AI Article Synopsis

  • The study investigated how SERPINB2 influences various biological processes in nasopharyngeal carcinoma cells, including cell growth, migration, and response to radiation.
  • It was found that upon SERPINB2 overexpression, cell proliferation decreased and cell cycle arrest occurred at the G2/M phase, indicating a potential mechanism for inhibiting tumor growth.
  • Additionally, SERPINB2 overexpression reduced the cells' ability to invade and migrate, as well as enhancing their sensitivity to radiation therapy, suggesting a new approach for improving treatment outcomes in this type of cancer.

Article Abstract

The aim of this study was to evaluate the effect of SERPINB2 on cell proliferation, cell cycle, epithelial-mesenchymal transition (EMT), invasion, migration, and radiosensitivity in nasopharyngeal carcinoma cells. Both CNE2R and CNE2 cells were transfected with pEGFP-N1-SERPINB2. Cell proliferation was measured by MTT assay, cell cycle by flow cytometry, and SERpINB2 expression by quantitative real-time polymerase chain reaction (qRT-PCR). Western blot was carried out to detect the protein expression. In addition, SERPINB2 and β-catenin were located intracellularly using an immunofluorescent assay, and cell migration and invasion were measured by wound healing and Transwell assays, respectively. Radiosensitivity was assessed using colony formation and MTT assays. SERPINB2 expression was downregulated in CNE2R cells. After transfection with pEGFP-N1-SERPINB2, the OD values were decreased, and there was an increased fraction in the G2/M phase. Moreover, SERPINB2 overexpression could inhibit the invasion and migration capabilities of CNE2R and CNE2 cells, with downregulation of vimentin, N-cadherin, nuclear β-catenin, matrix metalloproteinase (MMP)-2 and MMP-9, and upregulation of E-cadherin. Moreover, transfection with the SERPINB2 plasmid reduced the growth rate of CNE2R cells at doses of 2, 4 and 6 Gy, and also decreased the surviving fractions. Overexpression of SERPINB2 could reduce the proliferation, invasion and migration capabilities of CNE2R and CNE2 cells, and led to G2/M arrest via EMT inhibition, and this may be a potential strategy for enhancing the radiation sensitivity of nasopharyngeal carcinoma cells.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6530626PMC
http://dx.doi.org/10.1093/jrr/rrz003DOI Listing

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