4.2 Article

hsa_circ_0023305 Enhances Laryngeal Squamous Cell Carcinoma Progression and Modulates TRPM7 via miR-218-5p Sponging

Journal

BIOMED RESEARCH INTERNATIONAL
Volume 2021, Issue -, Pages -

Publisher

HINDAWI LTD
DOI: 10.1155/2021/9968499

Keywords

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Funding

  1. Academic Leaders Training Program of Pudong Health Bureau of Shanghai [PWRd2018-05]
  2. Research Grant for Health Science and Technology of Shanghai Municipal Health Commission [202140405]
  3. Top Talent Training Program of Gongli Hospital of Shanghai Pudong New Area [GLRb2018-02]
  4. Key Discipline Construction Project of Shanghai Health Bureau [ZK2019C-06]

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Recent research has revealed the mechanism of hsa_circ_0023305 in laryngeal squamous cell carcinoma (LSCC), showing its promotion of LSCC progression by regulating miR-218-5p and TRPM7. This study provides new insights into the role of circRNAs in cancer development and potential therapeutic targets for LSCC.
Recently, circular RNAs have been shown to function as critical regulators of many human cancers. However, the circRNA mechanism in laryngeal squamous cell carcinoma (LSCC) remains elusive. Recent investigations using bioinformatics analysis revealed high expression of hsa_circ_0023305 in LSCC tissues compared to normal tissues. Furthermore, we discovered that hsa_circ_0023305 expression level was positively correlated to tumor/node/metastasis (TNM) stage as well as lymph node metastasis in LSCC. Moreover, higher hsa_circ_0023305 levels were correlated to poorer LSCC patient outcomes. Knockdown of hsa_circ_0023305 significantly inhibited LSCC cell proliferation, invasion, and migration abilities. Our team validated that hsa_circ_0023305 functioned as a miR-218-5p sponge from a mechanistic perspective, targeting the melastatin-related transient receptor potential 7 (TRPM7) in LSCC cells. TRPM7 regulates a nonselective cation channel and promotes cancer proliferation and metastasis. Our data demonstrated that miR-218-5p was downregulated in LSCC and that miR-218-5p upregulation repressed LSCC proliferation and invasion both in vivo and in vitro. Additionally, we found that hsa_circ_0023305-mediated upregulation of TRPM7 inhibited miR-218-5p and contributed to LSCC migration, proliferation, and invasion. In summary, these data propose a new mechanism by which the hsa_circ_0023305/miR-218-5p/TRPM7 network enhances LSCC progression.

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