Long non-coding RNA UCA1 regulates the proliferation, migration and invasion of human lung cancer cells by modulating

T Jun1, F-S Zheng, K-M Ren

  • 1Department of The First Thoracic Surgery, Shengjing Hospital of China Medical University, Shenyang, Liaoning Province, People's Republic of China. zhaojz@sj-hospital.org.

Abstract

Insights

Long non-coding RNA UCA1 is upregulated in lung cancer. Silencing UCA1 inhibits cancer cell growth, migration, and invasion by downregulating MAPK1 through miR-143, suggesting UCA1 as a therapeutic target.

Area of Science:

  • Oncology
  • Molecular Biology
  • Gene Regulation

Background:

  • Lung cancer accounts for 25% of all cancers and 20% of cancer mortality.
  • Limited treatment options necessitate novel therapeutic targets.
  • Long non-coding RNAs (LncRNAs) play crucial roles in cellular functions and are potential therapeutic targets.

Purpose of the Study:

  • Investigate the therapeutic potential of UCA1 in lung cancer.
  • Elucidate the mechanism by which UCA1 affects cancer cell growth.

Main Methods:

  • Quantitative Reverse-Transcriptase Polymerase Chain Reaction (qRT-PCR) for expression analysis.
  • Cell Counting Kit-8 (CCK-8) assay for cell proliferation.
  • Apoptosis assays (AO/EB) and flow cytometry for cell cycle analysis.
  • Wound healing and Transwell assays for cell migration and invasion.

Main Results:

  • UCA1 was significantly upregulated in lung cancer cells.
  • UCA1 silencing inhibited proliferation, induced G2/M cell cycle arrest and apoptosis in SK-MES-1 cells.
  • UCA1 silencing suppressed migration and invasion.
  • UCA1 upregulated miR-143, which also suppressed proliferation, migration, and invasion.
  • Both UCA1 silencing and miR-143 overexpression decreased MAPK1 expression.

Conclusions:

  • UCA1 regulates lung cancer cell growth by inhibiting MAPK1 via miR-143 upregulation.
  • UCA1 and miR-143 are potential therapeutic targets for lung cancer management.

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