The role of SEMG1 overexpression in OSCC tumorigenesis and its relation with metabolic molecules

Author:

Wang Jing12345,Zhong Nian‐Nian1,Yi Jing‐Rui1,Liu Xuan‐Hao1,Wang Han‐Qi1,Liu Bing16ORCID,Man Qi‐Wen16ORCID,Bu Lin‐Lin16ORCID

Affiliation:

1. State Key Laboratory of Oral & Maxillofacial Reconstruction and Regeneration, Key Laboratory of Oral Biomedicine Ministry of Education, Hubei Key Laboratory of Stomatology School & Hospital of Stomatology, Wuhan University Wuhan China

2. Central Laboratory Peking University School and Hospital of Stomatology Beijing China

3. National Clinical Research Center for Oral Diseases Beijing China

4. National Engineering Laboratory for Digital and Material Technology of Stomatology Beijing China

5. Beijing Key Laboratory of Digital Stomatology Beijing China

6. Department of Oral & Maxillofacial‐Head Neck Oncology School & Hospital of Stomatology, Wuhan University Wuhan China

Abstract

AbstractObjectivesThis study aimed to investigate the expression and biological significance of Semenogelin 1 (SEMG1), a member of the cancer‐testis antigen family, in oral squamous cell carcinoma (OSCC). Further, we explored its potential association with metabolism‐related molecules.MethodsSEMG1 expression levels in OSCC were determined through immunohistochemistry, flow cytometry, and Western blot analyses. To decipher the biological implications of SEMG1 in OSCC, the CAL27 OSCC cell line was either stably overexpressed with SEMG1 or subjected to SEMG1‐shRNA knockdown. The relationship between clinicopathological parameters and SEMG1 expression in OSCC patients was also assessed.ResultsSEMG1 was found to be overexpressed in OSCC, though its expression was not influenced by the pathological grade. The fluorescent dihydroethidium assay indicated that SEMG1 augmented reactive oxygen species production. The mitochondrial membrane potential assay suggested a significant upregulation of mitochondrial membrane potential by SEMG1. Cell cycle assessments highlighted that SEMG1 overexpression led to a notable rise in cells entering the S‐phase. Additionally, a strong correlation between SEMG1 expression and both ENO1 and PKM2 expression in OSCC was observed.ConclusionsThe findings underscore the elevated expression of SEMG1 in OSCC and its contributory role in the tumorigenesis of OSCC patients.

Funder

National Natural Science Foundation of China

Fundamental Research Funds for the Central Universities

Natural Science Foundation of Hubei Province

Publisher

Wiley

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