AI Article Synopsis

  • Cervical cancer ranks as the fourth most common cancer among women and is a leading cause of cancer-related deaths due to advanced stages and treatment resistance.
  • Researchers investigated the role of an epigenetic regulator, polycomb repressor complex 1 (PRC1), specifically focusing on the subunit CBX2, which is found to be increased in cervical cancer and linked to poor patient outcomes.
  • The study revealed that CBX2 enhances cancer cell growth, provides resistance to treatments like cisplatin and radiation, and helps maintain cancer stem cell properties, suggesting it could be a key factor for cervical cancer prognosis and a potential target for future therapies.

Article Abstract

Cervical cancer is the fourth most common malignancy and the fourth leading cause of cancer-related death among women. Advanced stages and resistance to treatment in cervical cancer induce cancer-related deaths. Although epigenetics has been known to plays a vital role in tumor progression and resistance, the function of epigenetic regulators in cervical cancer is an area of investigation. In this study, we focused on an epigenetic regulator, polycomb repressor complex 1 (PRC1) in cervical cancer. Through bioinformatics analysis and immunochemistry, we subsequently identified CBX2, the deregulated subunit of PRC1, which is up-regulated in cervical cancer and associated with poor prognosis and unfavorable clinicopathological characteristics. We provided functional evidence demonstrating that CBX2 promoted cervical cancer cell proliferation. Furthermore, CBX2 exhibited an anti-apoptotic effect, which induced resistance to cisplatin and ionizing radiation in cervical cancer cells. Moreover, CBX2 was involved in maintaining cancer stemness. These findings suggest CBX2 plays an important role in cervical cancer progression and resistance to treatment, and may serve as a potential biomarker for prognosis and resistance as well as a potential therapeutic target.

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Source
http://dx.doi.org/10.1016/j.jbc.2025.108170DOI Listing

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