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Updated: Nov 19, 2025

Identification and Characterization of Metastatic Factors by Gene Transfer into the Novel RIP-Tag; RIP-tva Murine Model
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Published on: October 16, 2017

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RBM10 regulates human TERT gene splicing and inhibits pancreatic cancer progression

Wenjing Xiao1,2, Xin Chen3, Xia Li4

  • 1School of Materials Science and Engineering, Southwest Jiaotong University Chengdu 611756, China.

American Journal of Cancer Research
|February 1, 2021
PubMed

Insights

Pancreatic cancer involves altered splicing of the hTERT gene. The splicing factor RBM10 suppresses tumor growth by promoting a non-functional hTERT isoform, offering a potential therapeutic target.

Area of Science:

  • Molecular Biology
  • Cancer Research
  • Genetics

Background:

  • Alternative splicing of the human telomerase reverse transcriptase (hTERT) gene to produce the full-length hTERT (hTERT-FL) isoform reactivates telomerase, a key event in pancreatic cancer (PrCa) pathogenesis.
  • The precise mechanisms regulating hTERT splicing in PrCa remain largely unknown.

Purpose of the Study:

  • To investigate the role of the splicing factor RBM10 in regulating hTERT alternative splicing in pancreatic cancer.
  • To elucidate the functional consequences of RBM10-mediated hTERT splicing on cancer progression and telomerase activity.

Main Methods:

  • Bioinformatics analysis to identify candidate splicing factors.
  • In vitro and in vivo experiments assessing the impact of RBM10 modulation on PrCa cell proliferation.
  • RNA immunoprecipitation (RIP) and RNA pull-down assays to determine RBM10 binding and its effect on hTERT splicing.

Main Results:

  • RBM10 acts as a splicing factor that promotes the production of a function-less hTERT isoform (hTERT-s) by excluding exons 7 and 8.
  • RBM10 expression is inversely correlated with pancreatic cancer progression.
  • Modulation of RBM10 levels significantly affects PrCa cell proliferation in vitro and in xenograft models.
  • RBM10-mediated splicing suppresses telomerase activity and telomere shortening.

Conclusions:

  • RBM10 plays a critical role in regulating hTERT alternative splicing in pancreatic cancer.
  • RBM10 acts as a tumor suppressor by inhibiting telomerase activity through the generation of hTERT-s.
  • RBM10 represents a potential therapeutic target for pancreatic cancer treatment.
Keywords:
Alternative RNA splicingRBM10hTERTpancreatic cancer

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