Loss of XIST lncRNA unlocks stemness and cellular plasticity in ovarian cancer

Ikrame Naciri & Sha Sun et al. · 2024-11-15

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.

Funding
Cancer Research Training and Education CoordinationElucidating the molecular basis of lncRNA evolution for mammalian dosage compensationElucidating the molecular basis of lncRNA evolution for mammalian dosage compensationCancer Research Training and Education Coordination

NCI NIH HHS

P30 CA062203

NIGMS NIH HHS

R01 GM141424

HHS | NIH | National Institute of General Medical Sciences (NIGMS)

R01GM141424

HHS | NIH | National Cancer Institute (NCI)

P30CA062203

HHS | NIH | National Cancer Institute

P30CA062203

HHS | NIH | National Institute of General Medical Sciences

R01GM141424