CXCL6 fuels the growth and metastases of esophageal squamous cell carcinoma cells both in vitro and in vivo through upregulation of PD‐L1 via activation of STAT3 pathway

CXCL6 fuels the growth and metastases of esophageal squamous cell carcinoma cells both in vitro and in vivo through upregulation of PD‐L1 via activation of STAT3 pathway
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DOI:
10.1002/jcp.30236
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发表时间:
2020-12
影响因子:
5.6
通讯作者:
Shutao Zheng;Tongxue Shen;Qing Liu;Tao Liu;A. Tuerxun;Qiqi Zhang;Lifei Yang;Xiujuan Han;Xiaomei Lu
Shutao Zheng;Tongxue Shen;Qing Liu;Tao Liu;A. Tuerxun;Qiqi Zhang;Lifei Yang;Xiujuan Han;Xiaomei Lu
中科院分区:
生物学2区
文献类型:
--
作者:
Shutao Zheng;Tongxue Shen;Qing Liu;Tao Liu;A. Tuerxun;Qiqi Zhang;Lifei Yang;Xiujuan Han;Xiaomei Lu

文献摘要

相似文献

CXCL 6,C-X-C基序趋化因子配体6的收缩,其生物学作用在食管鳞状细胞癌(ESCC)中很少被描述。为了解CXCL 6在食管鳞癌生长和转移中的临床病理学和生物学作用,采用免疫组化方法检测105例食管鳞癌组织中CXCL 6的表达,并统计分析CXCL 6表达与临床病理参数的相关性。使用伤口愈合和Transwell试验评价了在迁移和侵袭中介导的作用。MTT法和流式细胞仪检测细胞增殖活性。在体内,建立了人食管鳞癌细胞株(CXCL 6)裸鼠移植瘤尾静脉注射模型。结果发现,相对于正常对照,CXCL 6在ESCC中显著升高;上调的CXCL 6仅与分化程度显著相关。体外实验发现CXCL 6能促进食管鳞癌细胞的增殖、迁移和侵袭;裸鼠实验也充分证实了CXCL 6能促进食管鳞癌细胞在体内的生长和转移。从机制上讲,发现CXCL 6能够通过激活STAT 3通路促进上皮-间质转化并上调PD-L1表达。总的来说,我们在这里显示的所有数据表明,CXCL 6可以在体内和体外增强ESCC细胞的生长和转移。
CXCL6, contraction of C‐X‐C motif chemokine ligand 6, whose biological roles have been rarely described in esophageal squamous cell carcinoma (ESCC). To understand the clinicopathological and biological roles played by CXCL6 in the growth and metastasis of ESCC, immunohistochemistry was used to detect the expression of CXCL6 in ESCC tissues, totaling 105 cases; and the correlation was statistically analyzed between CXCL6 expression and clinicopathological parameters. The role mediated in migration and invasion was evaluated using wound‐healing and Transwell assays. MTT and flow cytometry were used to assay the proliferative variation. In vivo, tail vein injection model was established in nude mice xenografted with human ESCC cell lines whose CXCL6 were artificially manipulated. It was found that relative to normal control, CXCL6 was profoundly higher in ESCC; upregulated CXCL6 only significantly correlated with differentiation degree. In vitro, CXCL6 was found to promote the proliferation, migration, and invasion of ESCC cells; which was fully corroborated by nude mice experiment that CXCL6 can promote the growth and metastases of ESCC cells in vivo. Mechanistically, CXCL6 was discovered to be capable of promoting epithelial‐mesenchymal transition and upregulating PD‐L1 expression through activation of the STAT3 pathway. Collectively, all the data we showed here demonstrate that CXCL6 can enhance the growth and metastases of ESCC cells both in vivo and in vitro.