Background/Aims. TRPV1 is a nonselective Ca2+ channel which has recently been observed in many cancers, while its effect on cell proliferation, apoptosis, metabolism, and cancer development in colorectal cancer (CRC) is still unclear. In this study, we hypothesized that TRPV1 is a tumor suppressor in CRC development as well as the underlying mechanism. Methods. Immunohistochemistry assay was applied to detect the expression of TRPV1 protein in CRC tissues. HCT116 cell proliferation and apoptosis were measured by CCK-8 and flow cytometry, respectively. Cellular Ca2+ concentration was measured by Fluo-4/AM-based flow cytometer. Apoptosis-related proteins were measured by Western blotting. Results. In this study, we found that TRPV1 expression was significantly decreased in CRC tissues, compared with CRC-adjacent tissues and normal tissues, respectively. Then, we found that the TRVP1 agonist capsaicin treatment inhibited CRC growth and induced apoptosis by activating P53. Subsequent mechanistic study revealed that the TRPV1 induced cytosolic Ca2+ influx to regulate cell apoptosis and p53 activation through calcineurin. Conclusions. This study suggests that TRPV1 served as a tumor suppressor in CRC and contributed to the development of novel therapy of CRC.

LIN28B is involved in “stemness” and tumourigenesis by negatively regulating the maturation of let-7 microRNA family members. In this study, we showed that LIN28B expression promotes migration and recurrence of colon cancer. Immunohistochemistry and reverse-transcription polymerase chain reactions were performed to detect LIN28B expression in colon cancer tissue microarrays, paraffin-embedded surgical resected tissues and cancer cells. Loss-of-function, migration and proliferation analyses were performed to delineate the potential roles of LIN28B in colon cancer. LIN28B was upregulated in colon cancer tissue compared to normal mucosa, and its overexpression correlated with reduced patient survival and increased tumour recurrence. LIN28B suppression inhibited the migration of SW480 colon cancer cells and facilitated the cytotoxicity induced by oxaliplatin in SW480 and HCT116 colon cancer cells. In conclusion, LIN28B overexpression contributes to colon tumourigenesis, and LIN28B may serve as a diagnostic tool and therapeutic target for colon cancer.

Background: We conducted a meta-analysis to assess the efficacy and safety of mirabegron on overactive bladder (OAB) induced by benign prostatic hyperplasia (BPH) in men receiving tamsulosin therapy. Methods: We performed the analysis by using the Preferred Reporting Items for Systematic Reviews and Meta-Analyses. The databases including MEDLINE, EMBASE, and the Cochrane Controlled Trials Register were retrieved to get information regarding randomized controlled trials of mirabegron on OAB induced by BPH in men receiving tamsulosin therapy. We also searched the references of included literatures. Results: Three randomized controlled trials containing a total of 1317 BPH patients were included in the analysis. Co-primary efficacy end points: the mean number of micturitions per day [the mean difference (MD) = –0.27, 95% confidence interval (CI): –0.46 to –0.09, P = .004], the urgency episodes per day (the MD = –0.50, 95% CI: –0.77 to –0.22, P = .0004), the total OAB symptom score (the MD = –0.69, 95% CI: –1.00 to –0.38, P < .0001), and mean volume voided (the MD = 10.76, 95% CI: 4.87–16.64, P = .0003) indicated that mirabegron was effective in treating OAB induced by BPH in men receiving tamsulosin therapy. Safety assessments that included treatment-emergent adverse events (odds ratio = 0.88, 95% CI: 0.68–1.13, P = .31) indicated that mirabegron was well tolerated with the exception of post-void residual urine volume (MD = 12.02, 95% CI: 6.01–18.04, P < .0001). Conclusions: This analysis demonstrates that mirabegron is an effective and safe treatment for OAB symptoms induced by BPH in men receiving tamsulosin therapy with a low occurrence of side effects. Besides, we should be aware that the administration of mirabegron might have the risk of increasing post-void residual urine volume.

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Background: Vibegron is a new β3-adrenergic receptor agonist which has been demonstrated for the treatment of overactive bladder (OAB). We carried out meta-analysis to evaluate the efficiency of vibegron vs antimuscarinic monotherapy for treating OAB. Methods: Randomized controlled trials (RCTs) of Vibegron vs antimuscarinic monotherapy for OAB were searched systematically by using EMBASE, MEDLINE, and the Cochrane Controlled Trials Register. The RevMan version 5.3.0. was used to analysis the data. Results: Three RCTs involving a total of 1751 patients were studied in the Systematic review and Meta-analysis. Efficacy end points: the mean number of micturitions episodes/d ( P = .16); the mean number of urgency episodes/d ( P = .05); mean number of urgency incontinence episodes/d ( P = .11) and mean number of incontinence episodes/d ( P = .14) indicated that vibegron and antimuscarinic had no significant differences in terms of OAB treatment. Mean volume voided/micturition showed a distinct difference in the two groups ( P = .009). With regard to dry mouth and drug related treatment-emergent adverse event (TEAE), vibegron showed better tolerance than antimuscarinic. Serious adverse event (SAE) and discontinuations due to adverse event (AE) did not show a significant difference between the two groups. Conclusions: The therapeutic effect of vibegron is similar to that of antimuscarinic, but vibegron does not increase the risk of AE.