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Showing 2 results for Hepatocellular Carcinoma.
D.b. Xiao, H. Xu, J.c. Li, K.k. Peng, X.l. Jiang, D.x. Wang, Ph.d., F.f. Zhu,
Volume 22, Issue 2 (4-2024)
Abstract
Background: miR-144-3p exerts inhibitory roles in hepatocellular carcinoma (HCC). This paper aims to explore that miR-144-3p and its predictive target gene, SLIT- and NTRK-like family member 4 (SLITRK4), in HCC progression. Materials and Methods: The levels of SLITRK4 and miR-144-3p were determined by western blot and qPCR. A loss- and gain-of-function test was used to test whether the relationship between miR-144-3p and SlitrK4 affected the growth of HCC cells. StarBase examined the miR-144-3p target prediction using SLITRK4. Through the use of a luciferase reporter experiment, miR-144-3p's targeting SLITRK4 was identified. The salvage experiment confirmed that miR-144-3p interacts SLITRK4 to regulate the progression of HCC. Results: Findings showned that the expression of miR-144-3p decreased in HCC tissue and cells. MiR-144-3p inhibits deterioration progression of HCC cell progression. MiR-144-3p targeted SLITRK4 and negatively modulated SLITRK4 levels. Besides, miR-144-3p upregulation decreased HCC migration and invasion activity, while SLITRK4 overexpression reduced this inhibition effects. Conclusions: MiR-144-3p regulates invasion and proliferation activity in HCC by targeting SLITRK4. MiR-144-3P/ SLITRK4 axis might provide a potential anti-cancer therapy pathway for clinical diagnosis, treatment and prognosis in hepatoma.
Q. Chen, M.m. Wang, X-K. Meng, M.d., Q.l. Wu,
Volume 23, Issue 1 (1-2025)
Abstract
Background: Hepatocellular carcinoma (HCC) cell development was investigated in relation to the regulation of Sec61 translocon alpha 1 subunit (SEC61A1) by microRNA (miR)-18a-5p. Materials and Methods: After collection of clinical samples, the transfection of interfering vectors of miR-18a-5p or SEC61A1 was into HCC cells to figure out their roles in development of HCC. The Pearson test and starBase analyzed the association and target prediction of miR-18a-5p. Subsequently, through the dual luciferase reporter experiment, SEC61A1 can be regulated via miR-18a-5p. The salvage experiment revealed that miR-18a-5p influence the degradation process of Hepatocellular carcinoma through combining SEC61A1. Results: In HCC cells, we found that SEC61A1 was elevated and miR-18a-5p was downregulated. HCC cells deteriorating was considerably slowed down by the enhanced miR-18a-5p level. The outcomes demonstrated that miR-18a-5p can interact and regulate SEC61A1. Additionally, the effects of earlier therapy on HCC cell proliferation can be restored by overexpressing SEC61A1. Conclusion: Overall, in HCC cells and tissues miR-18a-5p was significantly downregulated, and inhibited the proliferative ability of HCC cells by targeting SEC61A1.
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