Long noncoding RNA CASC2c inhibited cell proliferation in hepatocellular carcinoma by inactivated ERK1/2 and

Q Y Li1, K Yang2, F G Liu3

  • 1Department of Pathology, Qilu Hospital of Shandong University, Qingdao, 266035, China.

Abstract

Insights

The long non-coding RNA CASC2c is downregulated in hepatocellular carcinoma (HCC). Overexpression of CASC2c inhibits HCC cell growth and promotes apoptosis by affecting ERK1/2 and Wnt/β-catenin pathways.

Area of Science:

  • Molecular Biology
  • Cancer Research
  • Genetics

Background:

  • Long non-coding RNAs (lncRNAs) are implicated in tumorigenesis, but their specific roles are often unclear.
  • CASC2 is a lncRNA with multiple transcript variants (CASC2a, CASC2b, CASC2c), with CASC2a/b studied more extensively than CASC2c in malignancies.

Purpose of the Study:

  • To investigate the role of the lncRNA CASC2c in the proliferation and apoptosis of hepatocellular carcinoma (HCC) cells.
  • To explore the underlying molecular mechanisms of CASC2c in HCC and other cancers.

Main Methods:

  • Quantitative real-time polymerase chain reaction (qRT-PCR) was used to assess CASC2c expression levels in HCC tissues and cells.
  • Functional studies were conducted in HCC, gastric cancer (GC), and colorectal cancer (CRC) cell lines to evaluate the effects of CASC2c overexpression.

Main Results:

  • CASC2c was significantly downregulated in HCC tissues and cells.
  • Overexpression of CASC2c inhibited HCC cell growth, migration, and invasion, while promoting apoptosis.
  • CASC2c overexpression decreased p-ERK1/2 levels in HCC, GC, and CRC cells, and affected β-catenin expression differently across cancer types.

Conclusions:

  • The lncRNA CASC2c plays a critical role in HCC tumorigenesis and progression.
  • CASC2c may serve as a potential biomarker or therapeutic target for cancer treatment.
  • Down-regulation of ERK1/2 and Wnt/β-catenin signaling pathways is implicated in CASC2c's function.

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