Journal
DISCOVER ONCOLOGY
Volume 13, Issue 1, Pages -Publisher
SPRINGER
DOI: 10.1007/s12672-022-00561-7
Keywords
LSCC; ROCK1; Tumorigenesis and progression; FAK
Categories
Funding
- Research Grant for Health Science and Technology of Pudong Health Bureau of Shanghai [PW2020B-10]
- Young Medical Talents Training Program of Pudong Health Bureau of Shanghai [PWRq2021-06]
- National Fund Cultivation project [2022GPY-B04]
- Pudong New Area health system discipline leader project [PWRd2021-04]
- Shanghai Pudong Science & Technology Development Foundation [PKJ2021-Y13]
- Subject Construction Project of Pudong Health Committee of Shanghai [PWZy202006]
- Technology of Pudong Health Bureau of Shanghai [PW2019D-4]
- Key specialty Construction Project of Health Bureau of Shanghai [ZX2019C06]
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ROCK1 promotes tumorigenesis and progression of LSCC through the FAK signaling pathway. Its overexpression is correlated with advanced stage and poor survival prognosis. Inhibition of FAK activity impairs the tumor-promoting effects.
Laryngeal squamous cell carcinoma (LSCC) is one of the most common head and neck squamous cell carcinomas (HNSCC). Rho-associated kinase1 (ROCK1) is considered to promote progression of numerous cancers, however, its role in LSCC is still unknown. Here, the expression level of ROCK1 is higher in LSCC tissues than non-tumor tissues, and the expression level of ROCK1 is positively correlated with advanced stage and poor survival prognosis. ROCK1 knockdown in TU686 and TU212 cells dramatically inhibits cellular proliferation, migration and invasion. Whereas the overexpression of ROCK1 reversed these changes. FAK signaling pathway plays an essential role in promoting LSCC progression. Inhibiting FAK activity with TAE226 observably impairs the tumor-promoting effects. In conclusion, ROCK1 promotes LSCC tumorigenesis and progression via the FAK signaling pathway, targeting the ROCK1 molecule may represent potential targets for clinical LSCC treatment.
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