LncRNA MT1JP inhibits the malignant progression of hepatocellular carcinoma through regulating AKT.

OBJECTIVE: The purpose of this study was to investigate the expression profile of long non-coding RNA (IncRNA) MT1JP in hepatocellular carcinoma (HCC), and to explore the relationship between its expression level and the clinical indicators, as well as the prognosis of HCC patients. PATIENTS AND METHODS: In this study, the expression level of MT1JP in 45 pairs of tumor tissue specimens and paracancerous ones collected from HCC patients were examined through quantitative Real Time-Polymerase Chain Reaction (qRT-PCR) method, and the interplay between MT1JP expression and clinical indicators, as well as the prognosis of HCC patients, was also analyzed. Meanwhile, the expression of MT1JP in HCC cell lines was further verified by qRT-PCR. In addition, MT1JP overexpression model was constructed using lentivirus in HCC cell lines (Hub7 and HepG2), and then, Cell Counting Kit-8 (CCK-8), cell colony formation assay, and flow cytometry were performed to examine the impact of MT1JP on the HCC cell functions. Additionally, whether MT1JP exerts its biological characteristics through protein kinase B (AKT) was finally explored. RESULTS: In this experiment, qRT-PCR results showed that the expression level of IncRNA MT1JP in tumor tissues of HCC patients was remarkably lower than that in adjacent tissues, and the difference was statistically significant. Meanwhile, compared with patients with high expression of MT1JP, patients with low expression of MT1JP had a higher pathological staging and a lower overall survival rate. In addition, overexpression of MT1JP remarkably attenuated the proliferation ability of HCC cells but enhanced cell apoptosis rate at the same time. Finally, Western blot results revealed that the overexpression of MT1JP may markedly reduce the AKT expression, thereby suppressing the malignant progression of HCC. CONCLUSIONS: LncRNA MT1JP expression is remarkably decreased in HCC tumor tissue samples, which is associated with pathological stage and poor prognosis of HCC patients. In addition, MT1JP may inhibit the malignant progression of HCC by downregulating AKT.