Down-regulation of lncRNA PCGEM1 inhibits cervical carcinoma by modulating the miR-642a-5p/LGMN axis

Yuanlin Liu1, Ye Wang2, Xiang Shen3

  • 1Department of Obstetrics and Gynecology, Affiliated Hospital of Nantong University, Nantong 226001, China.

Insights

Long non-coding RNA PCGEM1 (PCGEM1) promotes cervical carcinoma progression. Knocking down PCGEM1 inhibits cancer cell proliferation, migration, and invasion by regulating the miR-642a-5p/LGMN axis.

Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • Long non-coding RNAs (lncRNAs) play crucial roles in tumorigenesis.
  • The specific role of PCGEM1 in cervical carcinoma is not well understood.
  • PCGEM1 is implicated in the development of various cancers.

Purpose of the Study:

  • To investigate the role and mechanism of PCGEM1 in cervical carcinoma.
  • To elucidate the regulatory pathway involving PCGEM1, miR-642a-5p, and LGMN in cervical cancer.

Main Methods:

  • Real-time quantitative polymerase chain reaction (RT-qPCR) to assess gene expression.
  • Bioinformatics analysis and luciferase reporter assays to confirm targeting.
  • Cell proliferation, migration, invasion, and cell cycle assays.
  • Gene knockdown and inhibition experiments.

Main Results:

  • PCGEM1 was upregulated in cervical carcinoma tissues and cells.
  • PCGEM1 knockdown suppressed proliferation, migration, and invasion, inducing G1 arrest.
  • PCGEM1 targets miR-642a-5p, which was downregulated in cervical cancer.
  • PCGEM1 knockdown increased miR-642a-5p expression.
  • Inhibition of miR-642a-5p partially reversed PCGEM1 knockdown effects.
  • miR-642a-5p targets LGMN, which was upregulated in cervical cancer.
  • LGMN suppression partially restored cellular functions inhibited by miR-642a-5p inhibitor.

Conclusions:

  • PCGEM1 promotes cervical carcinoma progression.
  • PCGEM1 knockdown inhibits cervical cancer cell proliferation, migration, and invasion.
  • The PCGEM1/miR-642a-5p/LGMN axis is a key regulatory pathway in cervical carcinoma.

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