4.7 Article

Association of CASC18/miR-20a-3p/TGFB2 ceRNA axis with occult lymph node metastasis in tongue squamous cell carcinoma

Journal

MOLECULAR MEDICINE
Volume 27, Issue 1, Pages -

Publisher

SPRINGER
DOI: 10.1186/s10020-021-00345-9

Keywords

CASC18; TGFB2; ceRNA; Occult lymph node metastasis; Tongue squamous cell carcinoma

Funding

  1. National Natural Science Foundation of China [81703005]
  2. Natural Science Foundation of Hunan Province [2017JJ3195, 2018JJ3317, 2021JJ30427]
  3. Research Project of Health and Family Planning Commission of Hunan Province [C2019080, 202102082037]
  4. Key Clinical Specialty Construction Project (Head&Neck Surgery) of Provincial Health Commission of Hunan province

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A novel CASC18/miR-20a-3p/TGFB2 ceRNA axis was identified in OLNM of TSCC. Higher CASC18 expression was positively correlated with the presence of OLNM and worse outcome of TSCC patients, while knockdown of CASC18 inhibited cell migration and invasion.
Background Tongue squamous cell carcinoma (TSCC) ranks as the most prevalent malignancy in the oral cavity. TSCC patients with occult lymph node metastasis (OLNM) are thought to be at risk of worse outcome. However, regulatory mechanisms underlying OLNM remain less investigated. Methods In the present study, CASC18/miR-20a-3p/TGFB2 axis was identified and evaluated by bioinformatic and qRT-PCR analyses. Effects of CASC18 knockdown on cell migration and invasion were determined by wound healing and transwell assays. Western blot, ELISA, RNA pulldown and luciferase reporter assays were performed for mechanism verification. Results CASC18 was identified up-regulating in TSCC tumours, and especially in those from patients with OLNM. Importantly, we found higher CASC18 expression was positively correlated with the presence of OLNM and worse outcome of TSCC patients. Furthermore, we demonstrated that CASC18 knockdown repressed cell migration and invasion through inhibiting epithelial-mesenchymal transition, which could be partly rescued by miR-20a-3p inhibitor. Regarding the molecular mechanism, we further confirmed that CASC18 functioned as a ceRNA to sponge miR-20a-3p to enhanceTGFB2 expression and secretion. Conclusion In conclusion, we have reported a novel CASC18/miR-20a-3p/TGFB2 ceRNA axis in OLNM of TSCC. Our findings will contribute to a deeper understanding of the molecular mechanism of OLNM in TSCC, and facilitate the development of diagnostic methods for assisting treatment decision-making.

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