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Overexpressed miR-122-5p Promotes Cell Viability, Proliferation, Migration And Glycolysis Of Renal Cancer By

Shuai Wang1, Wei Zheng1, Alin Ji1

  • 1Department of Urology, Zhejiang Provincial People's Hospital, People's Hospital of Hangzhou Medical College, Hangzhou 310014, Zhejiang Province, People's Republic of China.

Cancer Management and Research
|December 10, 2019
PubMed
Abstract

Insights

Overexpressed miR-122-5p promotes renal cancer progression by regulating pyruvate kinase M2 (PKM2). Silencing miR-122-5p inhibits cell viability, migration, and glycolysis, offering therapeutic potential for renal cancer.

Area of Science:

  • Oncology
  • Molecular Biology
  • Biochemistry

Background:

  • Renal cancer remains a deadly urological malignancy with limited effective treatments.
  • MicroRNAs (miRNAs) play crucial roles in cancer development and progression.
  • miR-122-5p has emerged as a potential regulator in various cancers.

Purpose of the Study:

  • To investigate the functional role and underlying mechanisms of miR-122-5p in renal cancer.
  • To explore the relationship between miR-122-5p and pyruvate kinase M2 (PKM2) in renal cancer cells.

Main Methods:

  • Quantitative real-time PCR (RT-qPCR) and Western blot to detect miR-122-5p and PKM2 expression.
  • Cell Counting Kit-8 (CCK-8) assay for cell viability.
  • Flow cytometry for cell cycle and apoptosis analysis.
  • Wound healing assay for cell migration.
  • Measurement of glucose consumption and lactate production.
  • Western blot for autophagy-related proteins.

Main Results:

  • miR-122-5p was upregulated in renal cancer cells, particularly in 786-O cells.
  • Silencing miR-122-5p or PKM2 significantly reduced renal cancer cell viability.
  • Knockdown of miR-122-5p or PKM2 induced G1 phase arrest, increased apoptosis, and inhibited cell migration.
  • Silencing miR-122-5p promoted autophagy, while siPKM2 transfection increased glucose consumption.

Conclusions:

  • Overexpressed miR-122-5p promotes renal cancer cell viability, proliferation, migration, glycolysis, and autophagy.
  • miR-122-5p negatively regulates PKM2 expression in renal cancer.
  • Targeting miR-122-5p presents a potential therapeutic strategy for renal cancer.
Keywords:
PKM2cell viabilityglycolysismiR-122-5prenal cancer

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