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

Research output: Contribution to journalArticle

6 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 languageEnglish
Pages (from-to)787-794
Number of pages8
JournalAnticancer Research
Volume38
Issue number2
Publication statusPublished - 2018 Feb 1

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Neoplastic Stem Cells
Colorectal Neoplasms
Cadherins
Down-Regulation
Cell Self Renewal
transglutaminase 2
Catenins
Vimentin
RNA Interference
Cell Line

Keywords

  • CCSC
  • EMT
  • stemness
  • TGM2

ASJC Scopus subject areas

  • Oncology
  • Cancer Research

Cite this

Transglutaminase 2 Regulates Self-renewal and Stem Cell Marker of Human Colorectal Cancer Stem Cells. / Kang, Sanghee; Oh, Sang Cheul; Min, Byung Wook; Lee, Dae Hee.

In: Anticancer Research, Vol. 38, No. 2, 01.02.2018, p. 787-794.

Research output: Contribution to journalArticle

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