LncRNA CASC2 inhibited the viability and induced the apoptosis of hepatocellular carcinoma cells through regulating miR‐24‐3p

Abstract

Cancer susceptibility candidate 2 (CASC2), a recently discovered long non-coding RNA (lncRNA), was confirmed to play numerous roles in several human cancers. However, the involvement and concrete mechanism of CASC2 in hepatocellular carcinoma (HCC) still need to be further elucidated. The relative expressions of CASC2 and miR-24-3p in HCC tissue and cell lines were determined by quantitative real-time PCR (qRT-PCR). The effects of CASC2 and miR-24-3p on HCC cells were further assessed via cell viability and apoptosis. In vivo tumorigenesis assay was performed to verify the inhibition effect of CASC2 on the tumor growth and further clarify the important role of miR-24-3p in this mechanism. Compared with the paired normal tissues, the relative expression of CASC2 significantly reduced in the HCC tissues, while miR-24-3p as determined by qRT-PCR obviously increased in the HCC tissues. This observation was also found in HCC cell lines. Meanwhile, the expression of CASC2 was negatively related to miR-24-3p expression in the HCC tissues (r = -0.804, P < 0.001). CASC2 could negatively regulate the expression of miR-24-3p in vitro. Moreover, CASC2 overexpression resulted in the growth inhibitory and apoptosis-inducing effects on HCC cells, but the up-regulation of miR-24-3p greatly eliminated the CASC2-induced effects. The tumorigenesis of HCC cells was restrained significantly by CASC2 overexpression as shown by decreased tumor volume and growth rate. However, miR-24-3p up-regulation rescued the inhibition of CASC2 on the tumor growth in tumor-bearing mice. LncRNA CASC2 inhibited the viability and induced the apoptosis of HCC cells through regulating miR-24-3p.

Long non‑coding RNA CASC2 suppresses pancreatic cancer cell growth and progression by regulating the miR‑24/MUC6 axis

“…Furthermore, CASC2 altered cell-cell adhesion, as evidenced by the decrease in the levels of ITGB4 and p-FAK, together with attenuation of N-cadherin and MMP expression, enhancement of E-cadherin expression, and morphological alterations. These findings were consistent with previous reports in which CASC2 functioned as a tumor suppressor in numerous types of human cancer, including colorectal cancer, hepatocellular cancer, osteosarcoma and pancreatic cancer (7)(8)(9)(10)(11). To the best of our knowledge, this study was the first to indicate that CASC2 exerted its tumor-suppressive effects through altering cell-cell adhesion in pancreatic cancer.…”

“…Long non-coding RNAs (lncRNAs) have been implicated in the regulation of disease progression in numerous types of cancer by functioning as tumor suppressors or promoters (5,6). Increasing evidence indicates that lncRNA cancer susceptibility candidate 2 (CASC2) exhibits tumor-suppressive functions by acting as a competing endogenous RNA (ceRNA) for microRNAs (miRNAs/miRs) (7)(8)(9)(10). CASC2 was shown to be downregulated and suppress tumor progression in pancreatic cancer (11).…”

“…miR-24 has been reported to be upregulated in pancreatic cancer cells (12,13). While CASC2 was demonstrated to act as a sponge for miR-24 and regulated tumorigenesis of hepatocellular carcinoma (8,14), little is known about the interaction between CASC2 and miR-24 in pancreatic cancer.…”

Retracted Article: PVT1 depletion protects cartilage ATDC5 cells against LPS-induced inflammatory injury by regulating the miR-24/ADAMTS5 axis

“…31 Besides, miR-24 also bound to lncRNA cancer susceptibility candidate 2 (CASC2) and were involved in cell viability and apoptosis of hepatocellular carcinoma cells. 32 Notably, available evidence indicated miR-24 was downregulated in chondrocyte treated by IL-1b or from rats with osteoarthritis and elevated miR-24 inhibited apoptosis, promoted cell proliferation. 17,18 Hence, we probed a potential miRNA of PVT1 and found the possibility of binding of PVT1 and miR-24.…”

Competing Endogenous RNAs in Hepatocellular Carcinoma—The Pinnacle of Rivalry

“…51 Its forced overexpression also induces growth arrest of HCC tissues through regulating the expression of miR-24-3p. 52 In addition, Wang et al reported yet another lncRNA that regulates EMT, tumor suppressor candidate 7 (TUSC7), which acts to suppress EMT via regulating the expression of Eph tyrosine kinase receptor A4 by acting as a ceRNA for miR-10a. 53 Interestingly, EMT is controlled by lncRNA FTX as well through repressing Wnt/β-catenin signaling by sponging miR-374a.…”