AI Article Synopsis
- Plasticity in cancer enables tumor cells to switch states, contributing to tumor diversity and challenges in treatment.
- XIST long noncoding RNA is found to be down-regulated in ovarian cancer, correlating with increased cancer stemness and poorer patient outcomes.
- Reducing XIST levels in ovarian cancer cells enhances stemness and alters cell characteristics under specific conditions, highlighting XIST as a potential target for therapies in CSC-rich tumors.
Article Abstract
Plasticity, a key hallmark of cancer, enables cells to transition into different states, driving tumor heterogeneity. This cellular plasticity is associated with cancer progression, treatment resistance, and relapse. Cancer stem cells (CSCs) play a central role in this process, yet the molecular factors underlying cancer cell stemness remain poorly understood. In this study, we explored the role of XIST (X-inactive specific transcript) long noncoding RNA in ovarian cancer stemness and plasticity through in silico and in vitro analyses. We found that XIST is significantly down-regulated in ovarian tumors, with low XIST expression linked to a higher stemness index and lower overall survival. Knocking down XIST in ovarian cancer cells enhanced stemness, particularly increasing mesenchymal-like CSCs, and under hypoxic conditions, it promoted epithelial-like CSC markers. Our findings suggest that XIST loss leads to CSC enrichment and cellular plasticity in ovarian cancer, pointing to potential therapeutic targets for patients with low XIST expression.
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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC11588085 | PMC |
| http://dx.doi.org/10.1073/pnas.2418096121 | DOI Listing |
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