ACTN1 promotes HNSCC tumorigenesis and cisplatin resistance by enhancing MYH9-dependent degradation of GSK-3β and integrin β1-mediated phosphorylation of FAK.

"Declarations Ethics approval and consent to participateAll human samples were collected with the informed consent of the patients, and the experiments were approved by the Institutional Review Board at the First Affiliated Hospital of Sun Yat-sen University. All animal procedures complied with the guidelines of the Institutional Animal Care and Use Committee (IACUC) at Southern Medical University. Consent for publicationNot applicable. Competing interestsThe authors declare that they have no competing interests. Competing interests The authors declare that they have no competing interests."

"Funding This work was supported by National Natural Science Foundation of China (81901006, 82372905), Young Top-notch Talent of Pearl River Talent Plan (0920220228), Guangdong Provincial Science and Technology Project Foundation (2022A0505050038), Scientific Research Talent Cultivation Project of Stomatological Hospital, Southern Medical University (RC202005) and Science Research Cultivation Program of Stomatological Hospital, Southern Medical University (PY2020002)."