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KRT4 suppresses oral squamous cell carcinoma development by reducing ATG4B-mediated autophagy

XIAOXU LI, YUN WANG, JUAN FANG, ZHI WANG, XIAOAN TAO, JUAN XIA, BIN CHENG*
Guangdong Provincial Key Laboratory of Stomatology, Guanghua School of Stomatology, Hospital of Stomatology, Sun Yat-Sen University, Guangzhou, 510055, China
* Corresponding Author:BIN CHENG,

BIOCELL 2022, 46(2), 441-451. https://doi.org/ 10.32604/biocell.2021.014844

Received 03 November 2020; Accepted 12 January 2021; Issue published 20 October 2021

Abstract

Head and neck squamous cell carcinoma is the sixth most common tumor worldwide, and half of head and neck squamous cell carcinoma patients are with oral squamous cell carcinoma (OSCC). 300,000 new cases of OSCC were reported annually. Even with multi-modality treatment, the prognosis of OSCC remains unsatisfactory. Thus, it is urgent to discover novel therapeutic targets for OSCC. Some microarray studies have revealed that Keratin 4 (KRT4) is downregulated in OSCC, whereas its role in OSCC development remains unknown. The present study revealed that KRT4 suppressed OSCC progression by inducing cell apoptosis and inhibiting cell invasion. In addition, KRT4 over-expression inhibited autophagy by blocking the interaction of autophagy-related 4B cysteine peptidase (ATG4B) and microtubule-associated protein 1A/1B light chain 3 (LC3) to regulate apoptosis and invasion of OSCC. In conclusion, KRT4 played an important role in OSCC development through regulating ATG4B-mediated autophagy and may be a novel therapeutic drug target of OSCC.

Keywords

Oral squamous cell carcinoma, KRT4, Cancer-suppressive role, ATG4B, Autophagy

Cite This Article

LI, X., WANG, Y., FANG, J., WANG, Z., TAO, X. et al. (2022). KRT4 suppresses oral squamous cell carcinoma development by reducing ATG4B-mediated autophagy. BIOCELL, 46(2), 441–451.



This work is licensed under a Creative Commons Attribution 4.0 International License , which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
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