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HOTAIR Contributes to Stemness Acquisition of Cervical Cancer through Regulating miR-203 Interaction with ZEB1 on Epithelial-Mesenchymal Transition
Author(s) -
Wenying Zhang,
Jing Liu,
Qiongwei Wu,
Yu Liu,
Chengbin Ma
Publication year - 2021
Publication title -
journal of oncology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.228
H-Index - 54
eISSN - 1687-8469
pISSN - 1687-8450
DOI - 10.1155/2021/4190764
Subject(s) - hotair , gene knockdown , cancer stem cell , cancer research , epithelial–mesenchymal transition , cervical cancer , stem cell , metastasis , medicine , downregulation and upregulation , microrna , cancer cell , cancer , biology , cell culture , microbiology and biotechnology , long non coding rna , gene , genetics
Cervical cancer stem cells contribute respond to considerable recurrence and metastasis of patients with cervical cancer. The stemness properties were partly regulated by the interaction of lncRNAs and miRNAs. HOTAIR functions as an oncogenic lncRNA. Previous research studies revealed its role in regulating stemness properties in various cancers. However, the role of HOTAIR in cervical cancer stem cells is still unknown. Here, cisplatin-resistant and serum-free cultured cells exhibited stem cells properties. Cervical cancer stem cells exhibited greater invasion and migration compared with their parental cells, which was similar to cells overexpressing HOTAIR. HOTAIR was significantly overexpressed in cervical cancer stem cells, and knockdown of HOTAIR generated statistical downregulation of stemness markers. Additionally, HOTAIR expression was negatively correlated with the level of miR-203, which was found to be an inhibitory miRNA in regulating the expressions of stemness markers. Also, miR-203 expression was negatively correlated with ZEB1. These findings suggested that HOTAIR should be a positive contributor in stemness acquisition of cervical cancer cells, and this effect should correlate with the interaction with miR-203, which can be suppressed by ZEB1.

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