Long non-coding RNA MIR205HG regulates KRT17 and tumor processes in cervical cancer via interaction with SRSF1

Mingli Dong1, Zhennan Dong2, Xinyu Zhu3

  • 1Department of Obstetrics and Gynecology, Chinese PLA General Hospital, Beijing 100853, China.

Insights

Long non-coding RNA MIR205HG is upregulated in cervical cancer, promoting cancer cell proliferation and migration by regulating KRT17 expression via SRSF1. This finding offers a potential new therapeutic target for cervical cancer treatment.

Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • Aberrant expression of long non-coding RNAs (lncRNAs) is implicated in various cancers.
  • The specific role and regulatory mechanisms of MIR205HG in cervical cancer remain largely unexplored.

Purpose of the Study:

  • To investigate the expression pattern and functional role of MIR205HG in cervical cancer.
  • To elucidate the underlying molecular mechanism by which MIR205HG influences cervical cancer progression.

Main Methods:

  • Quantitative real-time PCR to assess MIR205HG and KRT17 expression levels.
  • Cell proliferation, migration, and apoptosis assays following KRT17 or MIR205HG manipulation.
  • Western blotting and RNA immunoprecipitation assays to determine the interaction between MIR205HG, SRSF1, and KRT17.

Main Results:

  • MIR205HG and KRT17 were found to be significantly upregulated in cervical cancer tissues and cell lines.
  • Silencing KRT17 inhibited cervical cancer cell proliferation and migration while promoting apoptosis.
  • MIR205HG depletion suppressed cancer progression, and rescue experiments confirmed MIR205HG targets SRSF1 to upregulate KRT17, impacting cell proliferation, migration, and apoptosis.

Conclusions:

  • MIR205HG acts as an oncogenic lncRNA in cervical cancer by modulating the MIR205HG/SRSF1/KRT17 axis.
  • This pathway influences key cellular processes including proliferation, migration, and apoptosis in cervical cancer.
  • MIR205HG represents a potential therapeutic target for cervical cancer intervention.

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