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Diffuse large B‑cell lymphoma (DLBCL) is the most common type of non‑Hodgkin lymphoma worldwide. Several studies have indicated that Homo sapiens (hsa)‑microRNA (miR)‑429 exerts a tumor‑suppressive effect on a variety of malignant tumors. To the best of our knowledge, the molecular function and mechanism of action of hsa‑miR‑429 in DLBCL have not been evaluated to date. The present study demonstrated that the expression of hsa‑miR‑429 in DLBCL cells was significantly reduced. hsa‑miR‑429 inhibited the proliferation of the DLBCL cell lines, SUDHL‑4 and DB, and promoted apoptosis. A dual luciferase reporter assay was used to demonstrate that chromobox 8 (CBX8) was the target gene of hsa‑miR‑429. Overexpression of CBX8 promoted the proliferation of SUDHL‑4 and DB cells and inhibited apoptosis, thereby playing a cancer‑promoting role. Transfection of hsa‑miR‑429 mimic into DB cells overexpressing CBX8 antagonized the effect of CBX8 on the proliferation of DB cells. Moreover, the apoptotic rate was increased in DB cells overexpressing CBX8 and transfected with hsa‑miR‑429 mimic, while the proportion of cells in the G 2 /M phase was significantly reduced. These results demonstrated the antagonistic effect of hsa‑miR‑429 on the oncogenic function of CBX8. Therefore, in DLBCL, the tumor suppressor effect of hsa‑miR‑429 may be achieved by targeted downregulation of CBX8, suggesting that hsa‑miR‑429 may be used as a diagnostic marker and a potential nucleic acid drug for DLBCL. CBX8 may also represent an effective therapeutic target for DLBCL.

8‑bromo‑7‑methoxychrysin (BrMC), a novel chrysin analog, was reported to have anti‑cancer activities. The aim of the present study was to investigate the molecular mechanism of 8‑bromo‑7‑methoxychrysin (BrMC)‑induced apoptosis via the Akt/forkhead box O3a (FOXO3a) pathway in cisplatin (DDP)‑sensitive and ‑resistant ovarian cancer cells. The human ovarian cancer cell lines A2780 and A2780/DDP were cultured in vitro. Various molecular techniques were used to assess the expression of FOXO3a and B cell lymphoma 2 (Bcl‑2)‑interacting mediator of cell death (Bim) in cisplatin‑sensitive and ‑resistant ovarian cancer cells. Different concentrations of BrMC induced apoptosis in cisplatin‑sensitive and ‑resistant ovarian cancer cells. BrMC‑induced apoptotic cell death occurred mainly by the activation of Akt, which was accompanied by the overexpression of transcription factor FOXO3a, with a concomitant increase in the expression levels of Bim. Silencing Bim expression by using small interfering RNA, attenuated the induction of apoptosis by BrMC treatment. The results indicated that BrMC‑induced apoptosis in cisplatin‑sensitive and ‑resistant ovarian cancer cells may occur via the regulation of Akt/FOXO3a, leading to Bim transcription.

Hepatocellular carcinoma (HCC) is the third leading cause of cancer‑associated mortality in the 21st century. microRNA (miR)‑23b has been shown to be involved in the pathogenesis of many cancers, including breast and prostate cancer. However, the role of miR‑23b in HCC remains unclear. The present study revealed a negative correlation between miR‑23b expression in HCC tissues and progression of carcinomas. Compared to normal tissues, miR‑23b expression was significantly downregulated in HCC tissues, whereas the expression of interleukin (IL)‑11 and IL‑11 receptor α (IL‑11Rα) was significantly upregulated, indicating that miR‑23b expression is negatively correlated with IL‑11 and IL‑11Rα expression. In addition, miR‑23b inhibited proliferation and promoted apoptosis of SMMC‑7721 cells. This effect was mediated by IL‑11, which was found to be the direct target of miR‑23b in this study. These results indicated that miR‑23b regulates IL‑11 and IL‑11Rα expression, and might act as an anti‑oncogenic agent in the progression of HCC by directly downregulating IL‑11 expression. [ABSTRACT FROM AUTHOR]