骨苷通过PI3K/AKT通路调节icam1介导的细胞粘附抑制肺腺癌的进展

IF 3 2区医学 Q3 BIOCHEMISTRY & MOLECULAR BIOLOGY

Molecular Carcinogenesis Pub Date : 2025-07-13 DOI:10.1002/mc.70007

Shangwei Xu, Chunji Chen, Hongwei Liu, Shuai Jiang, Zheng Li, Yun Wu

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引用次数: 0

摘要

肺癌具有高侵袭性和致死率的特点，对其分子机制进行深入的研究尤为必要。在我们的研究中，我们发现骨胰素（OGN）缺乏与肺腺癌（LUAD）的不良预后密切相关。OGN过表达可抑制LUAD细胞的增殖、迁移和侵袭。通过转录组测序分析和实验验证，我们发现这种ogn介导的肿瘤抑制作用与ICAM1下调诱导的细胞粘附功能有关，并受到PI3K/AKT信号通路的调控。本研究揭示了OGN参与LUAD进展的具体机制，为LUAD肿瘤抑制研究提供了新的证据和潜在靶点。

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Osteoglycin Inhibits the Progression of Lung Adenocarcinoma by Modulating ICAM1-Mediated Cell Adhesion via the PI3K/AKT Pathway.

Lung cancer is characterized by high aggressiveness and lethality, processing in-depth molecular mechanism investigation is particularly necessary. In our study, we found that osteoglycin (OGN) deficiency is strongly associated with a poor prognosis in lung adenocarcinoma (LUAD). OGN overexpression could inhibit the proliferation, migration, and invasion of LUAD cells. Through transcriptome sequencing analysis and experimental validation, we revealed that such OGN-mediated tumor suppression effect was related to cell adhesion function induced by ICAM1 downregulation, along with regulation by the PI3K/AKT signaling pathway. The present study demonstrated the specific mechanism of OGN involvement in LUAD progression, providing new evidence and potential targets for research on cancer suppression in LUAD.

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来源期刊

Molecular Carcinogenesis 医学-生化与分子生物学

CiteScore

7.30

自引率

2.20%

发文量

112

审稿时长

2 months

期刊介绍： Molecular Carcinogenesis publishes articles describing discoveries in basic and clinical science of the mechanisms involved in chemical-, environmental-, physical (e.g., radiation, trauma)-, infection and inflammation-associated cancer development, basic mechanisms of cancer prevention and therapy, the function of oncogenes and tumors suppressors, and the role of biomarkers for cancer risk prediction, molecular diagnosis and prognosis.