S100A9 promotes the proliferation and migration of cervical cancer cells by inducing epithelial‑mesenchymal transition and activating the Wnt/β‑catenin pathway
Autor: | Aifang Li, Hui Sun, Huan Li, Liang Duan, Xueru Li, Lan Zhou, Shimei Yuan, Jiali Zhao, He Zha, Yue Gu, Jiaqing Xie |
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Rok vydání: | 2019 |
Předmět: |
0301 basic medicine
Cancer Research Wnt/β-catenin signaling pathway Epithelial-Mesenchymal Transition cervical cancer proliferation Uterine Cervical Neoplasms Vimentin Biology migration medicine.disease_cause HeLa 03 medical and health sciences 0302 clinical medicine Cell Movement Cell Line Tumor medicine Calgranulin B Humans Epithelial–mesenchymal transition S100A9 Wnt Signaling Pathway Cell Proliferation Oncogene EMT Wnt signaling pathway Cancer Articles medicine.disease biology.organism_classification Up-Regulation Gene Expression Regulation Neoplastic 030104 developmental biology Oncology 030220 oncology & carcinogenesis Catenin Cancer research biology.protein Female Carcinogenesis HeLa Cells |
Zdroj: | International Journal of Oncology |
ISSN: | 1791-2423 1019-6439 |
DOI: | 10.3892/ijo.2019.4793 |
Popis: | S100 calcium‑binding protein A9 (S100A9), a member of the S100 protein family, is often upregulated in various cancers, including cervical cancer. Elevated S100A9 expression is thought to serve an important role in tumorigenesis; however, the exact role of S100A9 in the modulation of cervical cancer and the underlying molecular mechanism remain unknown. In the present study, we aimed to investigate the effects of S100A9 on the proliferation and migration of cervical cancer cells, as well as the molecular mechanisms underlying these effects. Our results demonstrated that endogenous expression of S100A9 in SiHa and CaSki cell lines was significantly higher than in the HeLa cell line. As expected, overexpression of S100A9 enhanced the proliferation and migration of cervical cancer cells. In addition, S100A9 overexpression induced epithelial‑mesenchymal transition (EMT) as determined by reduced expression levels of the epithelial marker E‑cadherin, whereas the expression levels of the mesenchymal marker vimentin were upregulated. Furthermore, it was reported that the effects of S100A9 in the modulation of cervical cancer cells were mediated through the Wnt/β‑catenin signaling pathway as β‑catenin knockdown significantly suppressed the ability of S100A9 to enhance the proliferation and migration of cervical cancer cells. Collectively, these findings suggest that S100A9 promoted the proliferation and migration of cervical cancer cell lines. Furthermore, the underlying molecular mechanisms may be partially attributed to the induction of EMT and activation of the Wnt/β‑catenin signaling pathway. |
Databáze: | OpenAIRE |
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