MEIS3 Expression Predicts Poor Prognosis in Ovarian Cancer and Represents a Potential Therapeutic Target
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Abstract
Ovarian cancer is the most lethal gynecologic malignancy, marked by late-stage diagnosis, high recurrence, and inevitable platinum resistance. The molecular mechanisms driving tumor progression and chemoresistance remain incompletely understood, underscoring the need for new prognostic biomarkers and therapeutic targets. The MEIS (Myeloid Ecotropic Viral Integration Site) family of TALE homeobox transcription factors is a relevant regulatory node in several malignancies, but its role in gynecologic cancers remains poorly defined. This review combines the literature with original bioinformatic analyses of MEIS1, MEIS2, and MEIS3 expression, prognostic significance, genomic alterations, functional dependency, and molecular correlations in ovarian cancer. GEPIA2 analysis showed significant downregulation of MEIS2 and MEIS3 in tumor versus normal tissue, and Kaplan–Meier analysis showed that high MEIS3 expression was an adverse prognostic factor (HR = 1.32, p = 0.0073). cBioPortal profiling identified MEIS alterations in 20% of ovarian serous cystadenocarcinoma cases, mainly copy-number changes. MEIS3 also correlated positively with the EMT regulators ZEB1, VIM, and SNAI1, supporting a model in which MEIS3 drives ovarian cancer progression via EMT and stemness programs. These findings establish MEIS3 as a candidate prognostic biomarker and therapeutic target in ovarian cancer.
