Long non-coding RNA XIST inhibited breast cancer cell growth, migration, and invasion via miR-155/CDX1 axis

Ruinian Zheng1, Shunhuan Lin1, Ling Guan2

  • 1Department of Oncology, Dongguan People's Hospital, Southern Medical University, Dongguan, China.

Insights

Long non-coding RNA XIST (X inactive specific transcript) is downregulated in breast cancer, suppressing tumor growth and spread. It acts through the miR-155/CDX1 pathway, offering potential therapeutic targets for breast cancer.

Area of Science:

  • Molecular Biology
  • Oncology
  • Genetics

Background:

  • Long non-coding RNAs (lncRNAs) are key regulators in cellular processes.
  • X inactive specific transcript (XIST) shows potential as a tumor suppressor, but its role in breast cancer is not well understood.

Purpose of the Study:

  • To investigate the expression and function of XIST in breast cancer.
  • To elucidate the molecular mechanism underlying XIST's role in breast cancer.

Main Methods:

  • Quantitative real-time PCR to assess XIST expression.
  • Cell proliferation, migration, and invasion assays to evaluate XIST function.
  • Luciferase reporter assays to identify direct targets of XIST and miR-155.

Main Results:

  • XIST expression was significantly decreased in breast cancer tissues and cell lines.
  • Overexpression of XIST inhibited breast cancer cell proliferation, migration, and invasion.
  • XIST directly targets miR-155, which in turn targets CDX1, forming the XIST/miR-155/CDX1 axis.

Conclusions:

  • XIST is downregulated in breast cancer and acts as a tumor suppressor.
  • The XIST/miR-155/CDX1 axis plays a critical role in regulating breast cancer progression.
  • XIST represents a potential therapeutic target for breast cancer treatment.

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