Anti-MAPK6 monoclonal antibody, clone 5F9

Emerging evidence showed miR499a could not only function as an oncogene but also as a tumor suppressor in various types of cancer, such as melanoma. However, whether miR499a was involved in hepatocarcinogenesis remains unknown. We previously reported that miR499a was up-regulated in HBV-mediated hepatocellular carcinoma (HCC). In this study, we found that HBV could induce the expression of miR499a by promoting its promoter activity. In addition, we reported that miR499a increased cell proliferation and cell migration of HCC cells. MAPK6 was further identified as a target of miR499a, which could also be down-regulated by HBV. Moreover, we demonstrated that MAPK6 could rescue the cell growth induced by miR499a and HBV. These findings indicated that miR499a might play an oncogene role by targeting MAPK6 in the development and progression of HBV-related HCC.

Long noncoding RNAs (lncRNAs) or microRNAs belong to the two most important noncoding RNAs and they are involved in a lot of cancers, including non-small-cell lung cancer (NSCLC). Therefore, currently, we focused on the biological and clinical significance of lncRNA nuclear enriched abundant transcript 1 (NEAT1) and hsa-mir-98-5p in NSCLC. It was observed that NEAT1 was upregulated while hsa-mir-98-5p was downregulated respectively in NSCLC cell lines compared to human normal lung epithelial BES-2B cells. Inhibition of NEAT1 can suppress the progression of NSCLC cells and hsa-mir-98-5p can reverse this phenomenon. Bioinformatics search was used to elucidate the correlation between NEAT1 and hsa-mir-98-5p. Additionally, a novel messenger RNA target of hsa-mir-98-5p, mitogen-activated protein kinase 6 (MAPK6), was predicted. Overexpression and knockdown studies were conducted to verify whether NEAT1 exhibits its biological functions through regulating hsa-mir-98-5p and MAPK6 in vitro. NEAT1 was able to increase MAPK6 expression and hsa-mir-98-5p mimics can inhibit MAPK6 via downregulating NEAT1 levels. We speculated that NEAT1 may act as a competing endogenous lncRNA to upregulate MAPK6 by attaching hsa-mir-98-5p in lung cancers. Taken these together, NEAT1/hsa-mir-98-5p/MAPK6 is involved in the development and progress in NSCLC. NEAT1 could be recommended as a prognostic biomarker and therapeutic indicator in NSCLC diagnosis and treatment.