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FYN通过激活STAT3介导的上皮-间质转化促进胃癌转移。

FYN promotes gastric cancer metastasis by activating STAT3-mediated epithelial-mesenchymal transition.

作者信息

Yu Jie, Zhou ZhiJun, Wei ZheWei, Wu Jing, OuYang Jun, Huang WeiBin, He YuLong, Zhang ChangHua

机构信息

Department of Gastrointestinal Surgery, the First Affiliated Hospital of Sun Yat-sen University, 58 Zhongshan 2(nd) Road, Guangzhou, Guangdong 510080, China.

Department of Gastrointestinal Surgery, the Seventh Affiliated Hospital of Sun Yat-sen University, 628 Zhenyuan Road, Shenzhen, Guangdong 518000, China.

出版信息

Transl Oncol. 2020 Nov;13(11):100841. doi: 10.1016/j.tranon.2020.100841. Epub 2020 Aug 4.

DOI:10.1016/j.tranon.2020.100841
PMID:32763503
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7408597/
Abstract

Gastric cancer is one of the most lethal cancers worldwide. FYN, a gene that is differentially expressed in gastric cancer, is considered a critical metastasis regulator in several solid tumors, but its role in gastric cancer is still unclear. This study aimed to evaluate the role of FYN and test whether FYN promotes migration and invasion of gastric cancer cells in vitro and in vivo via STAT3 signaling. FYN was overexpressed in gastric cancer and positively correlated with metastasis. FYN knockdown significantly decreased cancer cell migration and invasion, whereas FYN overexpression increased cancer migration and invasion. Genetic inhibition of FYN decreased the number of metastatic lung nodules in vivo. Several epithelial-mesenchymal transition markers were positively correlated with FYN expression, indicative of FYN involvement in this transition. Furthermore, gene set enrichment analysis of a Cancer Genome Atlas dataset revealed that the STAT3 signaling pathway was positively correlated with FYN expression. STAT3 inhibition reversed the FYN-mediated epithelial-mesenchymal transition and suppressed metastasis. In conclusion, FYN promotes gastric cancer metastasis possibly by activating STAT3-mediated epithelial mesenchymal transition and may be a novel therapeutic target for gastric cancer.

摘要

胃癌是全球致死率最高的癌症之一。FYN是一种在胃癌中差异表达的基因，在几种实体瘤中被认为是关键的转移调节因子，但其在胃癌中的作用仍不清楚。本研究旨在评估FYN的作用，并测试FYN是否通过STAT3信号通路在体外和体内促进胃癌细胞的迁移和侵袭。FYN在胃癌中过表达且与转移呈正相关。敲低FYN可显著降低癌细胞的迁移和侵袭，而过表达FYN则增加癌细胞的迁移和侵袭。对FYN的基因抑制减少了体内转移性肺结节的数量。几种上皮-间质转化标志物与FYN表达呈正相关，表明FYN参与了这一转化过程。此外，对癌症基因组图谱数据集的基因集富集分析显示，STAT3信号通路与FYN表达呈正相关。抑制STAT3可逆转FYN介导的上皮-间质转化并抑制转移。总之，FYN可能通过激活STAT3介导的上皮-间质转化促进胃癌转移，可能是胃癌的一个新的治疗靶点。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bcaa/7408597/83603fdb414b/mmc3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bcaa/7408597/71d1d4cc38b0/gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bcaa/7408597/c283b7ec65c8/gr2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bcaa/7408597/6a268cae09f2/gr3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bcaa/7408597/d8d373b0308e/gr4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bcaa/7408597/55c6c3786605/gr5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bcaa/7408597/e71a8f7ab0a3/gr6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bcaa/7408597/45e25541420d/mmc1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bcaa/7408597/75d12255a437/mmc2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bcaa/7408597/83603fdb414b/mmc3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bcaa/7408597/71d1d4cc38b0/gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bcaa/7408597/c283b7ec65c8/gr2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bcaa/7408597/6a268cae09f2/gr3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bcaa/7408597/d8d373b0308e/gr4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bcaa/7408597/55c6c3786605/gr5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bcaa/7408597/e71a8f7ab0a3/gr6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bcaa/7408597/45e25541420d/mmc1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bcaa/7408597/75d12255a437/mmc2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bcaa/7408597/83603fdb414b/mmc3.jpg

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