Background

Gastric cancer (GC) is threatening public health as there are at least one million new cases reported each year. Rhomboid domain-containing protein 1 (SEC61G) has been identified to regulate tumor cell survival, metastasis and cellular response by regulating glycolysis. However, the function of SEC61G in gastric cancer is not fully understood.

Objectives

To investigate the effect of SEC61G on proliferation, epidermal growth factor receptor (EGFR) and glycolysis levels on GC, as well as the sensitivity of GC to etoposide.

Results

SEC61G is highly expressed in gastric cancer tissues and gastric cell lines. SEC61G knockdown suppresses the cell viability and EdU incorporation. Meanwhile, SEC61G knockdown attenuated the phosphorylation of EGFR and AKT. SEC61G knockdown suppressed the migration, invasion, glucose uptake, lactate release and ATP production, while elevated oxygen consumption rate (OCR), promoting the sensitivity of gastric cancer to etoposide.

Conclusions

SEC61G knockdown weakened the proliferation, EGFR phosphorylation and glycolysis of gastric cancer cells, as well as increased the sensitivity of gastric cancer to etoposide, which make SEC61G a promising therapeutic target for gastric cancer treatment.

中文翻译：

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SEC61G敲低通过EGFR和糖酵解介导的途径增强胃癌细胞对依托泊苷的敏感性

背景

胃癌 (GC) 正在威胁公众健康，每年至少报告一百万个新病例。含菱形结构域的蛋白 1 (SEC61G) 已被鉴定可通过调节糖酵解来调节肿瘤细胞的存活、转移和细胞反应。然而，SEC61G 在胃癌中的功能尚不完全清楚。

目标

探讨SEC61G对GC增殖、表皮生长因子受体(EGFR)和糖酵解水平的影响，以及GC对依托泊苷的敏感性。

结果

SEC61G在胃癌组织和胃细胞系中高表达。SEC61G 敲低会抑制细胞活力和 EdU 掺入。同时，SEC61G 敲低减弱了 EGFR 和 AKT 的磷酸化。SEC61G敲低抑制了胃癌的迁移、侵袭、葡萄糖摄取、乳酸释放和ATP产生，同时提高了耗氧率（OCR），促进了胃癌对依托泊苷的敏感性。

结论

SEC61G敲低减弱了胃癌细胞的增殖、EGFR磷酸化和糖酵解，并增加了胃癌对依托泊苷的敏感性，这使得SEC61G成为胃癌治疗的有前景的治疗靶点。