Gastric cancer (GC) is one of the most prevalent malignancies worldwide. Endoplasmic reticulum (ER) stress plays a key role in the progression of GC. Rapid proliferation of tumor cells interferes with ER homeostasis, leading to ER stress and triggering unfolded protein response. Therefore, it is very necessary to investigate abnormally expressed ER resident proteins (ERp) in cancer cells. This study aimed to investigate the possible roles of ERp44. The mRNA and protein expression of genes were detected using qRT-PCR and western blot. Cell apoptosis was calculated using flow cytometry. Cell proliferation was determined using CCK-8 and colony formation assay. Cell migration was detected by wound healing, and cell invasion was measured by transwell assay. We found that ERp44 was obviously decreased in GC tissues. Furthermore, ERp44 overexpression distinctly suppressed the proliferation, migration, and invasion of MGC-803 and KATO III cells. In contrast, apoptosis was promoted by ERp44 overexpression. Furthermore, mechanistic studies revealed that overexpression of ERp44 inhibited malignant biological processes by regulating the eIF-2α/CHOP signaling pathway. Taken together, our data demonstrated that ERp44 regulated the proliferation, migration, invasion, and apoptosis via ERp44/eIF-2α/CHOP axis in GC. Targeting the ERp44and ER stress may be a promising strategy for GC.

胃癌 (GC) 是全球最普遍的恶性肿瘤之一。内质网 (ER) 应激在 GC 的进展中起着关键作用。肿瘤细胞的快速增殖会干扰内质网稳态，导致内质网应激并触发未折叠蛋白反应。因此，非常有必要研究癌细胞中异常表达的内质网常驻蛋白（ERp）。本研究旨在探讨ERp44的可能作用。使用qRT-PCR和western blot检测基因的mRNA和蛋白表达。使用流式细胞术计算细胞凋亡。使用CCK-8和集落形成测定法测定细胞增殖。通过伤口愈合检测细胞迁移，并通过transwell测定法测量细胞侵袭。我们发现ERp44在 GC 组织中明显减少。此外，ERp44过表达明显抑制了 MGC-803 和 KATO III 细胞的增殖、迁移和侵袭。相反，ERp44过表达促进细胞凋亡。此外，机制研究表明，ERp44的过表达通过调节 eIF-2α/CHOP 信号通路来抑制恶性生物学过程。总之，我们的数据表明，ERp44通过 GC 中的ERp44 /eIF-2α/CHOP 轴调节增殖、迁移、侵袭和凋亡。针对ERp44和 ER 压力可能是 GC 的一个有前途的策略。