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<p>The long non-coding RNA (lncRNA) HOX transcript antisense RNA (HOTAIR), a tumor suppressor associated with various human cancers, regulates multiple cellular processes. However, the role of HOTAIR in papillary thyroid carcinoma remains unclear. Therefore, the purpose of the present study was to investigate the effect of HOTAIR on the proliferation and migration of PTC cells, and to explore its possible mechanism. The initial step involves conducting an analysis in The Cancer Genome Atlas database of the HOTAIR expression level between PTC and normal tissue samples. Reverse transcription-quantitative PCR was conducted to detect HOTAIR and microRNA (miRNA, miR)-206 expression in each cell line. We assessed cell proliferation using the CCK-8 and MTT assays. We employed the wound-healing and transwell assays to evaluate cell migration. The HOTAIR/miR-206/c-Met targeting relations were verified through dual-luciferase reporter assay. We analyzed changes in protein expression downstream of the c-Met/AKT/mTOR pathway by Western blotting. Our results showed that HOTAIR was highly expressed in PTC cells. Silencing HOTAIR significantly inhibited the proliferation and migration of PTC cells. Conversely, miR-206 expression was downregulated in PTC cells. Importantly, overexpressing miR-206 significantly inhibited PTC cell proliferation and migration. In conclusion, HOTAIR acts as a sponge for miR-206, thereby alleviating its repression of c-Met and activating the AKT/mTOR signaling pathway in PTC cells.</p>

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LncRNA HOTAIR promotes cell proliferation and migration in papillary thyroid carcinoma cells by sponging miR-206/c-Met axis

  • 期刊论文

  • 发表日期：

    2025年8月29日

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  • Xifeng Du,
  • Yufei Hao,
  • Min Liu,
  • Zhihui Hu,
  • Tao Yang,
  • Lizhen Lan

摘要

The long non-coding RNA (lncRNA) HOX transcript antisense RNA (HOTAIR), a tumor suppressor associated with various human cancers, regulates multiple cellular processes. However, the role of HOTAIR in papillary thyroid carcinoma remains unclear. Therefore, the purpose of the present study was to investigate the effect of HOTAIR on the proliferation and migration of PTC cells, and to explore its possible mechanism. The initial step involves conducting an analysis in The Cancer Genome Atlas database of the HOTAIR expression level between PTC and normal tissue samples. Reverse transcription-quantitative PCR was conducted to detect HOTAIR and microRNA (miRNA, miR)-206 expression in each cell line. We assessed cell proliferation using the CCK-8 and MTT assays. We employed the wound-healing and transwell assays to evaluate cell migration. The HOTAIR/miR-206/c-Met targeting relations were verified through dual-luciferase reporter assay. We analyzed changes in protein expression downstream of the c-Met/AKT/mTOR pathway by Western blotting. Our results showed that HOTAIR was highly expressed in PTC cells. Silencing HOTAIR significantly inhibited the proliferation and migration of PTC cells. Conversely, miR-206 expression was downregulated in PTC cells. Importantly, overexpressing miR-206 significantly inhibited PTC cell proliferation and migration. In conclusion, HOTAIR acts as a sponge for miR-206, thereby alleviating its repression of c-Met and activating the AKT/mTOR signaling pathway in PTC cells.