Tim-4 promotes migration and invasion of NSCLC depending on N-linked glycosylation at Asn291
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- 英文论文题名：Tim-4 promotes migration and invasion of NSCLC depending on N-linked glycosylation at Asn291
- 论文作者：Wang Hongxing ; Liu Wen ; Liang Xiaohong ; Ma Chunhong ; Gao Lifen
- 英文论文作者：Wang Hongxing ; Liu Wen ; Liang Xiaohong ; Ma Chunhong ; Gao Lifen ; Department of Immunology ; Shandong University School of Medicine
- 年：2016
- 作者机构：Department of Immunology,Shandong University School of Medicine;
- 英文论文关键词：Tim-4 ; migration and invasion ; N-linked glycosylation ; lung cancer
- 会议召开时间：2016-11-04
- 会议录名称：第十一届全国免疫学学术大会壁报交流集
- 英文会议录名称：Proceedings of 2016 CSI Congress on Immunology
- 语种：英文
- 分类号：R734.2
- 学会代码：IGMD
- 会议名称：第十一届全国免疫学学术大会
- 会议地点：中国安徽合肥
- 主办单位：中国免疫学会
- 学会名称：中国免疫学会
- 页数：1
- 文件大小：290k
- 原文格式：D
- 会议级别：全国
摘要
Background:Tim-4 is a novel cell-surface glycoprotein belonging to TIM family.Tim-4 is selectively expressed on antigen presenting cells.We and other labs report that Tim-4 is also expressed on multiple tumor cells and tumor microenviroments up-regulate Tim-4 expression.Recently,we identify Tim-4 as a new player in non-small cell lung cancer(NSCLC) growth and proliferation.However,the role of Tim-4 in NSCLC migration and invasion remains unclear.Objective:This study aims to investigate the role of Tim-4 in driving migration and invasion of NSCLC cells and further explore the possible effects of N-linked glycosylation at Asn291.Methods:Tim-4 expression were detected by q PCR and flow cytometry respectively.Tim-4 expression vector and mutation plasmid with N-linked glycosylation at Asn291 or si RNA were transfected into A549 cells.The lung cancer cell migration and invasion was assayed by transwell and wound healing assay.Western blot was performed to analyze the EMT-related proteins.Results:We found that IL-6 induced Tim-4 m RNA and protein expression in lung cancer cells in a time and dose dependent manner.Tim-4 overexpression promoted migration and invasion of lung cancer cells.Consistently,Tim-4 overexpression decreased E-cadherin expression,but increased expression of Snail,Slug and Vimentin.Tim-4 knockdown significantly inhibited the migration and invasion of lung cancer cells induced by IL-6 stimulation.Accordingly,Tim-4 interference reversed EMT-related protein expression in IL-6 treated lung cancer cells.Wild type Tim-4 overexpression rescued this effect,while Tim-4 mutation with N-linked glycosylation at Asn291 did not work.Conclusions:These data indicate that Tim-4 plays a key role in migration and invasion of NSCLC.Tim-4 blocking might be a new option in preventing lung cancer metastases.
Background:Tim-4 is a novel cell-surface glycoprotein belonging to TIM family.Tim-4 is selectively expressed on antigen presenting cells.We and other labs report that Tim-4 is also expressed on multiple tumor cells and tumor microenviroments up-regulate Tim-4 expression.Recently,we identify Tim-4 as a new player in non-small cell lung cancer(NSCLC) growth and proliferation.However,the role of Tim-4 in NSCLC migration and invasion remains unclear.Objective:This study aims to investigate the role of Tim-4 in driving migration and invasion of NSCLC cells and further explore the possible effects of N-linked glycosylation at Asn291.Methods:Tim-4 expression were detected by q PCR and flow cytometry respectively.Tim-4 expression vector and mutation plasmid with N-linked glycosylation at Asn291 or si RNA were transfected into A549 cells.The lung cancer cell migration and invasion was assayed by transwell and wound healing assay.Western blot was performed to analyze the EMT-related proteins.Results:We found that IL-6 induced Tim-4 m RNA and protein expression in lung cancer cells in a time and dose dependent manner.Tim-4 overexpression promoted migration and invasion of lung cancer cells.Consistently,Tim-4 overexpression decreased E-cadherin expression,but increased expression of Snail,Slug and Vimentin.Tim-4 knockdown significantly inhibited the migration and invasion of lung cancer cells induced by IL-6 stimulation.Accordingly,Tim-4 interference reversed EMT-related protein expression in IL-6 treated lung cancer cells.Wild type Tim-4 overexpression rescued this effect,while Tim-4 mutation with N-linked glycosylation at Asn291 did not work.Conclusions:These data indicate that Tim-4 plays a key role in migration and invasion of NSCLC.Tim-4 blocking might be a new option in preventing lung cancer metastases.
Background:Tim-4 is a novel cell-surface glycoprotein belonging to TIM family.Tim-4 is selectively expressed on antigen presenting cells.We and other labs report that Tim-4 is also expressed on multiple tumor cells and tumor microenviroments up-regulate Tim-4 expression.Recently,we identify Tim-4 as a new player in non-small cell lung cancer(NSCLC) growth and proliferation.However,the role of Tim-4 in NSCLC migration and invasion remains unclear.Objective:This study aims to investigate the role of Tim-4 in driving migration and invasion of NSCLC cells and further explore the possible effects of N-linked glycosylation at Asn291.Methods:Tim-4 expression were detected by q PCR and flow cytometry respectively.Tim-4 expression vector and mutation plasmid with N-linked glycosylation at Asn291 or si RNA were transfected into A549 cells.The lung cancer cell migration and invasion was assayed by transwell and wound healing assay.Western blot was performed to analyze the EMT-related proteins.Results:We found that IL-6 induced Tim-4 m RNA and protein expression in lung cancer cells in a time and dose dependent manner.Tim-4 overexpression promoted migration and invasion of lung cancer cells.Consistently,Tim-4 overexpression decreased E-cadherin expression,but increased expression of Snail,Slug and Vimentin.Tim-4 knockdown significantly inhibited the migration and invasion of lung cancer cells induced by IL-6 stimulation.Accordingly,Tim-4 interference reversed EMT-related protein expression in IL-6 treated lung cancer cells.Wild type Tim-4 overexpression rescued this effect,while Tim-4 mutation with N-linked glycosylation at Asn291 did not work.Conclusions:These data indicate that Tim-4 plays a key role in migration and invasion of NSCLC.Tim-4 blocking might be a new option in preventing lung cancer metastases.
引文