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.
Mol Med Rep. 2021 Jul;24(1). doi: 10.3892/mmr.2021.12162. Epub 2021 May 26.
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, , 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.
食管癌（EC）是全球第六大癌症相关死亡原因，其发病率逐年递增。因此，进一步阐明 EC 发展的机制可能有助于确定其治疗的新型生物标志物和靶点。本研究旨在确定神经胶质瘤扩增序列（GBAS）的功能作用，GBAS 是一种新鉴定的基因，已被报道在多种癌症中发挥关键作用，包括在 EC 细胞的恶性行为中，如细胞活力、集落形成、细胞凋亡和细胞周期进程。本研究结果显示，通过 Celigo 细胞计数分析和集落形成试验分别证实，下调 GBAS 显著抑制 TE-1 和 KYSE-150 细胞系中的细胞活力和集落形成，而通过 Annexin V APC 染色下调 GBAS 可显著增加 EC 细胞的凋亡率。此外，下调 GBAS 后，通过 PI 染色，TE-1 和 KYSE-150 细胞的细胞周期进程被阻滞在 G1 期。综上所述，本研究结果表明，GBAS 可能通过调节细胞活力、凋亡和细胞周期进程在 EC 中发挥作用。
