胃癌（GC）是一种普遍存在的恶性肿瘤，对人类健康构成严重威胁。Aurora A（AURKA）的过表达常与各种癌症的自我更新和致瘤性相关。Chebulagic酸（CA）已被证明具有潜在的肿瘤抑制剂作用，基于其抵制多种肿瘤生物活性的能力。然而，CA通过调节AURKA/β-连环蛋白/Wnt信号通路抑制GC进展的可能机制尚未得到研究。本研究调查了GC中AURKA表达水平。我们进一步在MKN1和NUGC3胃癌细胞系中检测了CA对细胞增殖、迁移和凋亡的影响，并评估了其抑制肿瘤生长的效果。我们证明AURKA在GC中高度表达并与不良预后相关。我们证明CA治疗显著抑制了GC细胞的增殖和迁移，并诱导了凋亡。与车组相比，CA治疗严重减少了肿瘤的体积、重量和转移。CA还在体外和体内抑制了AURKA和AURKA/β-连环蛋白/Wnt信号通路的表达。总之，本研究结果表明，AURKA的高表达可能是GC患者不良预后的独立因素，CA显著抑制了GC的肿瘤生物学功能并抑制了AURKA/β-连环蛋白/Wnt通路。版权所有©2023 Zhao, Shi, Ma, Pan, Wang, Yuan, Dong和Ying。

Gastric cancer (GC) is a prevalent malignant neoplasm that poses a serious threat to human health. Overexpression of Aurora A (AURKA) is frequently associated with the self-renewal and tumorigenicity of various cancers. Chebulagic acid (CA) has been examined as a potential tumor suppressor based on its ability against numerous tumor biological activities. However, the possible mechanisms of CA inhibition of the progression of GC by mediating the AURKA/β-catenin/Wnt signaling pathway have not been investigated. The present study investigated the level of AURKA expression in GC. We further examined the effect of CA on cell proliferation, migration, and apoptosis in the MKN1 and NUGC3 GC cell lines, and its efficacy in suppressing tumor growth was assessed in tumor bearing mice model. We demonstrated that AURKA was highly expressed in GC and associated with poor prognosis. We demonstrated that treatment with CA significantly inhibited the proliferation and migration of GC cells and induced apoptosis. Compared to the vehicle group, CA treatment severely diminished the volume and weight and the metastasis of tumors. CA also inhibited the expression of AURKA and the AURKA/β-catenin/Wnt signaling pathway in vitro and in vivo. Collectively, the present results demonstrated that high expression of AURKA may be an independent factor of poor prognosis in patients with GC, and CA significantly suppressed the tumor biological functions of GC and inhibited the AURKA/β-catenin/Wnt pathway.Copyright © 2023 Zhao, Shi, Ma, Pan, Wang, Yuan, Dong and Ying.