LncRNA HOTAIR enhances RCC2 to accelerate cervical cancer progression by sponging miR-331-3p

• Gulimire Buranjiang ^[1] ; Ailikemu Abuduwanke ^[2] ; Xiaowen Li ^[3] ; Guzalinuer Abulizi ^[4]
  1. [1] Department of Gynecologic Oncology Radiation Therapy (Ward II), Xinjiang Medical University, Xinjiang Medical University Third Clinical Medical College (Affiliated Tumor Hospital), Urumqi, Xinjiang, China
  2. [2] Department of Internal Neurology, Xinjiang Uygur Autonomous Region Children’s Hospital, Urumqi, Xinjiang, China
  3. [3] Department of Gynecologic Oncology Radiation Therapy (Ward II), Xinjiang Medical University, Third Clinical Medical College (Affiliated Tumor Hospital), Urumqi, Xinjiang, China
  4. [4] Department of Gynecological Surgery (Ward V), Xinjiang Medical UniversityXinjiang Medical UniversityThird Clinical Medical College (Affiliated Tumor Hospital), Urumqi, Xinjiang, China

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• Localización: Clinical & translational oncology, ISSN 1699-048X, Vol. 25, Nº. 6, 2023, págs. 1650-1660
• Idioma: inglés
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• Resumen

  • Purpose Long noncoding RNAs (lncRNAs) have been gradually regarded as influential indicators of various cancers. The present study aimed to identify the effects of lncRNA HOTAIR on cervical cancer progression.

    Methods RNA and protein expressions were quantified by RT-qPCR and western blot assays. Fluorescence in situ hybridization (FISH) assay was carried out to examine the intracellular location of HOTAIR. Cancer cell viability and mobility were detected by CCK-8, colony formation, transwell and wound healing assays. Binding relationships between miR-331-3p and HOTAIR/RCC2 were validated by luciferase reporter assay.

    Results RT-qPCR assays showed that HOTAIR levels were notably upregulated in cervical cancer tissues and cell lines. Furthermore, a fluorescence in situ hybridization (FISH) assay suggested that HOTAIR was mostly located in the cytoplasm of cancer cells, indicating a sponging function. CCK-8, colony formation, Transwell and wound-healing assays indicated that knockdown of HOTAIR in HeLa and SiHa cells significantly reduced cell growth, migration and invasion. Subsequently, miR-331-3p was proven to be the target molecule of HOTAIR. In addition, results from Pearson's correlation analysis indicated negative correlation between HOTAIR and miR-331-3p in cervical cancer tissues. HOTAIR negatively modulated miR-331-3p expression. Ultimately, the target gene of miR-331-3p was verified to be RCC2, and miR-331-3p negatively modulated RCC2 expression. In addition, analysis on clinical cervical cancer tissues confirmed the negative correlation between miR-331-3p and RCC2. HOTAIR and RCC2 showed oncogenic functions in HeLa and SiHa cells, while miR-331-3p exerted the reverse effect.

    Conclusions HOTAIR plays a carcinogenic role in cervical cancer by targeting the miR-331-3p/RCC2 axis. Moreover, clinical cervical cancer tissues confirmed the negative correlation between miR-331-3p with lncRNA HOTAIR and RCC2. These data suggested an underlying therapeutic target for cervical cancer.