Article Sidebar
Published:
Apr 19, 2023DOI:
10.4314/tjpr.v22i3.6Keywords:
Article Details
Submission of a manuscript to this journal is a representation that the manuscript has not been published previously and is not under consideration for publication elsewhere.
All authors named in each manuscript would be required to sign a form (to be supplied by the Editor) so that they may retain their copyright in the article but to assign to us (the Publishers) and its licensees in perpetuity, in all forms, formats and media (whether known or created in the future) to (i) publish, reproduce, distribute, display and store the contribution, (ii) translate the contribution into other languages, create adaptations, reprints, include within collections and create summaries, extracts and/or abstracts of the contribution, (iii) create any other derivative works(s) based on the contribution, (iv) to exploit all subsidiary rights in the contribution, (v) the inclusion of electronic links from the contribution to third party material where-ever it may be located, and (vi) license any thrid party to do any or all of the above.
Main Article Content
ANKRD22 enhances cancer stem cell growth and cisplatin resistance in cervical cancer via NUSAP1/Wnt/β catenin pathway
Abstract
Purpose: To investigate the role of ankyrin repeat domain 22 (ANKRD22) and nucleolar spindle-associated protein 1 (NUSAP1)-mediated Wnt/β-catenin pathway in cervical cancer (CC).
Methods: ANKRD22 levels were evaluated in tissue samples collected from CC patients. The CC cells were transfected with an ANKRD22 silencing vector. Cell proliferation and migration were determined via colony formation, BrdU, scratch and Transwell assays. Sphere formation test was performed to determine the effect of ANKRD22 on the cancer stem cell (CSC)-like traits of CC cells. The effect of ANKRD22 on CSC-like traits was further evaluated by determining the expressions of the CSC markers, Oct4, SOX2, and Nanog, while cisplatin resistance was assessed by CCK-8 assay. The effect of ANKRD22 on the NUSAP1-mediated Wnt/β-catenin pathway was evaluated by determining the expression levels of β-catenin, matrix metalloproteinase-7, and adenomatous polyposis coli. Moreover, ANKRD22-mediated tumor growth was monitored in vivo using an animal model.
Results: ANKRD22 was overexpressed in cancer tissues from CC patients (p < 0.05). ANKRD22 knockdown suppressed CC cell proliferation, migration, invasion, and CSC traits, and also positively regulated Wnt/β-catenin pathway through NUSAP1 (p < 0.05). However, the inhibition of ANKRD22 suppressed tumor growth in vivo through NUSAP1. In addition, the silencing of ANKRD22 alleviated cisplatin resistance in CC cells (p < 0.05).
Conclusion: ANKRD22 activates NUSAP1/Wnt/β-catenin pathway, and enhances CSC-like characteristics and cisplatin resistance, thus exacerbating the malignant behaviors of CC cells. Therefore, ANKRD22 could serve as a promising target for CC treatment.
