top-emitting organic light-emitting devices (TOLEDs) by using an ultrasmooth Ag anode. A template-stripping process has been employed to create the ultrasmooth Ag anode on a photopolymer substrate. The flexible TOLEDs obtained by this method keep good electroluminescence properties under a small bending radius and after repeated bending. The efficiency of the flexible TOLEDs is improved by 60% compared with the conventional TOLEDs deposited on Si substrate due to the enhanced hole injection from the ultrasmooth anode.

Overexpression of a hematopoietic transcriptional regulator EDAG induces myelopoiesis and suppresses lymphopoiesis in transgenic mice.

Erythroid differentiation-associated gene (EDAG) is a hematopoietic tissue-specific gene that is highly expressed in the earliest CD34+ lin- bone marrow (BM) cells and involved in the proliferation and differentiation of hematopoietic cells. To investigate the role of EDAG in hematopoiesis, we established an EDAG transgenic mouse model driven by human CD11a promoter. The transgenic mice showed increased mortality with severe organ infiltration by neutrophils, and the homeostasis of hematopoiesis was broken. The myelopoiesis was enhanced with expansion of myeloid cells in BM, increased peripheral granulocytes and extramedullary myelopoiesis in spleen. In contrast to myeloid cells, the lymphoid commitment was severely impaired with the B lymphopoiesis blocked at the transition from pro/pre-B I to pre-B II stage in BM and T thymocytes development blocked at the most immature stage (DN I). Moreover, we showed that EDAG was a transcriptional regulator which had transactivation activity and regulated the expression of several key transcription factors such as PU.1 and Pax5 in transgenic hematopoietic stem cells. These data suggested that EDAG was a key transcriptional regulator in maintaining the homeostasis of hematopoietic lineage commitment.