Knockdown of GBAS regulates esophageal cancer cell viability and apoptosis

Peng,Jun; Ma,Ke; Rong,Hao; Xiao,Bo; Zhu,Jiang; He,Jin-Tao

doi:10.3892/mmr.2021.12162

Knockdown of GBAS regulates esophageal cancer cell viability and apoptosis

Authors:
- Jun Peng
- Ke Ma
- Hao Rong
- Bo Xiao
- Jiang Zhu
- Jin-Tao He
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Affiliations: Department of Thoracic Surgery, Sichuan Cancer Hospital and Institute, Sichuan Cancer Center, School of Medicine, University of Electronic Science and Technology of China, Chengdu, Sichuan 610054, P.R. China
Published online on: May 21, 2021 https://doi.org/10.3892/mmr.2021.12162
Article Number: 523
Copyright: © Peng et al. This is an open access article distributed under the terms of Creative Commons Attribution License.

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Abstract

Esophageal cancer (EC) is the sixth leading cause of cancer‑related mortality worldwide, with the incidence gradually increasing each year. Therefore, further clarifying the mechanism underlying the development of EC may be beneficial for identifying novel biomarkers and targets for its treatment. The present study aimed to determine the functional roles of glioblastoma‑amplified sequence (GBAS), a newly identified gene that has been reported to play crucial roles in multiple types of cancer, including in the malignant behavior of EC cells, such as cell viability, colony formation, cell apoptosis and cell cycle progression. The results of the present study revealed that, in vitro, the knockdown of GBAS significantly suppressed cell viability and colony formation in TE‑1 and KYSE‑150 cell lines, using a Celigo cell count analysis and colony formation assay respectively, whereas the apoptotic rate of EC cells was significantly increased by the knockdown of GBAS using Annexin V APC staining. Furthermore, following GBAS knockdown, the cell cycle progression of TE‑1 and KYSE‑150 cells was arrested in the G1 phase using PI staining. In conclusion, the findings of the present study suggested that GBAS may serve a role in EC by regulating cell viability, apoptosis and cell cycle progression.

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