We investigated the role of lncRNA nuclear enriched abundant transcript 1_2 (NEAT1_2) in radioresistance of HCC and its molecular mechanism in this study.
Since data on NEAT1 in HCC chemosensitivity are completely lacking and chemoresistance is linked to poor prognosis, we aimed to study NEAT1 expression in HCC chemoresistance and its link to HCC prognosis.
The effects of down-regulation or up-regulation of NEAT1 expression in HCC cell lines were analysed from the perspectives of cell viability and apoptosis.
The results revealed that NEAT1 expression was associated with tumor size and differentiation where NEAT1 was upregulated in both HCC tissues and cell lines.
We found that NEAT1 was greatly upregulated in human HCC cell lines including Huh7, Hep3B, HepG2, Bel-7404, and SK-Hep1 cells compared to the normal human liver cell line LO2.
The pooled standard mean deviation (SMD) indicated that NEAT1 was down-regulated in esophageal carcinoma (ESCA, SMD = -0.35, 95% CI: -0.5~-0.20, P < 0.0001) and hepatocellular carcinoma (HCC, SMD = -0.47, 95% CI: -0.60~-0.34, P < 0.0001), while in pancreatic cancer (PC), NEAT1 was up-regulated (SMD = 0.45, 95% CI: 0.2~0.71, P = 0.001).
Long non-coding RNA NEAT1 overexpression is associated with unfavorable prognosis in patients with hepatocellular carcinoma after hepatectomy: A Chinese population-based study.
Thus, the <i>NEAT1-hnRNP A2</i> regulation mechanism promotes HCC pathogenesis and may provide a potential target for the prognosis and treatment of HCC.
High levels of NEAT1 promoted the clinical features of HCC, including the number of tumor nodes, metastasis, clinical TNM stage, the status of portal vein tumor embolus, vaso-invasion and the infiltration of tumor cells.