In the last few decades, YAP has been shown to be critical in regulating tumor progression. YAP activity can be regulated by many kinase cascade pathways and proteins through phosphorylation and promotion of cytoplasmic localization. Other factors can also affect YAP activity by modulating its binding to different transcription factors (TFs). Programmed cell death (PCD) is a genetically controlled suicide process present with the scope of eliminating cells unnecessary or detrimental for the proper development of the organism. In some specific states, PCD is activated and facilitates the selective elimination of certain types of tumor cells. As a candidate oncogene correlates with many regulatory factors, YAP can inhibit or induce different forms of PCD, including apoptosis, autophagy, ferroptosis and pyroptosis. Furthermore, YAP may act as a bridge between different forms of PCD, eventually leading to different outcomes regarding tumor development. Researches on YAP and PCD may benefit the future development of novel treatment strategies for some diseases. Therefore, in this review, we provide a general overview of the cellular functions of YAP and the relationship between YAP and PCD.
As a gastrointestinal malignancy, colorectal cancer (CRC) is a main cause of cancer-related deaths worldwide. Mex-3 RNA-binding family member A (MEX3A) is upregulated in multiple types of tumors and plays a critical role in tumor proliferation and metastasis. However, the function of MEX3A in CRC angiogenesis has not been fully understood. Hence, the aim of this study was to explore the role of MEX3A in CRC angiogenesis and investigate its underlying mechanisms. MEX3A expression in CRC was first investigated by bioinformatics means and then measured by qRT-PCR and Western blot. CCK-8 assay was employed to test cell viability. Angiogenesis assay was used to assess angiogenesis. The protein levels of VEGF, FGF and SDF-1 were evaluated using Western blot. The expression levels of MYC, HK2 and PGK1 were investigated by qRT-PCR. Extracellular acidification rate (ECAR) and oxygen consumption rate (OCR) were determined by Seahorse XP 96. The levels of pyruvate, lactate, citric acid and malate were measured by corresponding kits. Bioinformatics analysis demonstrated high MEX3A expression in CRC tissues and MEX3A enrichment in glycolysis and angiogenesis pathways. Cell assays showed high MEX3A expression in CRC cells and its promoting effects in CRC cell proliferation and glycolysis as well as angiogenesis. Rescue experiment confirmed that glycolysis inhibitor 2-DG could offset the promoting effects of MEX3A on the proliferation, angiogenesis and glycolysis of CRC cells. In conclusion, MEX3A could facilitate CRC angiogenesis by activating the glycolytic pathway, suggesting that MEX3A may be a novel therapeutic target for CRC.
Background The mortality of cervical cancer (CC) is quite high and advanced CC is hard to cure. Accordingly, to find the mechanism of CC progression at molecular level is imminent. Methods The mRNA expression data were acquired from The Cancer Genome Atlas database, and squalene epoxidase (SQLE) level in the tumor and adjuvant tissues of CC was analyzed. The pathway enrichment analysis of target mRNAs was performed based on the GSEA database. The cancerous tissues and para‐cancerous tissues of CC patients were collected for immunohistochemistry. SQLE and p53 mRNA expression was ensured by qRT‐polymerase chain reaction. SQLE and p53 protein levels were determined by western blot. Cell functional assays focused on evaluating the malignant behaviors of cancer cells in each treatment group. Nude mouse xenograft models were constructed for tumorigenicity analysis. Results Bioinformatics analysis revealed that SQLE expression was high in CC tissues, which was linked to the poor prognosis. SQLE could affect the p53 signaling pathway. Cell functional assays demonstrated that SQLE expression was promoted in CC cell lines, and overexpressing SQLE facilitated the malignant phenotypes of CC cells, whereas silencing SQLE suppressed CC progression in vitro and in vivo. Besides, the repressed p53 signaling pathway could reverse the effect caused by silenced SQLE. Conclusion SQLE could promote CC progression by modulating the p53 signaling pathway.
Purpose This study aims to evaluate the pain relief function of chemical sphincterotomy in patients undergoing haemorrhoid surgery and compare, through a meta-analysis, the different drugs used to treat this condition. Methods We conducted a search in databases including PubMed, EMBASE and Web of Science. The methodological quality was evaluated using the Revised Cochrane risk-of-bias tool for randomized trials (ROB2). The pain score was assessed using a visual analogue scale (VAS) on day 1, day 2, and day 7, and a meta-analysis was conducted based on the use of random effects models. In addition, the subgroup analysis was evaluated based on the kind of experimental drugs. Heterogeneity and publication bias were assessed. Results Fourteen studies with a total of 681 patients were included in this meta-analysis, and all studies were randomized controlled trials RCTs. Chemical sphincterotomy showed better pain relief function than placebo on day 1 (SMD: 1.16, 95% CI 0.52 to 1.80), day 2 (SMD: 2.12, 95% CI 1.37 to 2.87) and day 7 (SMD: 1.97, 95% CI 1.17 to 2.77) after surgery. In the subgroup meta-analysis, we found that different drugs for chemical sphincterotomy provided different pain relief. Conclusion Chemical sphincterotomy effectively relieves pain after haemorrhoidectomy, and calcium channel blockers have the best effect.
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