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UBE2T regulates FANCI monoubiquitination to promote NSCLC progression by activating EMT

  • Authors:
    • Jiguang Zhang
    • Jingdong Wang
    • Jincheng Wu
    • Jianyuan Huang
    • Zhaoxian Lin
    • Xing Lin
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    Affiliations: Shengli Clinical Medical College, Fujian Medical University, Fuzhou, Fujian 350001, P.R. China
    Copyright: © Zhang et al. This is an open access article distributed under the terms of Creative Commons Attribution License.
  • Article Number: 139
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    Published online on: June 14, 2022
       https://doi.org/10.3892/or.2022.8350
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Abstract

Fanconi anemia complementation group I (FANCI) is a critical protein for maintaining DNA stability. However, the exact role of FANCI in tumors remains to be elucidated. The present study aimed to explore the role and potential mechanism of action of FANCI in non‑small cell lung cancer (NSCLC). To quantify the expression levels of FANCI and ubiquitin‑conjugating enzyme E2T (UBE2T) in NSCLC tissues, reverse‑transcription quantitative PCR and western blotting were employed. Cell Counting Kit‑8, wound healing and Transwell assays along with flow cytometry analysis and tumor xenograft were used to investigate the biological effects of FANCI in NSCLC in vitro and in vivo. The binding of FANCI with UBE2T was confirmed using a co‑immunoprecipitation assay. Epithelial‑to‑mesenchymal transition (EMT) protein markers were quantified via western blotting. The results showed that FANCI expression level was higher in NSCLC tumor tissues, compared with adjacent tissues. In A549 and H1299 cells, knockdown of FANCI inhibited cell proliferation, migration, invasion, cell cycle and EMT in vitro. Tumor growth was repressed in vitro, upon downregulation of FANCI expression. UBE2T was observed to directly bind to FANCI and regulate its monoubiquitination. Overexpression of UBE2T reversed the effects induced by FANCI knockdown in NSCLC cells. Furthermore, it was noted that FANCI interacted with WD repeat domain 48 (WDR48). Overexpression of WDR48 reversed the effects of FANCI on cell proliferation, migration and EMT. In conclusion, FANCI was identified to be a putative oncogene in NSCLC, wherein FANCI was monouniubiquitinated by UBE2T to regulate cell growth, migration and EMT through WDR48. The findings suggested that FANCI could be used as a prognostic biomarker and therapeutic target for NSCLC.
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Copy and paste a formatted citation
Spandidos Publications style
Zhang J, Wang J, Wu J, Huang J, Lin Z and Lin X: UBE2T regulates FANCI monoubiquitination to promote NSCLC progression by activating EMT. Oncol Rep 48: 139, 2022.
APA
Zhang, J., Wang, J., Wu, J., Huang, J., Lin, Z., & Lin, X. (2022). UBE2T regulates FANCI monoubiquitination to promote NSCLC progression by activating EMT. Oncology Reports, 48, 139. https://doi.org/10.3892/or.2022.8350
MLA
Zhang, J., Wang, J., Wu, J., Huang, J., Lin, Z., Lin, X."UBE2T regulates FANCI monoubiquitination to promote NSCLC progression by activating EMT". Oncology Reports 48.2 (2022): 139.
Chicago
Zhang, J., Wang, J., Wu, J., Huang, J., Lin, Z., Lin, X."UBE2T regulates FANCI monoubiquitination to promote NSCLC progression by activating EMT". Oncology Reports 48, no. 2 (2022): 139. https://doi.org/10.3892/or.2022.8350
Copy and paste a formatted citation
x
Spandidos Publications style
Zhang J, Wang J, Wu J, Huang J, Lin Z and Lin X: UBE2T regulates FANCI monoubiquitination to promote NSCLC progression by activating EMT. Oncol Rep 48: 139, 2022.
APA
Zhang, J., Wang, J., Wu, J., Huang, J., Lin, Z., & Lin, X. (2022). UBE2T regulates FANCI monoubiquitination to promote NSCLC progression by activating EMT. Oncology Reports, 48, 139. https://doi.org/10.3892/or.2022.8350
MLA
Zhang, J., Wang, J., Wu, J., Huang, J., Lin, Z., Lin, X."UBE2T regulates FANCI monoubiquitination to promote NSCLC progression by activating EMT". Oncology Reports 48.2 (2022): 139.
Chicago
Zhang, J., Wang, J., Wu, J., Huang, J., Lin, Z., Lin, X."UBE2T regulates FANCI monoubiquitination to promote NSCLC progression by activating EMT". Oncology Reports 48, no. 2 (2022): 139. https://doi.org/10.3892/or.2022.8350
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