The relationship between miR-26a-5p and Wnt5a was analyzed by dual luciferase report. Results The database and clinical samples showed that miR-26a-5p level was low while Wnt5a was high in GC. MiR-26a-5p level decreased in patients with stage III+IV, lymphatic metastasis and tumor ≥3cm, and Wnt5a was contrary to that of the miR-26a-5p, with diagnostic value. Overexpressed miR-26a-5p and inhibited Wnt5a enhanced apoptosis, decreased proliferation and invasion, reduced Bcl-2 and β-catenin proteins, and elevated Caspase 3, E-cadherin and Bax proteins, while inhibited miR-26a-5p and over-expressed Wnt5a showed the opposite results. Dual luciferase report confirmed that miR-26a-5p targeted to regulate Wnt5a, and rescue experiments found that these effects could be counteracted by reducing miR-26a-5p level. Conclusion Overexpressed miR-26a-5p can inhibit Wnt5a expression, promote cell apoptosis, and suppress cell proliferation and invasion in GC. © 2020 Li et al.Background Increasing researches have revealed a critical role of long noncoding RNAs (lncRNAs) in tumor progression. LINC00665 is a poorly investigated lncRNA. In this research, we sought to determine the potential role of LINC00665 in prostate cancer (PC) progression. Methods LINC00665 expression was analyzed by bioinformatics method and qRT-PCR. Proliferation was determined via CCK8 and colony formation assays. Transwell assay was conducted to analyze migration and invasion. Xenograft assay was used to test the roles of LINC00665 in vivo. Luciferase reporter assay, pulldown assay and RIP assay were utilized to confirm the interaction between LINC00665 and miR-1224-5p. Results LINC00665 expression was increased in PC samples in contrast to control tissues, according to bioinformatics analysis and qRT-PCR validation. LINC00665 high expression was related to a poor prognosis. LINC00665 knockdown markedly attenuated growth and metastasis of PC cells and impaired tumor propagation in vivo. Mechanistic investigation revealed that LINC00665 was the sponge for miR-1224-5p. By inhibiting miR-1224-5p level, LINC00665 dramatically promoted the expression of SND1 in PC cells. Ectopic expression of SND1 significantly rescued the effects of LINC00665 silencing. Conclusion LINC00665 is a novel oncogenic gene in PC by targeting miR-1224-5p/SND1 pathway and may be a therapeutic target. © 2020 Chen et al.Non-small cell lung cancer (NSCLC) is the leading cause of cancer-related death worldwide and has a poor prognosis. Current treatments for advanced NSCLC included traditional chemotherapy, radiotherapy, targeted therapy, and immunotherapy. The efficacy of targeted therapy relies on oncogene addiction. Mesenchymal-epithelial transition factor (MET) gene can encode unconventional receptor tyrosine kinases with pleiotropic functions, when signals are abnormally activated, it can initiate and maintain tumor transformation, promote cell proliferation, survival, tumor invasion and angiogenesis. Thus, it is a promising therapeutic target. Previous studies have shown that elevated levels of HGF and/or overexpression of c-Met are associated with poor prognosis in lung cancer. In preclinical and clinical trials, c-MET inhibitors have shown some antitumor activity in NSCLC. Although the efficacy results of MET inhibitors in Phase III clinical trials are disappointing, given the molecular heterogeneity of NSCLC, only subgroups of patients with MET gene alterations may benefit from c-MET inhibitors. The challenge for the future is to screen out the potential beneficiaries. To solve this problem, there is need for large data analysis for the detection methods and treatment effects, to establish standards that meet the MET activation status, and determine reliable thresholds to achieve effective patient stratification and clinical decision making. This article summarized the structure of the hepatocyte growth factor (HGF)/c-Met axis, the different mechanisms of MET addiction, as well as MET amplification as acquired resistance mechanism to epidermal growth factor receptor-tyrosine kinase inhibitors, the latest advances of MET inhibitors, and immuotherapy in the treatment of NSCLC with MET alterations. © 2020 Liang and Wang.Background Bladder cancer is a serious threat to human health. It is meaningful to study the pathogenesis of bladder cancer. Long non-coding RNAs (lncRNAs) are reported to promote or inhibit bladder cancer development. selleck chemicals However, the role of lncRNA BCAR4 in the regulation of bladder cancer remains unclear. Purpose This study was to explore the role of lncRNA BCAR4 in the progression of bladder cancer cell. Methods RT-PCR was used to examine the expression of BCAR4 and miR-644a. CCK8 assay, colony formation assay, Transwell assay were used to detect the progression of bladder cancer cells after transfecting of indicated plasmids. Results The expression of BCAR4 was higher in bladder cancer cell lines than normal urothelial cell line. Moreover, the expression of BCAR4 was associated with the advanced stage and metastasis of bladder cancer. Through knockdown of BCAR4, we discovered that knockdown of BCAR4 significantly decreased the proliferation, migration and invasive abilities of bladder cancer cells. Mechanically, we showed that BCAR4 can bind to miR-644a directly and targets TLX1. Moreover, we also showed that miR-644a was also highly expressed in bladder cancer cells and inhibition of miR-644a or overexpression of TLX1 can increased the migration abilities of bladder cancer caused by knockdown of BCAR4. Conclusion We showed that BCAR4 sponged miR-644a to modulate the expression of TLX1 and promote bladder cancer development. © 2020 Wang et al.Background Several studies have indicated that the anoikis effector Bcl-2 inhibitor of transcription 1 (Bit1) can promote or inhibit tumor progression depending on the nature of the malignancy. However, its regulatory effects on gliomas are unknown. Methods This study aimed at assessing Bit1 expression in glioma tissues and cells, its subsequent effects on glioma cell apoptosis, proliferation, invasion, and migration, and the underlying molecular mechanisms. Results The findings showed that lower Bit1 expressions in glioma tissues as well as a negative correlation between Bit1 expression and glioma grade. Additional findings also revealed that Bit1 silencing significantly inhibited anoikis and enhanced glioma cell proliferation, invasion, and migration. Further analysis showed that the decrease in Bit1 expressions led to malignancy proliferation and anoikis resistance through activation of the IL-6/STAT3 signaling pathway. Conclusion Our data suggested that Bit1 may play an anti-oncogenic role in glioma cells and that a decrease in its expressions might induce glioma cell proliferation, migration, and invasion through the IL-6/STAT3 signaling pathway.