Long non‑coding RNA B3GALT5‑AS1 contributes to the progression of gastric cancer via interacting with CSNK2A1

Wang,Ping; Sun,Guang-Bin; Dou,Guang-Xian; Wang,Bai-Qing

doi:10.3892/etm.2021.10359

Long non‑coding RNA B3GALT5‑AS1 contributes to the progression of gastric cancer via interacting with CSNK2A1

Authors:
- Ping Wang
- Guang-Bin Sun
- Guang-Xian Dou
- Bai-Qing Wang
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Affiliations: Center of Digestive Endoscopy, Tianjin Fifth Central Hospital, Tianjin 300451, P.R. China
Published online on: June 30, 2021 https://doi.org/10.3892/etm.2021.10359
Article Number: 927
Copyright: © Wang et al. This is an open access article distributed under the terms of Creative Commons Attribution License.

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Abstract

Gastric cancer is a type of cancer that is characterized by high morbidity and mortality rates. Long non‑coding RNA (lncRNA) β‑1,3‑galactosyltransferase 5‑AS1 (B3GALT5‑AS1) was previously found to be highly expressed in the serum of patients with gastric cancer. However, the regulatory effects of B3GALT5‑AS1 in gastric cancer remain poorly understood. The present study aimed to investigate the effects of B3GALT5‑AS1 in gastric cancer cell lines. The expression levels of B3GALT5‑AS1 were determined in different gastric cancer cell lines (AGS, HGC‑27 and MKN‑45) using reverse transcription‑quantitative PCR. The potential interaction between B3GALT5‑AS1 and casein kinase 2 a1 (CSNK2A1) was evaluated using an RNA binding protein immunoprecipitation and RNA pull down assays. Western blot analysis was performed to measure protein expression levels. Cell Counting Kit‑8 assay was utilized to determine cell viability, whilst cell invasion and migration were assessed using Transwell and wound healing assays, respectively. Apoptotic cells were evaluated using TUNEL assays. The results showed that B3GALT5‑AS1 expression was upregulated in MKN‑45 cells compared with the control group. In addition, B3GALT5‑AS1 could bind to CSNK2A1 to regulate its expression. B3GALT5‑AS1 knockdown attenuated cell viability, invasion and migration, whilst promoting cell apoptosis. These effects were partly reversed by CSNK2A1 overexpression. Overall, results of the present study revealed that interference with B3GALT5‑AS1 impeded gastric cancer cell migration and invasion whilst promoting apoptosis by regulating CSNK2A1 expression. These findings suggested that B3GALT5‑AS1 and CSNK2A1 may serve a tumorigenic role in the progression of gastric cancer and serve as therapeutic targets for this type of cancer.

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