Cancer-related Molecular Pathways
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Insight is provided into IRES-mediated translation of Δ160p53, which can be considered a novel target for cancer treatment and its role in cancer regulation.
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Mutations in p53 and its 12 isoforms can alter its functions. As N-terminally truncated isoforms of p53 (delta40p53, delta133p53, and delta160p53) participate in tetramer formation, they are important regulators of cancer fate. Although delta40p53- and delta133p53-mediated regulation of cancer is well reported, the mechanism underlying delta160p53 production and its functional role remains unclear. We investigated the internal ribosomal entry site (IRES)-mediated translation of Δ160p53 and its role in cancer regulation. As differential synthesis of delta160p53 was observed under different stress conditions, IRES-mediated translation of this isoform was demonstrated using bicistronic luciferase constructs. No cryptic promoters or splicing sites were detected in the IRES sequence. Cell death and late apoptosis were significantly decreased, while proliferation, the number of cells in the S phase, and drug resistance were induced by delta160p53. Furthermore, delta160p53 did not induce p53-responsive promoters. RNA sequencing analysis of delta160p53 overexpression showed similar results, along with the inhibition of other tumor suppressor genes. Overall, our results provide insights into IRES-mediated translation of delta160p53, which can be considered a novel target for cancer treatment.
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@article{Ghosh2026IRES,
title = {IRES-mediated translation of delta160p53 regulates p53 functions and fine-tunes cancer homeostasis},
author = {P K Ghosh and Piyanki Das and Sahana Ghosh and Risabh Sahu and Sabari Shree V and Subrata Patra and Arindam Maitra and Saumitra Das},
journal = {bioRxiv (Cold Spring Harbor Laboratory)},
year = {2026},
doi = {10.64898/2026.08.21.744132},
url = {https://doi.org/10.64898/2026.08.21.744132}
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