Bibliographic Details
Title: |
NDUFA4 promotes the progression of head and neck paraganglioma by inhibiting ferroptosis. |
Authors: |
Wang, Zhigang, Tao, Erxing, Chen, Yiming, Wang, Qi, Liu, Min, Wei, Liang, Xu, Siyi 1905029@tongji.edu.cn, Chen, Wei 2000806@tongji.edu.cn, Zhong, Chunlong drchunlongzhong@tongji.edu.cn |
Source: |
Biochemistry & Cell Biology. Dec2023, Vol. 101 Issue 6, p523-530. 8p. |
Subject Terms: |
*PARAGANGLIOMA, *LENTIVIRUS diseases, *REACTIVE oxygen species, *MEMBRANE potential, *CELL survival |
Abstract: |
NDUFA4 is a component of respiratory chain–oxidative phosphorylation pathway. NDUFA4 is highly expressed in tumor tissues, but little is known about the function of NDUFA4 in head and neck paraganglioma (HNPGL). We examined NDUFA4 expression in tissues from 10 HNPGL patients and 6 controls using qRT-PCR and Western blotting. NDUFA4 knockdown PGL-626 cells were established by using lentivirus infection and puromycin screening. Cell viability, ATP production, lipid reactive oxygen species, and mitochondrial membrane potential assays were performed to investigate the ferroptotic effects in NDUFA4 deficiency HNPGL cancer cells. Xenograft mouse model was created to detect the synergetic antitumor action between NDUFA4 deficiency and Metformin. NDUFA4 was upregulated in tumor tissues of HNPGL patients. NDUFA4 knockdown impaired the assembly of mitochondrial respiratory chain complexes and decreased the production of ATP and reduced cancer cell viability. Mechanistically, NDUFA4 knockdown increased cell ferroptosis, which further promoted Metformin-induced ferroptosis in PGL-626 cells. Therefore, NDUFA4 deficiency enhanced Metformin-mediated inhibition of the HNPGL progression in mice. In conclusion, NDUFA4 promotes the progression of HNPGL, and NDUFA4 knockdown enhances Metformin-mediated inhibition of the HNPGL progression in a mouse model. [ABSTRACT FROM AUTHOR] |
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Database: |
Academic Search Complete |