COTE-1通过AMPK/mTOR信号通路调节自噬活性，促进小细胞肺癌癌症的增殖和侵袭。

IF 4.6 Q2 MATERIALS SCIENCE, BIOMATERIALS ACS Applied Bio Materials Pub Date : 2023-10-01 DOI:10.1016/j.mcp.2023.101918

Yuhui Ma , Huijing Feng , Yuxuan Wang , Lina Hu , Xuan Su , Nan Li , Xu Li

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引用次数: 0

摘要

背景：COTE-1已被发现能促进癌症的增殖和侵袭。然而，COTE-1在SCLC中的作用机制尚不清楚。探讨COTE-1在小细胞肺癌中的作用，有望为小细胞肺癌的预后和治疗提供一个潜在的靶点。方法：用免疫组织化学方法检测COTE-1和ki-67的表达。PCR检测COTE-1的表达水平。CCK8法检测细胞增殖活性。伤口愈合测试检测到细胞迁移能力。Transwell侵袭试验检测细胞侵袭能力。通过透射电子显微镜观察自噬体的数量。WB检测自噬相关蛋白和AMPK/mTOR通路相关蛋白的表达水平。通过建立小鼠SCLC异种移植瘤模型，研究COTE-1表达水平对SCLC肿瘤组织增殖的影响。结果：COTE-1在SCLC组织和细胞中的表达高于正常组织和细胞。在COTE-1高表达的SCLC细胞中，自噬蛋白的表达水平显著增加，细胞内自噬体的数量增加，增殖活性、迁移和侵袭能力增强。COTE-1通过激活AMPK/mTOR信号通路，在营养缺乏的情况下促进SCLC细胞的自噬、增殖和侵袭。COTE-1激活自噬促进小细胞肺癌小鼠移植瘤的增殖和发展。结论：COTE-1通过介导基于AMPK/mTOR途径的自噬促进癌症小细胞的增殖、迁移和侵袭。

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COTE-1 promotes the proliferation and invasion of small cell lung cancer by regulating autophagy activity via the AMPK/mTOR signaling pathway

Background

COTE-1 has been found to promote the proliferation and invasion of non-small cell lung cancer. However, the mechanism of COTE-1 in SCLC is still unclear. Exploring the role of COTE-1 in SCLC is expected to provide a potential target for the prognosis and treatment of SCLC.

Methods

The expression of COTE-1 and ki-67 was detected by immunohistochemical staining. PCR detected COTE-1 expression level. Cell proliferation activity was detected by CCK8 assay. A wound healing test detected cell migrative ability. Transwell invasion assay detected cell invasive ability. The numbers of autophagosomes were observed by transmission electron microscopy. WB detected the expression levels of autophagy-related proteins and AMPK/mTOR pathway-related proteins. The effect of COTE-1 expression level on the proliferation of SCLC tumor tissues was investigated by establishing a mouse SCLC xenograft tumor model.

Results

The expression of COTE-1 in SCLC tissues and cells was higher than that in normal tissues and cells. In SCLC cells with high COTE-1 expression, the expression level of autophagy proteins was notably increased, the number of intracellular autophagosomes increased, and the proliferative activity, migration and invasion abilities were enhanced. COTE-1 promotes autophagy, proliferation, and invasion of SCLC cells under nutrient deprivation by activating the AMPK/mTOR signaling pathway. Activation of autophagy by COTE-1 promotes the proliferation and development of xenograft tumors in a mouse model of SCLC.