METTL3-stabilized lncRNA SNHG7 accelerates glycolysis in prostate cancer via SRSF1/c-Myc axis

Related Experiment Video

Updated: Sep 27, 2025

Sequencing Small Non-coding RNA from Formalin-fixed Tissues and Serum-derived Exosomes from Castration-resistant Prostate Cancer Patients
12:13

Sequencing Small Non-coding RNA from Formalin-fixed Tissues and Serum-derived Exosomes from Castration-resistant Prostate Cancer Patients

Published on: November 19, 2019

6.9K

Jun Liu1, Jun-Fang Yuan2, Yu-Zhong Wang3

  • 1The Second Affiliated Hospital, Department of Urology, Hengyang Medical School, University of South China, Hengyang, Hunan, 421001, PR China.

Experimental Cell Research
|April 11, 2022
PubMed
Abstract

Insights

Methyltransferase-like 3 stabilizes long non-coding RNA SNHG7, promoting prostate cancer cell glycolysis. This occurs through the serine/arginine-rich splicing factor 1 and c-Myc pathway, impacting tumor progression.

Area of Science:

  • Oncology
  • Molecular Biology
  • Biochemistry

Background:

  • Long non-coding RNAs (lncRNAs) are increasingly recognized for their roles in cancer metabolism.
  • The lncRNA small nucleolar RNA host gene 7 (SNHG7) exhibits oncogenic properties in prostate cancer (PCa).
  • The precise mechanisms by which SNHG7 influences PCa metabolism remain largely unexplored.

Purpose of the Study:

  • To elucidate the role and underlying mechanisms of SNHG7 in prostate cancer metabolism.
  • To investigate the interplay between SNHG7, N6-methyladenosine (m6A) modification, and key regulatory proteins in PCa.

Main Methods:

  • Gene expression and RNA stability were quantified using qRT-PCR in PCa tissues and cells.
  • Cell proliferation was assessed via CCK-8 assays, while glycolysis was evaluated by measuring glucose uptake, lactate, ATP, and ECAR.
  • Interactions between SNHG7, SRSF1, and c-Myc were analyzed using bioinformatics and RNA immunoprecipitation (RIP) assays.

Main Results:

  • SNHG7 and c-Myc showed elevated expression in PCa tissues and cells.
  • METTL3-mediated m6A modification enhanced SNHG7 stability, and SNHG7 knockdown inhibited PCa cell proliferation and glycolysis.
  • SNHG7 was found to regulate c-Myc by interacting with SRSF1, promoting glycolysis via the SRSF1/c-Myc axis.

Conclusions:

  • METTL3-stabilized SNHG7 accelerates glycolysis in prostate cancer through the SRSF1/c-Myc pathway.
  • This study enhances the understanding of m6A modifications in lncRNA metabolism and their contribution to tumor progression.
Keywords:
GlycolysisMETTL3Prostate cancerSNHG7SRSF1c-Myc

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