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<p>Epithelial ovarian cancer (EOC) is the most common subtype of ovarian cancer and is a highly recurrent and lethal malignancy of the female reproductive system. Accumulating evidence has indicated that long non-coding RNAs (lncRNAs) play pivotal roles in tumorigenesis. Long intergenic non-protein coding RNA 704 (LINC00704) has been recognized as an oncogenic lncRNA in several malignancies. However, its specific role in EOC remains unclear. In this study, RT-qPCR revealed the upregulation of LINC00704 in EOC tissues and cell lines. CCK-8 and EdU assays showed that LINC00704 knockdown inhibited EOC cell proliferation. Flow cytometry analysis demonstrated that LINC00704 silencing induced EOC cell cycle arrest and apoptosis. Transwell assays indicated the inhibitory effects of LINC00704 silencing on EOC cell migration and invasion. Mechanistically, bioinformatics analysis, RNA pull-down, luciferase reporter and RNA immunoprecipitation assays revealed that LINC00704 upregulated SLC44A1 expression by competitively binding to miR-323a-3p. Moreover, rescue experiments showed that SLC44A1 overexpression could reverse LINC00704 silencing-mediated effects on the malignant behaviors of EOC cells. In conclusion, LINC00704 promotes EOC cell aggressiveness in vitro by regulating the miR-323a-3p/SLC44A1 axis.</p>

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LINC00704 facilitates cell proliferation, migration, and invasion via miR-323a-3p/SLC44A1 axis in epithelial ovarian cancer

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年4月29日

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  • Xiaojuan Kong,
  • Lei Lei,
  • Zhengjiao Ma

摘要

Epithelial ovarian cancer (EOC) is the most common subtype of ovarian cancer and is a highly recurrent and lethal malignancy of the female reproductive system. Accumulating evidence has indicated that long non-coding RNAs (lncRNAs) play pivotal roles in tumorigenesis. Long intergenic non-protein coding RNA 704 (LINC00704) has been recognized as an oncogenic lncRNA in several malignancies. However, its specific role in EOC remains unclear. In this study, RT-qPCR revealed the upregulation of LINC00704 in EOC tissues and cell lines. CCK-8 and EdU assays showed that LINC00704 knockdown inhibited EOC cell proliferation. Flow cytometry analysis demonstrated that LINC00704 silencing induced EOC cell cycle arrest and apoptosis. Transwell assays indicated the inhibitory effects of LINC00704 silencing on EOC cell migration and invasion. Mechanistically, bioinformatics analysis, RNA pull-down, luciferase reporter and RNA immunoprecipitation assays revealed that LINC00704 upregulated SLC44A1 expression by competitively binding to miR-323a-3p. Moreover, rescue experiments showed that SLC44A1 overexpression could reverse LINC00704 silencing-mediated effects on the malignant behaviors of EOC cells. In conclusion, LINC00704 promotes EOC cell aggressiveness in vitro by regulating the miR-323a-3p/SLC44A1 axis.