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The TNF‐α‐induced expression of miR‐130b protects cervical cancer cells from the cytotoxicity of TNF‐α

Tumour necrosis factor alpha (‐α) is a multifunctional cytokine and has the capacity both to promote cell growth and to kill tumour cells by inducing cell apoptosis. However, many tumour cells develop resistance to the toxic effects of ‐α. Thus, understanding the mechanism underlying the resistance... Full description

Journal Title: FEBS Open Bio April 2018, Vol.8(4), pp.614-627
Main Author: Yang, Lei
Other Authors: Wang, Yanli , Shi, Shuainan , Xie, Lili , Liu, Tao , Wang, Yuliang , Mu, Hong
Format: Electronic Article Electronic Article
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ID: ISSN: 2211-5463 ; E-ISSN: 2211-5463 ; DOI: 10.1002/2211-5463.12395
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recordid: wj10.1002/2211-5463.12395
title: The TNF‐α‐induced expression of miR‐130b protects cervical cancer cells from the cytotoxicity of TNF‐α
format: Article
creator:
  • Yang, Lei
  • Wang, Yanli
  • Shi, Shuainan
  • Xie, Lili
  • Liu, Tao
  • Wang, Yuliang
  • Mu, Hong
subjects:
  • Cervical Cancer Cell
  • Mir‐130b
  • Pten
  • Tnf ‐Α Resistance
ispartof: FEBS Open Bio, April 2018, Vol.8(4), pp.614-627
description: Tumour necrosis factor alpha (‐α) is a multifunctional cytokine and has the capacity both to promote cell growth and to kill tumour cells by inducing cell apoptosis. However, many tumour cells develop resistance to the toxic effects of ‐α. Thus, understanding the mechanism underlying the resistance of tumours to ‐α toxicity and finding ways to overcome this resistance are urgently needed. In this study, we discovered that two cervical cancer cell lines, Hela and Siha, showed null responses to ‐α cytotoxicity. However, in these cell lines, ‐α stimulation promoted the expression of miR‐130b and downregulated the expression of gene, which encodes a dual‐specificity phosphatase that acts as a tumour suppressor. Blockade of miR‐130b function or overexpression of gene sensitized cells to ‐α cytotoxicity. Regression analyses revealed that there were reverse relationships between the cellular levels of miR‐130b and in cervical cancer cells. Gain‐ and loss‐of‐function assays demonstrated that there were causal relationships between the increase in miR‐130b levels and the reduction in or protein levels. analysis revealed that there were two miR‐130b target sites within the 3′ of and experimental evidences demonstrated that miR‐130b repressed the expression of gene by binding directly to the 3′ of . These data suggest miR‐130b expression as a target to be inhibited to make tumour cells more sensitive to the toxic impact of TNF‐α. Tumour necrosis factor alpha (TNF‐α) stimulation induces the expression of miR‐130b in cervical cancer cells. Relying on the base pairing between its seed sequence and target site, miR‐130b binds to the 3′UTR of mRNA and impairs the expression of gene that desensitizes cells to TNF‐α cytotoxicity, characterized as reduced cell viability and an increase in the rate of apoptosis.
language:
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identifier: ISSN: 2211-5463 ; E-ISSN: 2211-5463 ; DOI: 10.1002/2211-5463.12395
fulltext: fulltext
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  • 2211-5463
  • 22115463
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titleThe TNF‐α‐induced expression of miR‐130b protects cervical cancer cells from the cytotoxicity of TNF‐α
creatorYang, Lei ; Wang, Yanli ; Shi, Shuainan ; Xie, Lili ; Liu, Tao ; Wang, Yuliang ; Mu, Hong
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subjectCervical Cancer Cell ; Mir‐130b ; Pten ; Tnf ‐Α Resistance
descriptionTumour necrosis factor alpha (‐α) is a multifunctional cytokine and has the capacity both to promote cell growth and to kill tumour cells by inducing cell apoptosis. However, many tumour cells develop resistance to the toxic effects of ‐α. Thus, understanding the mechanism underlying the resistance of tumours to ‐α toxicity and finding ways to overcome this resistance are urgently needed. In this study, we discovered that two cervical cancer cell lines, Hela and Siha, showed null responses to ‐α cytotoxicity. However, in these cell lines, ‐α stimulation promoted the expression of miR‐130b and downregulated the expression of gene, which encodes a dual‐specificity phosphatase that acts as a tumour suppressor. Blockade of miR‐130b function or overexpression of gene sensitized cells to ‐α cytotoxicity. Regression analyses revealed that there were reverse relationships between the cellular levels of miR‐130b and in cervical cancer cells. Gain‐ and loss‐of‐function assays demonstrated that there were causal relationships between the increase in miR‐130b levels and the reduction in or protein levels. analysis revealed that there were two miR‐130b target sites within the 3′ of and experimental evidences demonstrated that miR‐130b repressed the expression of gene by binding directly to the 3′ of . These data suggest miR‐130b expression as a target to be inhibited to make tumour cells more sensitive to the toxic impact of TNF‐α. Tumour necrosis factor alpha (TNF‐α) stimulation induces the expression of miR‐130b in cervical cancer cells. Relying on the base pairing between its seed sequence and target site, miR‐130b binds to the 3′UTR of mRNA and impairs the expression of gene that desensitizes cells to TNF‐α cytotoxicity, characterized as reduced cell viability and an increase in the rate of apoptosis.
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abstractTumour necrosis factor alpha (‐α) is a multifunctional cytokine and has the capacity both to promote cell growth and to kill tumour cells by inducing cell apoptosis. However, many tumour cells develop resistance to the toxic effects of ‐α. Thus, understanding the mechanism underlying the resistance of tumours to ‐α toxicity and finding ways to overcome this resistance are urgently needed. In this study, we discovered that two cervical cancer cell lines, Hela and Siha, showed null responses to ‐α cytotoxicity. However, in these cell lines, ‐α stimulation promoted the expression of miR‐130b and downregulated the expression of gene, which encodes a dual‐specificity phosphatase that acts as a tumour suppressor. Blockade of miR‐130b function or overexpression of gene sensitized cells to ‐α cytotoxicity. Regression analyses revealed that there were reverse relationships between the cellular levels of miR‐130b and in cervical cancer cells. Gain‐ and loss‐of‐function assays demonstrated that there were causal relationships between the increase in miR‐130b levels and the reduction in or protein levels. analysis revealed that there were two miR‐130b target sites within the 3′ of and experimental evidences demonstrated that miR‐130b repressed the expression of gene by binding directly to the 3′ of . These data suggest miR‐130b expression as a target to be inhibited to make tumour cells more sensitive to the toxic impact of TNF‐α. Tumour necrosis factor alpha (TNF‐α) stimulation induces the expression of miR‐130b in cervical cancer cells. Relying on the base pairing between its seed sequence and target site, miR‐130b binds to the 3′UTR of mRNA and impairs the expression of gene that desensitizes cells to TNF‐α cytotoxicity, characterized as reduced cell viability and an increase in the rate of apoptosis.
doi10.1002/2211-5463.12395
pages614-627
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date2018-04