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Article Abstract

BACKGROUND RNA binding protein RNPC1 has a tumor-suppressive role in various tumors, nevertheless, the role of RNPC1 in human endometrial cancer (EC) are never been reported. MATERIAL AND METHODS Western blot, quantitative polymerase chain reaction and sphere forming analysis were performed to evaluate the stem-like traits of cells and RNPC1-induced effects on EC cell stemness. RNA immunoprecipitation (RIP) was constructed to investigate the underlying mechanisms. RESULTS The spheres formed by EC cells, named EC spheres, exhibited a remarkably higher stemness than the parental cells, which is characterized as the increase of sphere forming ability, ALDH1 activity, stemness marker expression and migration ability. Notably, RNPC1 expression was decreased in poorly differentiated EC cells than that in EC cells with moderately differentiated. Additionally, RNPC1 expression was significantly decreased in EC spheres and RNPC1 overexpression attenuated the stemness of EC spheres. Moreover, RNPC1 overexpression decreased the migration ability of EC spheres. Mechanistic studies showed that RNPC1 overexpression activated the Hippo pathway through directly binding to MST1/2. Inhibition of MST1/2 rescued RNPC1-mediated effects on EC sphere stemness. CONCLUSIONS Therefore, our results indicate a novel RNPC1/MST1/2 signaling responsible for EC cell stemness.

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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7055196PMC
http://dx.doi.org/10.12659/MSM.921389DOI Listing

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Article Synopsis
  • RNPC1 is a RNA binding protein that is known for its tumor-suppressive role in various cancers, but its specific effects on endometrial cancer (EC) were previously unstudied.
  • Using methods like Western blot and quantitative PCR, researchers found that EC cells showed increased stem-like properties when grown as spheres, and RNPC1 levels were lower in less differentiated EC cells.
  • The study revealed that overexpressing RNPC1 reduced the stemness and migration abilities of EC spheres by activating the Hippo pathway through binding to MST1/2, highlighting a new signaling mechanism in EC cell biology.
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