LncRNA MEG8 plays an oncogenic role in hepatocellular carcinoma progression through miR-367-3p/14-3-3ζ/TGFβR1 axis

• Published in: Neoplasma 2021-01, Vol.68 (2), p.273
• Main Authors: Lou, Jiang, Yan, Wei, Li, Qing-Yu, Zhu, A-Kao, Tan, Bi-Qin, Dong, Rong, Zou, Xiao-Zhou, Liu, Ting
• Format: Article
• Language: English
• Subjects: 14-3-3 Proteins - genetics; Carcinoma, Hepatocellular - genetics; Cell Line, Tumor; Cell Proliferation - genetics; Humans; Liver Neoplasms - genetics; MicroRNAs - genetics; Receptor, Transforming Growth Factor-beta Type I; RNA, Long Noncoding - genetics
• ISSN: 0028-2685
• DOI: 10.4149/neo_2020_200730N785

Hepatocellular carcinoma (HCC) is one of the most common cancers worldwide, and it carries a poor prognosis. Clarifying the pathologic mechanisms of this disease will be beneficial for the diagnosis and treatment of HCC. LncRNA MEG8 is involved in several tumors but its role in HCC progression remains unknown. This study was designed to explore the role and regulatory mechanisms of MEG8 in HCC progression. MTT, EdU, wound-healing, and transwell assays were employed to analyze the proliferation, migration, and invasion of HCC cells. A luciferase assay was utilized to confirm the predicted binding site. RNA immunoprecipitation and co-immunoprecipitation were employed to verify the binding between MEG8 and miR-367-3p as well as 14-3-3ζ and TGFβR1. Real-time PCR and western blot were employed to detect the expression of interesting genes. Results revealed that MEG8 was increased in HCC tissues and cells, and was correlated with the poor prognosis of HCC patients. Inhibiting MEG8 significantly repressed the HCC cells' ability to proliferate, migrate, and invade. Moreover, MEG8 sponged miR-367-3p to upregulate 14-3-3ζ, the binding of which suppressed TGFβR1 degradation, thereby enhancing TGFβ signaling. In conclusion, this work exposed a novel role and regulatory mechanism of MEG8 in HCC and provided new insight into the treatment of HCC.