MicroRNA‐375‐3p enhances chemosensitivity to 5‐fluorouracil by targeting thymidylate synthase in colorectal cancer

Resistance to chemotherapy is a major challenge for the treatment of patients with colorectal cancer (CRC). Previous studies have found that microRNAs (miRNAs) play key roles in drug resistance; however, the role of miRNA‐373‐3p (miR‐375‐3p) in CRC remains unclear. The current study aimed to explore...

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Published inCancer science Vol. 111; no. 5; pp. 1528 - 1541
Main Authors Xu, Fei, Ye, Ming‐Liang, Zhang, Yu‐Peng, Li, Wen‐Jie, Li, Meng‐Ting, Wang, Hai‐Zhou, Qiu, Xiao, Xu, Yan, Yin, Jin‐Wen, Hu, Qian, Wei, Wan‐Hui, Chang, Ying, Liu, Lan, Zhao, Qiu
Format Journal Article
LanguageEnglish
Published England John Wiley & Sons, Inc 01.05.2020
John Wiley and Sons Inc
Subjects
5-Fluorouracil
Apoptosis
Binding sites
Biomarkers
Calcium carbonate
Cancer therapies
Cell adhesion & migration
Cell migration
chemosensitivity
Chemotherapy
Colon cancer
Colorectal cancer
Colorectal carcinoma
Drug delivery
Drug resistance
Drugs
Gene expression
MicroRNAs
miRNA
miR‐375‐3p
Nanoparticles
Original
Thymidylate synthase
Tumor microenvironment
Tumors
Xenografts
5-fluorouracil
colorectal cancer
nanoparticles
chemosensitivity
miR-375-3p
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Abstract Resistance to chemotherapy is a major challenge for the treatment of patients with colorectal cancer (CRC). Previous studies have found that microRNAs (miRNAs) play key roles in drug resistance; however, the role of miRNA‐373‐3p (miR‐375‐3p) in CRC remains unclear. The current study aimed to explore the potential function of miR‐375‐3p in 5‐fluorouracil (5‐FU) resistance. MicroRNA‐375‐3p was found to be widely downregulated in human CRC cell lines and tissues and to promote the sensitivity of CRC cells to 5‐FU by inducing colon cancer cell apoptosis and cycle arrest and by inhibiting cell growth, migration, and invasion in vitro. Thymidylate synthase (TYMS) was found to be a direct target of miR‐375‐3p, and TYMS knockdown exerted similar effects as miR‐375‐3p overexpression on the CRC cellular response to 5‐FU. Lipid‐coated calcium carbonate nanoparticles (NPs) were designed to cotransport 5‐FU and miR‐375‐3p into cells efficiently and rapidly and to release the drugs in a weakly acidic tumor microenvironment. The therapeutic effect of combined miR‐375 + 5‐FU/NPs was significantly higher than that of the individual treatments in mouse s.c. xenografts derived from HCT116 cells. Our results suggest that restoring miR‐375‐3p levels could be a future novel therapeutic strategy to enhance chemosensitivity to 5‐FU. Resistance to chemotherapy is a major challenge for the treatment of patients with colorectal cancer (CRC). Our results suggest that the restoration of microRNA‐375‐3p levels could be a future novel therapeutic strategy to modulate and enhance chemosensitivity to 5‐fluorouracil treatment in CRC.
AbstractList Resistance to chemotherapy is a major challenge for the treatment of patients with colorectal cancer (CRC). Previous studies have found that microRNAs (miRNAs) play key roles in drug resistance; however, the role of miRNA-373-3p (miR-375-3p) in CRC remains unclear. The current study aimed to explore the potential function of miR-375-3p in 5-fluorouracil (5-FU) resistance. MicroRNA-375-3p was found to be widely downregulated in human CRC cell lines and tissues and to promote the sensitivity of CRC cells to 5-FU by inducing colon cancer cell apoptosis and cycle arrest and by inhibiting cell growth, migration, and invasion in vitro. Thymidylate synthase (TYMS) was found to be a direct target of miR-375-3p, and TYMS knockdown exerted similar effects as miR-375-3p overexpression on the CRC cellular response to 5-FU. Lipid-coated calcium carbonate nanoparticles (NPs) were designed to cotransport 5-FU and miR-375-3p into cells efficiently and rapidly and to release the drugs in a weakly acidic tumor microenvironment. The therapeutic effect of combined miR-375 + 5-FU/NPs was significantly higher than that of the individual treatments in mouse s.c. xenografts derived from HCT116 cells. Our results suggest that restoring miR-375-3p levels could be a future novel therapeutic strategy to enhance chemosensitivity to 5-FU.
Resistance to chemotherapy is a major challenge for the treatment of patients with colorectal cancer (CRC). Previous studies have found that microRNAs (miRNAs) play key roles in drug resistance; however, the role of miRNA‐373‐3p (miR‐375‐3p) in CRC remains unclear. The current study aimed to explore the potential function of miR‐375‐3p in 5‐fluorouracil (5‐FU) resistance. MicroRNA‐375‐3p was found to be widely downregulated in human CRC cell lines and tissues and to promote the sensitivity of CRC cells to 5‐FU by inducing colon cancer cell apoptosis and cycle arrest and by inhibiting cell growth, migration, and invasion in vitro. Thymidylate synthase (TYMS) was found to be a direct target of miR‐375‐3p, and TYMS knockdown exerted similar effects as miR‐375‐3p overexpression on the CRC cellular response to 5‐FU. Lipid‐coated calcium carbonate nanoparticles (NPs) were designed to cotransport 5‐FU and miR‐375‐3p into cells efficiently and rapidly and to release the drugs in a weakly acidic tumor microenvironment. The therapeutic effect of combined miR‐375 + 5‐FU/NPs was significantly higher than that of the individual treatments in mouse s.c. xenografts derived from HCT116 cells. Our results suggest that restoring miR‐375‐3p levels could be a future novel therapeutic strategy to enhance chemosensitivity to 5‐FU. Resistance to chemotherapy is a major challenge for the treatment of patients with colorectal cancer (CRC). Our results suggest that the restoration of microRNA‐375‐3p levels could be a future novel therapeutic strategy to modulate and enhance chemosensitivity to 5‐fluorouracil treatment in CRC.
Resistance to chemotherapy is a major challenge for the treatment of patients with colorectal cancer (CRC). Previous studies have found that microRNAs (miRNAs) play key roles in drug resistance; however, the role of miRNA-373-3p (miR-375-3p) in CRC remains unclear. The current study aimed to explore the potential function of miR-375-3p in 5-fluorouracil (5-FU) resistance. MicroRNA-375-3p was found to be widely downregulated in human CRC cell lines and tissues and to promote the sensitivity of CRC cells to 5-FU by inducing colon cancer cell apoptosis and cycle arrest and by inhibiting cell growth, migration, and invasion in vitro. Thymidylate synthase (TYMS) was found to be a direct target of miR-375-3p, and TYMS knockdown exerted similar effects as miR-375-3p overexpression on the CRC cellular response to 5-FU. Lipid-coated calcium carbonate nanoparticles (NPs) were designed to cotransport 5-FU and miR-375-3p into cells efficiently and rapidly and to release the drugs in a weakly acidic tumor microenvironment. The therapeutic effect of combined miR-375 + 5-FU/NPs was significantly higher than that of the individual treatments in mouse s.c. xenografts derived from HCT116 cells. Our results suggest that restoring miR-375-3p levels could be a future novel therapeutic strategy to enhance chemosensitivity to 5-FU.
Resistance to chemotherapy is a major challenge for the treatment of patients with colorectal cancer (CRC). Previous studies have found that microRNAs (miRNAs) play key roles in drug resistance; however, the role of miRNA-373-3p (miR-375-3p) in CRC remains unclear. The current study aimed to explore the potential function of miR-375-3p in 5-fluorouracil (5-FU) resistance. MicroRNA-375-3p was found to be widely downregulated in human CRC cell lines and tissues and to promote the sensitivity of CRC cells to 5-FU by inducing colon cancer cell apoptosis and cycle arrest and by inhibiting cell growth, migration, and invasion in vitro. Thymidylate synthase (TYMS) was found to be a direct target of miR-375-3p, and TYMS knockdown exerted similar effects as miR-375-3p overexpression on the CRC cellular response to 5-FU. Lipid-coated calcium carbonate nanoparticles (NPs) were designed to cotransport 5-FU and miR-375-3p into cells efficiently and rapidly and to release the drugs in a weakly acidic tumor microenvironment. The therapeutic effect of combined miR-375 + 5-FU/NPs was significantly higher than that of the individual treatments in mouse s.c. xenografts derived from HCT116 cells. Our results suggest that restoring miR-375-3p levels could be a future novel therapeutic strategy to enhance chemosensitivity to 5-FU.Resistance to chemotherapy is a major challenge for the treatment of patients with colorectal cancer (CRC). Previous studies have found that microRNAs (miRNAs) play key roles in drug resistance; however, the role of miRNA-373-3p (miR-375-3p) in CRC remains unclear. The current study aimed to explore the potential function of miR-375-3p in 5-fluorouracil (5-FU) resistance. MicroRNA-375-3p was found to be widely downregulated in human CRC cell lines and tissues and to promote the sensitivity of CRC cells to 5-FU by inducing colon cancer cell apoptosis and cycle arrest and by inhibiting cell growth, migration, and invasion in vitro. Thymidylate synthase (TYMS) was found to be a direct target of miR-375-3p, and TYMS knockdown exerted similar effects as miR-375-3p overexpression on the CRC cellular response to 5-FU. Lipid-coated calcium carbonate nanoparticles (NPs) were designed to cotransport 5-FU and miR-375-3p into cells efficiently and rapidly and to release the drugs in a weakly acidic tumor microenvironment. The therapeutic effect of combined miR-375 + 5-FU/NPs was significantly higher than that of the individual treatments in mouse s.c. xenografts derived from HCT116 cells. Our results suggest that restoring miR-375-3p levels could be a future novel therapeutic strategy to enhance chemosensitivity to 5-FU.
Author Li, Wen‐Jie
Zhang, Yu‐Peng
Zhao, Qiu
Liu, Lan
Li, Meng‐Ting
Wei, Wan‐Hui
Hu, Qian
Qiu, Xiao
Wang, Hai‐Zhou
Yin, Jin‐Wen
Xu, Yan
Chang, Ying
Ye, Ming‐Liang
Xu, Fei
AuthorAffiliation 1 Department of Gastroenterology Zhongnan Hospital of Wuhan University Wuhan China
3 Department of Hematology Shenzhen People’s Hospital The Second Clinical Medical College of Jinan University Shenzhen China
2 Hubei Clinical Center and Key Laboratory of Intestinal and Colorectal Diseases Wuhan China
AuthorAffiliation_xml – name: 2 Hubei Clinical Center and Key Laboratory of Intestinal and Colorectal Diseases Wuhan China
– name: 3 Department of Hematology Shenzhen People’s Hospital The Second Clinical Medical College of Jinan University Shenzhen China
– name: 1 Department of Gastroenterology Zhongnan Hospital of Wuhan University Wuhan China
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  organization: Hubei Clinical Center and Key Laboratory of Intestinal and Colorectal Diseases
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  organization: Hubei Clinical Center and Key Laboratory of Intestinal and Colorectal Diseases
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  surname: Li
  fullname: Li, Wen‐Jie
  organization: Hubei Clinical Center and Key Laboratory of Intestinal and Colorectal Diseases
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  organization: Hubei Clinical Center and Key Laboratory of Intestinal and Colorectal Diseases
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  surname: Wang
  fullname: Wang, Hai‐Zhou
  organization: Hubei Clinical Center and Key Laboratory of Intestinal and Colorectal Diseases
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  surname: Qiu
  fullname: Qiu, Xiao
  organization: The Second Clinical Medical College of Jinan University
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  givenname: Yan
  surname: Xu
  fullname: Xu, Yan
  organization: Hubei Clinical Center and Key Laboratory of Intestinal and Colorectal Diseases
– sequence: 9
  givenname: Jin‐Wen
  surname: Yin
  fullname: Yin, Jin‐Wen
  organization: Hubei Clinical Center and Key Laboratory of Intestinal and Colorectal Diseases
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  surname: Hu
  fullname: Hu, Qian
  organization: Hubei Clinical Center and Key Laboratory of Intestinal and Colorectal Diseases
– sequence: 11
  givenname: Wan‐Hui
  surname: Wei
  fullname: Wei, Wan‐Hui
  organization: Hubei Clinical Center and Key Laboratory of Intestinal and Colorectal Diseases
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  surname: Chang
  fullname: Chang, Ying
  organization: Hubei Clinical Center and Key Laboratory of Intestinal and Colorectal Diseases
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  surname: Liu
  fullname: Liu, Lan
  organization: Hubei Clinical Center and Key Laboratory of Intestinal and Colorectal Diseases
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  orcidid: 0000-0002-1596-5505
  surname: Zhao
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  organization: Hubei Clinical Center and Key Laboratory of Intestinal and Colorectal Diseases
BackLink https://www.ncbi.nlm.nih.gov/pubmed/32073706$$D View this record in MEDLINE/PubMed
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Copyright 2020 The Authors. published by John Wiley & Sons Australia, Ltd on behalf of Japanese Cancer Association.
2020 The Authors. Cancer Science published by John Wiley & Sons Australia, Ltd on behalf of Japanese Cancer Association.
2020. This work is published under http://creativecommons.org/licenses/by-nc-nd/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.
Copyright_xml – notice: 2020 The Authors. published by John Wiley & Sons Australia, Ltd on behalf of Japanese Cancer Association.
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– notice: 2020. This work is published under http://creativecommons.org/licenses/by-nc-nd/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.
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Issue 5
Keywords 5-fluorouracil
colorectal cancer
nanoparticles
chemosensitivity
miR-375-3p
Language English
License Attribution-NonCommercial-NoDerivs
2020 The Authors. Cancer Science published by John Wiley & Sons Australia, Ltd on behalf of Japanese Cancer Association.
This is an open access article under the terms of the http://creativecommons.org/licenses/by-nc-nd/4.0/ License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non‐commercial and no modifications or adaptations are made.
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content type line 14
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Ming‐Liang Ye, Yu‐Peng Zhang, Wen‐Jie Li, and Meng‐Ting Li contributed equally.
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Snippet Resistance to chemotherapy is a major challenge for the treatment of patients with colorectal cancer (CRC). Previous studies have found that microRNAs (miRNAs)...
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StartPage 1528
SubjectTerms 5-Fluorouracil
Apoptosis
Binding sites
Biomarkers
Calcium carbonate
Cancer therapies
Cell adhesion & migration
Cell migration
chemosensitivity
Chemotherapy
Colon cancer
Colorectal cancer
Colorectal carcinoma
Drug delivery
Drug resistance
Drugs
Gene expression
MicroRNAs
miRNA
miR‐375‐3p
Nanoparticles
Original
Thymidylate synthase
Tumor microenvironment
Tumors
Xenografts
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Title MicroRNA‐375‐3p enhances chemosensitivity to 5‐fluorouracil by targeting thymidylate synthase in colorectal cancer
URI https://onlinelibrary.wiley.com/doi/abs/10.1111%2Fcas.14356
https://www.ncbi.nlm.nih.gov/pubmed/32073706
https://www.proquest.com/docview/2406485271
https://www.proquest.com/docview/2490474918
https://www.proquest.com/docview/2358578283
https://pubmed.ncbi.nlm.nih.gov/PMC7226198
Volume 111
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