AI Article Synopsis
- Cancer stem cells (CSCs) limit the success of current cancer treatments due to their ability to evade the immune system and their unique survival mechanisms.
- Recent research highlights the role of epigenetic changes—specifically histone modifications—in how CSCs develop resistance to therapies, suggesting that correcting these modifications could enhance treatment effectiveness.
- Strategies involving histone modification inhibitors, when combined with traditional chemotherapy or immunotherapy, are being explored to weaken CSCs and make them more susceptible to immune attacks.
Article Abstract
The development and immune evasion of cancer stem cells (CSCs) limit the efficacy of currently available anticancer therapies. Recent studies have shown that epigenetic reprogramming regulates the expression of characteristic marker proteins and tumor plasticity associated with cancer cell survival and metastasis in CSCs. CSCs also possess unique mechanisms to evade external attacks by immune cells. Hence, the development of new strategies to restore dysregulated histone modifications to overcome cancer resistance to chemotherapy and immunotherapy has recently attracted attention. Restoring abnormal histone modifications can be an effective anticancer strategy to increase the therapeutic effect of conventional chemotherapeutic and immunotherapeutic drugs by weakening CSCs or by rendering them in a naïve state with increased sensitivity to immune responses. In this review, we summarize recent findings regarding the role of histone modifiers in the development of drug-resistant cancer cells from the perspectives of CSCs and immune evasion. In addition, we discuss attempts to combine currently available histone modification inhibitors with conventional chemotherapy or immunotherapy.
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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC10394043 | PMC |
| http://dx.doi.org/10.1038/s12276-023-01014-z | DOI Listing |
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