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Updated: Jan 28, 2026

Heterotypic Three-dimensional In Vitro Modeling of Stromal-Epithelial Interactions During Ovarian Cancer Initiation and Progression
Published on: August 28, 2012
LncRNA HOXB-AS1 Accelerates Epithelial Ovarian Cancer Progression by Modulating the miR-671-5p/SPTBN2 Axis
Chao He1, Wenying Peng2, Xuyue Jia3
1Department of Obstetrics and Gynecology, The First Hospital of Qiqihar, Qiqihar, China.
Abstract:
Epithelial ovarian cancer has the characteristics of high malignancy and poor survival outcomes. Long non-coding RNAs (lncRNAs) can mediate the biological function through regulating the expression of miRNA or protein in cancers. This study investigated the expression, function, and potential mechanism of lncRNA HOXB-AS1 in epithelial ovarian cancer. The levels of HOXB-AS1, miR-671-5p, and SPTBN2 mRNA in tissue samples and cells were measured by RT-qPCR after extraction of total RNA. The correlations between HOXB-AS1, miR-671-5p, and SPTBN2 mRNA were analyzed by Pearson's correlation coefficients. Cellular Fe2+ and ROS contents were measured by a Cell Ferrous Iron Colorimetric Assay Kit and a Reactive Oxygen Species assay kit. SPTBN2's downstream effectors SLC7A11 and GPX4 were measured by Western blot assay. The changes in cell viability, migration abilities, and invasion capacities were analyzed using CCK-8 and Transwell assays. HOXB-AS1 expression was upregulated in epithelial ovarian cancer and correlated with the FIGO stage. The decreased miR-671-5p and increased SPTBN2 mRNA expression were observed in epithelial ovarian cancer tissues and cells. Silencing of HOXB-AS1 inhibited cellular viability and invasion behaviors by promoting Fe2+ and ROS levels. HOXB-AS1 could regulate miR-671-5p and SPTBN2 expression and participate in the functional activities of ovarian cancer cells. HOXB-AS1 repressed ferroptosis in a miR-671-5p/SPTBN2-dependent manner in epithelial ovarian cancer, thereby facilitating the progression of ovarian cancer, which might be a therapeutic target for treating ovarian cancer.
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