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Engineering Artificial Factors to Specifically Manipulate Alternative Splicing in Human Cells
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Published on: April 26, 2017

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Modulation of alternative splicing by anticancer drugs

Sayeed Ur Rehman1, Mohammed Amir Husain1, Tarique Sarwar1

  • 1Department of Biochemistry, Faculty of Life Sciences, Aligarh Muslim University, Aligarh, India.

Wiley Interdisciplinary Reviews. RNA
|April 28, 2015
PubMed

Insights

Alternative splicing generates diverse protein isoforms, impacting cancer cell growth and apoptosis. Anticancer drugs can manipulate splicing, offering potential for novel cancer therapies by promoting pro-apoptotic forms.

Area of Science:

  • Molecular Biology
  • Cancer Research
  • Pharmacology

Background:

  • Pre-messenger RNA (mRNA) alternative splicing produces distinct protein isoforms with varied functions.
  • Altered gene expression in cell growth and apoptosis is characteristic of cancer cells.
  • Alternative splicing patterns of key cancer-related genes are crucial for understanding and treating cancer.

Purpose of the Study:

  • To review current knowledge on alternative splicing in important cancer-related genes.
  • To discuss the generation of functionally distinct protein isoforms through alternative splicing.
  • To explore the role of anticancer drugs in modulating alternative splicing patterns and their therapeutic potential.

Main Methods:

  • Review of existing literature on alternative splicing in cancer.
  • Analysis of splicing patterns and resulting protein isoforms.
  • Examination of anticancer drug mechanisms in modulating gene splicing.

Main Results:

  • Chemotherapy resistance can arise from altered expression of anti-apoptotic or pro-apoptotic isoforms.
  • Anticancer drugs can either induce pro-apoptotic isoforms (sensitizing cells) or anti-apoptotic isoforms (conferring resistance).
  • Specific examples of gene splicing modulation by anticancer drugs are discussed.

Conclusions:

  • Alternative splicing plays a significant role in cancer development and treatment.
  • Anticancer drugs can modulate alternative splicing, influencing therapeutic outcomes.
  • Shifting splicing towards pro-apoptotic isoforms presents a promising therapeutic strategy for cancer treatment.

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