LncRNA CKMT2-AS1 Promotes Hepatocellular Carcinoma Development Via Sponging miR-142-5p and Targeting IFITM3

TL;DR

This study shows that the lncRNA CKMT2-AS1 promotes liver cancer by interacting with miR-142-5p and increasing IFITM3 levels, offering new insights into cancer progression.

Contribution

The study identifies a novel regulatory network involving CKMT2-AS1, miR-142-5p, and IFITM3 in hepatocellular carcinoma.

Findings

CKMT2-AS1 is upregulated in HCC tissues and cells, while miR-142-5p is downregulated.

CKMT2-AS1 sponges miR-142-5p, leading to increased IFITM3 expression and enhanced HCC progression.

Downregulating CKMT2-AS1 inhibits HCC cell proliferation, migration, and invasion.

Abstract

Hepatocellular carcinoma (HCC) stands as the foremost contributor to cancer-related mortality, underscoring its profound significance in the oncological landscape. This study explores the potential regulatory mechanisms of lncRNA CKMT2-AS1 in the functionality of HCC cells, thereby providing a basis for therapeutic approaches in the treatment of HCC.

Quantitative polymerase chain reaction (qPCR) was utilized to evaluate the expression of CKMT2-AS1 and miR-142-5p in HCC tissues and cells. The interactions between CKMT2-AS1 and miR-142-5p, as well as the interplay between IFITM3 and miR-142-5p, were confirmed through dual-luciferase assays. To assess the effects of CKMT2-AS1 transfection, alongside the co-transfection of CKMT2-AS1 and miR-142-5p interference plasmids, a series of experiments were conducted utilizing CCK-8 and transwell assays to evaluate changes in proliferation, migration, and invasion of HCC cells. Additionally, qPCR was employed to elucidate the influence of miR-142-5p on the expression of IFITM3 in HCC cells.

The study elucidated that CKMT2-AS1 was significantly upregulated in HCC tissues and cells, while miR-142-5p exhibited a marked downregulation, revealing a noteworthy negative correlation. Notably, the downregulation of CKMT2-AS1 hindered the function of HCC cells. Conversely, the downregulation of miR-142-5p effectively mitigated the inhibitory effects of CKMT2-AS1 on cellular activities. Furthermore, the upregulation of miR-142-5p resulted in a substantial decrease in the levels of IFITM3 in HCC cells. This investigation established a potential regulatory network, identifying IFITM3 as the downstream target mRNA.

The sponging effect of CKMT2-AS1 on miR-142-5p resulted in altered expression levels of IFITM3, subsequently influencing the progression of HCC.

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