Chromatin modified protein 4C (CHMP4C) facilitates the malignant development of cervical cancer cells

Despite improvements in prevention and treatment, cervical cancer (CC) still poses a serious threat to women’s health. CHMP4C (chromatin modified protein 4C) is a subunit of the endosomal sorting complex required for transport, which is expressed in both nucleus and cytoplasm. Here, we examined the...

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Bibliographic Details
Published in:FEBS open bio 2020-07, Vol.10 (7), p.1295-1303
Main Authors: Lin, Shu‐Li, Wang, Mei, Cao, Qing‐Qing, Li, Qing
Format: Article
Language:English
Subjects:
Bioinformatics
Cell migration
Cell proliferation
Cervical cancer
Cervix
Chromatin
chromatin modified protein 4C
Cytoplasm
Dehydrogenases
EMT
Experiments
Gene expression
Genomes
Human papillomavirus
Mesenchyme
proliferation
Proteins
Standard deviation
Statistical analysis
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Summary:Despite improvements in prevention and treatment, cervical cancer (CC) still poses a serious threat to women’s health. CHMP4C (chromatin modified protein 4C) is a subunit of the endosomal sorting complex required for transport, which is expressed in both nucleus and cytoplasm. Here, we examined the effect of CHMP4C on the biological behavior of CC cells and the underlying mechanisms. We report that CHMP4C expression is higher in CC tissues, and high CHMP4C expression is associated with lower survival. Up‐regulation of CHMP4C in C‐33A cells accelerates cell proliferation, migration and invasion, whereas down‐regulation of CHMP4C in Ca Ski cells had the opposite effect. Moreover, overexpression of CHMP4C induced activation of the epithelial–mesenchymal transition pathway, whereas depletion of CHMP4C inhibited activation. Our results suggest that CHMP4C contributes to the viability and motility of CC cells by modulating epithelial–mesenchymal transition and may facilitate the identification of novel biomarkers for CC therapy. Chromatin modified protein 4C is highly expressed in cervical cancer (CC) tissues and cell lines, and contributes to the proliferation, invasion and migration of CC cells by modulating the epithelial–mesenchymal transition. Our findings may facilitate the identification of novel biomarkers for CC therapy.
ISSN:2211-5463
2211-5463
DOI:10.1002/2211-5463.12880