AI Article Synopsis
- CIP2A is linked to the activation of oncogenic proteins and contributes to the growth of cancer cells, specifically in radioresistant head and neck cancer (HNC) with TP53 mutations.
- The study found that while radiation alone didn't significantly harm HN31 cancer cells or lower CIP2A levels, combining radiation with rapamycin heightened the cancer cells' sensitivity to radiation by reducing CIP2A expression and promoting cellular senescence.
- These findings indicate that targeting CIP2A with rapamycin could be a promising therapeutic approach to treat radioresistant HNC that have TP53 mutations by inducing senescence in cancer cells.
Article Abstract
Background: CIP2A may activate multiple oncogenic proteins and promote the proliferation of various cancer cells.
Methods: We investigated that the role of CIP2A in radioresistant head and neck cancer (HNC) cell line with TP53 mutation and the effect of the rapamycin on the response of HN31 with TP53 mutation cells to irradiation related to CIP2A expression.
Results: CIP2A expression was stimulated by p53 mutation and critical for the inhibition of senescence induction in response to radiation. The treatment with radiation alone neither induced cytotoxicity in HN31 cells nor completely suppressed the activation of CIP2A. However, the combination of radiation and rapamycin increase the radiosensitivity through the induction of senescence with downregulation of CIP2A expression both in vivo and in vitro.
Conclusion: Our results suggest that CIP2A may serve as a therapeutic target of rapamycin through induction of senescence in radioresistant HNC with TP53 mutation.
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| http://dx.doi.org/10.1002/hed.25868 | DOI Listing |
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