Complement component 3 is regulated by TWIST1 and mediates epithelial-mesenchymal transition

Min Soon Cho, Rajesha Rupaimoole, Hyun Jin Choi, Kyunghee Noh, Jichao Chen, Qianghua Hu, Anil K. Sood, Vahid Afshar-Kharghan

Research output: Contribution to journalArticle

29 Citations (Scopus)

Abstract

We have previously shown that complement component 3 (C3) is secreted by malignant epithelial cells. To understand the mechanism of upregulation of C3 expression in tumor cells, we studied the C3 promoter and identified that twist basic helix-loop-helix transcription factor 1 (TWIST1) binds to the C3 promoter and enhances its expression. Because TWIST1 mediates epithelial-mesenchymal transition (EMT), we studied the effect of C3 on EMTand found that C3 decreased E-cadherin expression on cancer cells and promoted EMT.We showed that C3-induced reduction in E-cadherin expression in ovarian cancer cells was mediated by C3a and is Kr€uppel-like factor 5 dependent. We investigated the association between TWIST1 and C3 in malignant tumors and in murine embryos. TWIST1 and C3 colocalized at the invasive tumor edges, and in the neural crest and limb buds of mouse embryos. Our results identified TWIST1 as a transcription factor that regulates C3 expression during pathologic and physiologic EMT.

Original languageEnglish (US)
Pages (from-to)1412-1418
Number of pages7
JournalJournal of Immunology
Volume196
Issue number3
DOIs
StatePublished - Feb 1 2016

Fingerprint

Complement C3
Epithelial-Mesenchymal Transition
Cadherins
Neoplasms
Embryonic Structures
Kruppel-Like Transcription Factors
Basic Helix-Loop-Helix Transcription Factors
Limb Buds
Neural Crest
Cellular Structures
Ovarian Neoplasms
Transcription Factors
Up-Regulation
Epithelial Cells

ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology

Cite this

Complement component 3 is regulated by TWIST1 and mediates epithelial-mesenchymal transition. / Cho, Min Soon; Rupaimoole, Rajesha; Choi, Hyun Jin; Noh, Kyunghee; Chen, Jichao; Hu, Qianghua; Sood, Anil K.; Afshar-Kharghan, Vahid.

In: Journal of Immunology, Vol. 196, No. 3, 01.02.2016, p. 1412-1418.

Research output: Contribution to journalArticle

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AU - Rupaimoole, Rajesha

AU - Choi, Hyun Jin

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AU - Chen, Jichao

AU - Hu, Qianghua

AU - Sood, Anil K.

AU - Afshar-Kharghan, Vahid

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AB - We have previously shown that complement component 3 (C3) is secreted by malignant epithelial cells. To understand the mechanism of upregulation of C3 expression in tumor cells, we studied the C3 promoter and identified that twist basic helix-loop-helix transcription factor 1 (TWIST1) binds to the C3 promoter and enhances its expression. Because TWIST1 mediates epithelial-mesenchymal transition (EMT), we studied the effect of C3 on EMTand found that C3 decreased E-cadherin expression on cancer cells and promoted EMT.We showed that C3-induced reduction in E-cadherin expression in ovarian cancer cells was mediated by C3a and is Kr€uppel-like factor 5 dependent. We investigated the association between TWIST1 and C3 in malignant tumors and in murine embryos. TWIST1 and C3 colocalized at the invasive tumor edges, and in the neural crest and limb buds of mouse embryos. Our results identified TWIST1 as a transcription factor that regulates C3 expression during pathologic and physiologic EMT.

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