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.
Long non-coding RNA HOTAIR has been revealed to participate in the tumorigenesis of various cancers. However, the mechanism of HOTAIR involvement in cervical cancer has not been identified. Hence, this study aimed to explore the oncogenic and chemoresistant roles of HOTAIR in cervical cancer, and its underlying mechanism. RT-PCR, Western blot, and Luciferase assay were employed to determine the relationship of HOTAIR with miR-29b and PTEN and to study the role of HOTAIR in cervical cancer. CCK8 assay, cell migration, and invasion assay were used to reveal the role of HOTAIR in cervical cancer cell proliferation and metastasis. The inhibitory dose of chemotherapeutics was determined by CCK8 assay using probit analysis. HOTAIR was found to bind with miR-29b, and a negative correlation existed between HOTAIR and miR-29b expression in cervical cancer cells. In addition, HOTAIR promoted the migration and proliferation of cervical cancer cell lines HeLa and Siha, showing effects opposite to miR-29b. Further, HOTAIR facilitated the resistance of both HeLa and Siha cells against cisplatin, paclitaxel and docetaxel, whereas miR-29 suppressed the resistance of both cervical cancer cells against the 3chemotherapeutics. In addition, HOTAIR enhanced epithelial-to-mesenchymal transition (EMT), while miR-29b exerted an inhibitory effect on EMT. In cervical cancer cells, miR-29b did not affect promoter methylation of PTEN but regulated PTEN expression by targeting SP1. Transfection of miR-29b mimics led to a significant downregulation of PI3K. HOTAIR promotes chemoresistance by facilitating EMT through the miR-29b/PTEN/PI3K axis in cervical cancer.
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