胃癌（GC）是全球第五大常见癌症，具有显着的异质性和不良预后的特点。因此，确定有效的预后因素并了解GC的潜在分子机制对于改善患者的预后至关重要。在本研究中，我们旨在探讨RECK（具有Kazal基序的逆转诱导富含半胱氨酸蛋白）在GC中的预后意义及其生物学功能的分子机制。采用多种生物信息学策略来检测其潜在功能和预后RECK 在 GC 中的效率。拯救实验揭示了RECK抑制肿瘤增殖、迁移和侵袭的分子机制是由AGS和HGC-27细胞中的ERK/MAPK信号介导的。利用综合生物信息学分析和蛋白质印迹分析，我们研究了 CALD1 和 RECK 之间的潜在相互作用。我们的研究结果表明，与正常样本相比，GC 样本中 RECK 的表达显着降低，RECK 被认为是 GC 患者预后的有希望的预测因子。此外，RECK 的上调与 GC 中的高免疫和低转移微环境呈明显正相关。从机制上讲，RECK 阻碍肿瘤细胞生长、迁移和侵袭的抗肿瘤作用是由 ERK/MAPK 信号通路介导的。此外，我们还发现RECK抑制了ERK磷酸化降低介导的CALD1磷酸化。RECK是一种有前途的预后生物标志物，可能会在GC患者中塑造高肿瘤免疫和低转移的微环境。此外，RECK 通过灭活 GC 细胞中的 ERK/MAPK 信号传导来发挥其肿瘤抑制作用。© 2023。作者。

Gastric cancer (GC) ranks as the fifth most common cancer worldwide and is characterized by its significant heterogeneity and unfavorable prognosis. Thus, identifying efficient prognostic factors and understanding the underlying molecular mechanisms in GC are essential for improving patient outcomes. In this study, we aimed to investigate the role of RECK (reversion-inducing cysteine-rich protein with Kazal motifs) in the prognostic significance and molecular mechanisms of its biological function in GC.Multiple bioinformatics strategies were performed to detect the potential functions and prognostic efficiency of RECK in GC. Rescue experiments revealed that the molecular mechanism by which RECK in inhibited tumor proliferation, migration, and invasion was mediated by ERK/MAPK signaling in AGS and HGC-27 cells. Using integrated bioinformatics analysis and western blot assay, we investigated the potential interaction between CALD1 and RECK.Our findings revealed significantly decreased RECK expression in GC samples compared to normal samples and RECK was identified as a promising predictor for the prognosis of GC patients. Moreover, upregulation of RECK demonstrated a distinctly positive association with a high-immunity and low-metastasis microenvironment in GC. Mechanistically, the antitumour effects of RECK on hampering tumor cell growth, migration, and invasion were mediated by the ERK/MAPK signaling pathway. In addition, we also illustrated that RECK inhibited the phosphorylation of CALD1 mediated by decreased phosphorylation of ERK.RECK is a promising prognostic biomarker and may shape a high-tumor-immunity and low-metastasis microenvironment in patients with GC. Moreover, RECK exerted its tumor-suppressive effects by the inactivation of ERK/MAPK signaling in GC cells.© 2023. The Author(s).