CLEC5A 通过激活 PI3K/AKT/mTOR 通路促进胃癌细胞的增殖。
CLEC5A promotes the proliferation of gastric cancer cells by activating the PI3K/AKT/mTOR pathway.
机构信息
Department of Gastrointestinal Surgery, Affiliated Hospital of Nantong University, Nantong, 226001, Jiangsu, China.
Medical College, Nantong University, Nantong, 226001, Jiangsu, China.
出版信息
Biochem Biophys Res Commun. 2020 Apr 9;524(3):656-662. doi: 10.1016/j.bbrc.2019.10.122. Epub 2020 Feb 6.
Gastric cancer (GC), as one of the most prevalent malignancies, contributes to the high morbidity and mortality worldwide. By analyzing the bioinformatics, qRT-PCR and IHC assays, we found that CLEC5A is overexpressed in GC and associated with poorer prognosis. CLEC5A silencing inhibits cell growth and DNA replication and induces cell cycle arrest and cell apoptosis. Bioinformatics analyses and Western blotting revealed that CLEC5A depletion led to the dysregulation of the PI3K/AKT/mTOR pathway. CLEC5A-mediated GC proliferation and anti-apoptosis were impaired by blocking the PI3K/AKT/mTOR pathway with LY294002. We hypothesize that CLEC5A is of vital importance to GC initiation and progression via the PI3K/AKT/mTOR pathway, and that our results might represent promising therapeutic strategies for GC patients.
胃癌（GC）是最常见的恶性肿瘤之一，在全球范围内导致高发病率和死亡率。通过生物信息学、qRT-PCR 和 IHC 分析，我们发现 CLEC5A 在 GC 中过表达，并与预后不良相关。CLEC5A 沉默抑制细胞生长和 DNA 复制，并诱导细胞周期停滞和细胞凋亡。生物信息学分析和 Western blot 显示，CLEC5A 耗竭导致 PI3K/AKT/mTOR 通路失调。用 LY294002 阻断 PI3K/AKT/mTOR 通路可损害 CLEC5A 介导的 GC 增殖和抗凋亡作用。我们假设 CLEC5A 通过 PI3K/AKT/mTOR 通路对 GC 的发生和发展至关重要，我们的结果可能为 GC 患者提供有前途的治疗策略。
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