[Effects of long non-coding RNA RP1-90L14.1 on the biological behaviors of cancer prostate LNCaP cells and its

Pin-Geng Wu1, Yu-Xi Zhang1, Zhe Zhang1

  • 1Department of Urology, The First Affiliated Hospital of China Medical University, Shenyang, Liaoning 110001, China.

Abstract

Insights

Long non-coding RNA RP1-90L14.1 significantly enhances prostate cancer cell proliferation, migration, and invasion. This lncRNA also promotes the expression of GRIN2A and BACE2, suggesting a role in prostate cancer progression.

Area of Science:

  • Molecular Biology
  • Oncology
  • Genetics

Background:

  • Prostate cancer is a significant health concern.
  • Long non-coding RNAs (lncRNAs) are increasingly recognized for their roles in cancer.
  • The specific function of lncRNA RP1-90L14.1 in prostate cancer is not fully understood.

Purpose of the Study:

  • To investigate the functional role of lncRNA RP1-90L14.1 in prostate cancer cell lines.
  • To determine the effect of RP1-90L14.1 on cell proliferation, migration, and invasion.
  • To examine the impact of RP1-90L14.1 on the expression of GRIN2A and BACE2.

Main Methods:

  • RT-PCR was used to detect lncRNA RP1-90L14.1 expression.
  • LNCaP cells were transfected with RP1-90L14.1 overexpression or vector plasmids.
  • Cell proliferation, migration, and invasion were assessed using CCK-8 and Transwell assays.
  • mRNA and protein levels of GRIN2A and BACE2 were determined by RT-PCR and Western blot.

Main Results:

  • RP1-90L14.1 expression was significantly higher in androgen-independent (LNCaP-AI) than androgen-dependent (LNCaP) prostate cancer cells.
  • Overexpression of RP1-90L14.1 significantly increased proliferation, migration, and invasion of LNCaP cells.
  • RP1-90L14.1 overexpression led to significantly increased mRNA and protein levels of GRIN2A and BACE2.

Conclusions:

  • lncRNA RP1-90L14.1 promotes the proliferation, migration, and invasion of prostate cancer cells.
  • RP1-90L14.1 upregulates the expression of GRIN2A and BACE2.
  • RP1-90L14.1 may function as an endogenous competitor influencing GRIN2A and BACE2 activity in prostate cancer.

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