Transglutaminase 2 regulates self-renewal and stem cell marker of human colorectal cancer stem cells

Sanghee Kang; Sang Cheul Oh; Byung Wook Min; Dae Hee Lee

doi:10.21873/anticanres.12285

Transglutaminase 2 regulates self-renewal and stem cell marker of human colorectal cancer stem cells

Sanghee Kang, Sang Cheul Oh, Byung Wook Min, Dae Hee Lee

Department of Biomedical Sciences

Research output: Contribution to journal › Article › peer-review

14 Citations (Scopus)

Abstract

Background/Aim: The aim of this study was to investigate the role of transglutaminase 2 (TGM2) in colorectal cancer stem cells (CCSCs). Materials and Methods: We used the TU12 cell line possessing CD133-expressing CCSCs. After isolating CD133 (−) and CD133 (+) CCSCs, we overexpressed and knocked-down TGM2 to investigate its role in human CCSCs. Results: The expression level of TGM2 was 25-fold higher in tumorigenic cells than non-tumorigenic cells. We found that knockdown of TGM2 by specific RNA interference markedly inhibited cell growth and caused down-regulation of the stemness markers, CD133, SOX2, and β-catenin. We further demonstrated that knockdown of TGM2 inhibited cell metastatic abilities by down-regulating N-cadherin and vimentin and up-regulating E-cadherin. These findings revealed that TGM2 expression is markedly increased in human colorectal cancer and that down-regulation of TGM2 in tumors may serve as a treatment for colorectal cancer patients. Therefore, this study indicate that TGM2 affects the metastatic potential and stemness of CCSCs by regulating EMT- and stemness-related proteins. Conclusion: The metastatic potential of CSCs arises from highly expressed TGM2.

Original language	English
Pages (from-to)	787-794
Number of pages	8
Journal	Anticancer research
Volume	38
Issue number	2
DOIs	https://doi.org/10.21873/anticanres.12285
Publication status	Published - 2018 Feb

Keywords

CCSC
EMT
Stemness
TGM2

ASJC Scopus subject areas

Oncology
Cancer Research

UN SDGs

This output contributes to the following UN Sustainable Development Goals (SDGs)

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10.21873/anticanres.12285

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title = "Transglutaminase 2 regulates self-renewal and stem cell marker of human colorectal cancer stem cells",

abstract = "Background/Aim: The aim of this study was to investigate the role of transglutaminase 2 (TGM2) in colorectal cancer stem cells (CCSCs). Materials and Methods: We used the TU12 cell line possessing CD133-expressing CCSCs. After isolating CD133 (−) and CD133 (+) CCSCs, we overexpressed and knocked-down TGM2 to investigate its role in human CCSCs. Results: The expression level of TGM2 was 25-fold higher in tumorigenic cells than non-tumorigenic cells. We found that knockdown of TGM2 by specific RNA interference markedly inhibited cell growth and caused down-regulation of the stemness markers, CD133, SOX2, and β-catenin. We further demonstrated that knockdown of TGM2 inhibited cell metastatic abilities by down-regulating N-cadherin and vimentin and up-regulating E-cadherin. These findings revealed that TGM2 expression is markedly increased in human colorectal cancer and that down-regulation of TGM2 in tumors may serve as a treatment for colorectal cancer patients. Therefore, this study indicate that TGM2 affects the metastatic potential and stemness of CCSCs by regulating EMT- and stemness-related proteins. Conclusion: The metastatic potential of CSCs arises from highly expressed TGM2.",

keywords = "CCSC, EMT, Stemness, TGM2",

author = "Sanghee Kang and Oh, {Sang Cheul} and Min, {Byung Wook} and Lee, {Dae Hee}",

note = "Funding Information: This work was supported by a Grant from the National Research Foundation (NRF) of Korea funded by the Korean government (MSIP) (NRF-2015R1D1A1A01058303) and the Grant of the Korea Health Technology R&D Project through the Korea Health Industry Development Institute (KHIDI), funded by the Ministry of Health & Welfare, Republic of Korea (grant number: HI15C1665). Publisher Copyright: {\textcopyright} 2018 International Institute of Anticancer Research. All Right Reserved.",

year = "2018",

month = feb,

doi = "10.21873/anticanres.12285",

language = "English",

volume = "38",

pages = "787--794",

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T1 - Transglutaminase 2 regulates self-renewal and stem cell marker of human colorectal cancer stem cells

AU - Kang, Sanghee

AU - Oh, Sang Cheul

AU - Min, Byung Wook

AU - Lee, Dae Hee

N1 - Funding Information: This work was supported by a Grant from the National Research Foundation (NRF) of Korea funded by the Korean government (MSIP) (NRF-2015R1D1A1A01058303) and the Grant of the Korea Health Technology R&D Project through the Korea Health Industry Development Institute (KHIDI), funded by the Ministry of Health & Welfare, Republic of Korea (grant number: HI15C1665). Publisher Copyright: © 2018 International Institute of Anticancer Research. All Right Reserved.

PY - 2018/2

Y1 - 2018/2

N2 - Background/Aim: The aim of this study was to investigate the role of transglutaminase 2 (TGM2) in colorectal cancer stem cells (CCSCs). Materials and Methods: We used the TU12 cell line possessing CD133-expressing CCSCs. After isolating CD133 (−) and CD133 (+) CCSCs, we overexpressed and knocked-down TGM2 to investigate its role in human CCSCs. Results: The expression level of TGM2 was 25-fold higher in tumorigenic cells than non-tumorigenic cells. We found that knockdown of TGM2 by specific RNA interference markedly inhibited cell growth and caused down-regulation of the stemness markers, CD133, SOX2, and β-catenin. We further demonstrated that knockdown of TGM2 inhibited cell metastatic abilities by down-regulating N-cadherin and vimentin and up-regulating E-cadherin. These findings revealed that TGM2 expression is markedly increased in human colorectal cancer and that down-regulation of TGM2 in tumors may serve as a treatment for colorectal cancer patients. Therefore, this study indicate that TGM2 affects the metastatic potential and stemness of CCSCs by regulating EMT- and stemness-related proteins. Conclusion: The metastatic potential of CSCs arises from highly expressed TGM2.

AB - Background/Aim: The aim of this study was to investigate the role of transglutaminase 2 (TGM2) in colorectal cancer stem cells (CCSCs). Materials and Methods: We used the TU12 cell line possessing CD133-expressing CCSCs. After isolating CD133 (−) and CD133 (+) CCSCs, we overexpressed and knocked-down TGM2 to investigate its role in human CCSCs. Results: The expression level of TGM2 was 25-fold higher in tumorigenic cells than non-tumorigenic cells. We found that knockdown of TGM2 by specific RNA interference markedly inhibited cell growth and caused down-regulation of the stemness markers, CD133, SOX2, and β-catenin. We further demonstrated that knockdown of TGM2 inhibited cell metastatic abilities by down-regulating N-cadherin and vimentin and up-regulating E-cadherin. These findings revealed that TGM2 expression is markedly increased in human colorectal cancer and that down-regulation of TGM2 in tumors may serve as a treatment for colorectal cancer patients. Therefore, this study indicate that TGM2 affects the metastatic potential and stemness of CCSCs by regulating EMT- and stemness-related proteins. Conclusion: The metastatic potential of CSCs arises from highly expressed TGM2.

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KW - EMT

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Transglutaminase 2 regulates self-renewal and stem cell marker of human colorectal cancer stem cells

Abstract

Keywords

ASJC Scopus subject areas

UN SDGs

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