Department of General Surgery, The Second Affiliated Hospital of Wenzhou Medical University, Wenzhou, 325000 Zhejiang, China.
Wenzhou Medical University, Wenzhou, 325035 Zhejiang, China.
J Immunol Res. 2022 Jun 2;2022:1917585. doi: 10.1155/2022/1917585. eCollection 2022.
Gastric cancer is a prevalent malignant tumor with high morbidity and poor prognosis. Asiaticoside (AC) has antitumor effects, while its role in gastric cancer is elusive. Thus, this study investigated the effect of AC on gastric cancer progression.
Cell viability and migration were determined using the CCK-8 and Transwell migration assay. Endoplasmic reticulum stress was detected through measuring the expressions of GRP78, Chop, and hnRNPA1 by Western blot. The luciferase assay confirmed the relationship between miR-635 and High Mobility Group AT-Hook 1 (HMGA1). The effect of AC on tumor growth was evaluated by establishing a xenograft tumor. The survival rate of mice was analyzed by Kaplan-Meier analysis.
AC suppressed gastric cancer cell viability and restrained cell migration. AC inhibited the expressions of the cell proliferation marker PCNA and EMT-related marker N-cadherin and increased E-cadherin expression. AC elevated the levels of GRP78 and Chop and suppressed the level of hnRNPA1. In addition, AC restrained gastric cancer proliferation and migration ability and induced endoplasmic reticulum stress by upregulating miR-635 expression. Furthermore, HMGA1 was proven to be a target of miR-635. AC constrained gastric cancer cell proliferation and migration and promoted endoplasmic reticulum stress by regulating HMGA1. Moreover, AC suppressed tumor growth and improved the survival time of mice. Additionally, AC elevated the expressions of miR-635, E-cadherin, GRP78, and Chop and inhibited Ki-67, HMGA1, N-cadherin, and hnRNPA1 expressions in tumor tissues of mice.
AC suppressed gastric cancer progression and induced endoplasmic reticulum stress via the miR-635/HMGA1 axis, providing a valuable drug against gastric cancer.
胃癌是一种发病率高、预后差的常见恶性肿瘤。积雪草苷（AC）具有抗肿瘤作用，但在胃癌中的作用尚不清楚。因此，本研究探讨了 AC 对胃癌进展的影响。
通过 CCK-8 和 Transwell 迁移实验测定细胞活力和迁移。通过 Western blot 测定内质网应激标志物 GRP78、Chop 和 hnRNPA1 的表达来检测内质网应激。荧光素酶实验证实了 miR-635 与高迁移率族蛋白 A1（HMGA1）之间的关系。通过建立异种移植瘤评估 AC 对肿瘤生长的影响。通过 Kaplan-Meier 分析分析小鼠的存活率。
AC 抑制胃癌细胞活力并抑制细胞迁移。AC 抑制细胞增殖标志物 PCNA 和 EMT 相关标志物 N-钙粘蛋白的表达，增加 E-钙粘蛋白的表达。AC 上调 GRP78 和 Chop 的水平，抑制 hnRNPA1 的水平。此外，AC 通过上调 miR-635 的表达抑制胃癌的增殖和迁移能力，并诱导内质网应激。此外，HMGA1 被证明是 miR-635 的靶标。AC 通过调节 HMGA1 抑制胃癌细胞增殖和迁移并促进内质网应激。此外，AC 抑制肿瘤生长并提高小鼠的生存时间。此外，AC 上调 miR-635、E-钙粘蛋白、GRP78 和 Chop 的表达，并抑制 Ki-67、HMGA1、N-钙粘蛋白和 hnRNPA1 在小鼠肿瘤组织中的表达。
AC 通过 miR-635/HMGA1 轴抑制胃癌进展并诱导内质网应激，为治疗胃癌提供了有价值的药物。
