| Literature DB >> 34021861 |
Chengyuan Yang1, Zichan Guo1, Zitong Zhao2, Yuan Wei1, Xiaoxia Wang3, Yongmei Song4.
Abstract
Esophageal squamous cell carcinoma (ESCC) is one of the most aggressive cancers and the primary cause of cancer-related mortality in China. micoRNA plays a vital role during tumor initiation and malignant progression. miR-4306 has been reported to negatively regulate aggressive cell phenotypes in triple-negative breast cancer (TNBC). Nevertheless, the function of miR-4306 in ESCC was still not clear. In this study, we detected miR-4306 expression by quantitative real-time reverse transcription-PCR (qRT-PCR) and found that miR-4306 expression was downregulated in human ESCC tissue samples and cell lines. Moreover, miR-4306 overexpression could restrain ESCC cell proliferation, migratory and invasive ability and epithelial-mesenchymal transition (EMT), promote cell apoptosis after treatment with or without cisplatin. In contrast, inhibiting the expression of miR-4306 showed the opposing results. Furthermore, we explored the molecular mechanism of effects of miR-4306 and found that miR-4306 inhibited the expression of SIX3 by interaction with SIX3 3'UTR in ESCC cells, and SIX3 overexpression significantly reversed the effect of miR-4306-mediated ESCC cells proliferation. The current study provided evidence of miR-4306 as a tumor suppression gene in ESCC.Entities:
Keywords: Esophageal squamous cell carcinoma; Invasion; SIX3; miR-4306; proliferation
Mesh:
Year: 2021 PMID: 34021861 DOI: 10.1007/s12013-021-00994-x
Source DB: PubMed Journal: Cell Biochem Biophys ISSN: 1085-9195 Impact factor: 2.194