ArticleAmerican journal of translational research2026
LncRNA CDIPTOSP-induced destabilization of KLF17 promotes ovarian cancer progression through STAU1-mediated mRNA decay.
Article in American journal of translational research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Ovarian cancer (OC) remains one of the most lethal gynecologic malignancies, largely due to its poorly understood pathogenesis, which limits the development of effective early detection and targeted therapy. This study was designed to explore the potential role of the long non-coding RNA CDIPTOSP in OC progression. We observed high expression of CDIPTOSP in OC tissues and cell lines. Knockdown of CDIPTOSP impeded the proliferation and migration of OC cells. Using the RNA pull-down-Liquid Chromatography-Tandem Mass Spectrometry (LC-MS/MS) approach, we found that CDIPTOSP bound staufen double-stranded RNA binding protein 1 (STAU1). In turn, CDIPTOSP-STAU1 interactions were essential for KLF transcription factor 17 (KLF17) mRNA destabilization. Notably, depletion of KLF17 could rescue the tumor-suppressive effects caused by CDIPTOSP knockdown, whereas overexpression of KLF17 abolished the tumor-promoting effects induced by overexpressing CDIPTOSP. In conclusion, our study provided the first evidence of the CDIPTOSP/STAU1/KLF17 axis in the regulation of OC progression.
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