Tripterine Restrains the Aggressiveness of Hepatocellular Carcinoma Cell via Regulating miRNA-532-5p/CXCL2 Axis.

INTRODUCTION: Triterpene has attracted considerable interests because it exhibits anticancer effects. However, the effects of tripterine on hepatocellular carcinoma (HCC) are not well studied. In the current study, the mechanism of tripterine on HCC cells growth and metastasis was examined. METHODS: The inhibitory effect on the growth and aggressiveness in HCC cells was analyzed by Cell Counting Kit-8 (CCK-8), wound healing and Transwell assay. The levels of microRNA-532-5p (miR-532-5p) in HCC cells and tissues were measured using qRT-PCR. The expression of chemokine (C-X-C Motif) ligand 2 (CXCL2) was determined by Western blotting and immunohistochemistry (IHC). Luciferase reporter gene assay was used to validate the binding between miR-532-5p and CXCL2. The impact of tripterine on the growth and metastasis of HCC cells in vivo was analyzed using transplanted tumor model and experimental lung metastasis model, respectively. RESULTS: We found that tripterine inhibited HCC cells proliferation, migration ability and invasion. Under tripterine treatment, the level of miR-532-5p was strikingly raised, and overexpression of miR­532-5p reduced cell viability and metastatic-related traits. In addition, we identified CXCL2 as a target of miR-532-5p in HCC. Rescue experiments indicated that overexpression of CXCL2 restored the migration and invasive capacity of HCC cells inhibited by miR-532-5p or tripterine treatment. Finally, the tumor growth and metastatic ability of HCC MHCC97H cell in vivo were also significantly restrained by tripterine. The expression of CXCL2 was distinctly decreased and miR-532-5p level was increased by tripterine in vivo. CONCLUSION: In conclusion, tripterine inhibits the growth, migration ability and invasiveness of HCC cells through intervening miR-532-5p/CXCL2.

miR-539 induces cell cycle arrest in nasopharyngeal carcinoma by targeting cyclin-dependent kinase 4.

Dysregulation of microRNAs has been demonstrated to contribute to malignant progression of cancers, including nasopharyngeal carcinoma (NPC). miR-539 was previously reported to be significantly downregulated in osteosarcoma. However, the potential role and mechanism of action of miR-539 in the initiation and progression of NPC remain largely unknown. Quantitative reverse transcription (RT)-PCR demonstrated that miR-539 was significantly downregulated in NPC tumour tissues compared with nontumour tissues. The cell viability, colony formation assay and tumourigenicity assays in nude mice showed that miR-539 could inhibit NPC cell growth in vitro and in vivo. The cyclin-dependent kinase 4 (CDK4) was verified as a miR-539 target gene using dual-luciferase reporter assays, quantitative RT-PCR and Western blotting and was involved in miR-539-regulated NPC cell growth. These results indicated that miR-539 plays an important role in the initiation and progression of NPC by targeting CDK4 and the miR-539/CDK4 pathway may contribute to the development of novel therapeutic strategies for NPC in the future.