High-mobility group box 1 (HMGB1) protein regulates tumor-associated cell migration through the interaction with BTB domain

Young Bok Ko, Boh Ram Kim, Sang Lyun Nam, Jung Bo Yang, Sang Yoon Park, Seung Bae Rho

Research output: Contribution to journalArticleResearchpeer-review

17 Citations (Scopus)

Abstract

High-mobility group box 1 (HMGB1) was shown to be strongly implicated in high incidences of metastasis and the poor clinical pathologic conditions found in various human tumors. In this study, we explored the possible mechanism of HMGB1 in tumor metastases in vitro, using a human carcinoma cell system. BTB, as a negative regulator of cell cycle progression, was identified as a HMGB1 interacting partner. The ectopic expression of HMGB1 activates cell growth by suppressing BTB-induced cell death, decreasing Bax and p53 expression, while enhancing Bcl-xL, Bcl-2, cyclin D1, and NF-κB expression. HMGB1 activates the FAK/PI3K/mTOR signaling cascade, and BTB prominently inhibits HMGB1-induced oncogenesis. The effect of HMGB1 on FAK/mTOR signaling was also confirmed through the silencing of HMGB1 expression. These insights provide evidence that HMGB1 enhances cell proliferation and suppresses apoptosis. Collectively, our results show an underlying mechanism for an HMGB1-associated promotion of carcinoma cells.

Original languageEnglish
Pages (from-to)777-783
Number of pages7
JournalCellular Signalling
Volume26
Issue number4
DOIs
StatePublished - 1 Apr 2014

Fingerprint

HMGB1 Protein
Cell Movement
Neoplasm Metastasis
Carcinoma
Neoplasms
Cyclin D1
Phosphatidylinositol 3-Kinases
Cell Cycle
Carcinogenesis
Cell Death
Cell Proliferation
Apoptosis
Incidence
Growth
BTB-POZ Domain

Keywords

  • Anti-apoptotic function
  • BTB/POZ domain
  • FAK/mTOR signaling
  • High-mobility group box 1
  • Yeast two-hybrid system

Cite this

Ko, Young Bok ; Kim, Boh Ram ; Nam, Sang Lyun ; Yang, Jung Bo ; Park, Sang Yoon ; Rho, Seung Bae. / High-mobility group box 1 (HMGB1) protein regulates tumor-associated cell migration through the interaction with BTB domain. In: Cellular Signalling. 2014 ; Vol. 26, No. 4. pp. 777-783.
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abstract = "High-mobility group box 1 (HMGB1) was shown to be strongly implicated in high incidences of metastasis and the poor clinical pathologic conditions found in various human tumors. In this study, we explored the possible mechanism of HMGB1 in tumor metastases in vitro, using a human carcinoma cell system. BTB, as a negative regulator of cell cycle progression, was identified as a HMGB1 interacting partner. The ectopic expression of HMGB1 activates cell growth by suppressing BTB-induced cell death, decreasing Bax and p53 expression, while enhancing Bcl-xL, Bcl-2, cyclin D1, and NF-κB expression. HMGB1 activates the FAK/PI3K/mTOR signaling cascade, and BTB prominently inhibits HMGB1-induced oncogenesis. The effect of HMGB1 on FAK/mTOR signaling was also confirmed through the silencing of HMGB1 expression. These insights provide evidence that HMGB1 enhances cell proliferation and suppresses apoptosis. Collectively, our results show an underlying mechanism for an HMGB1-associated promotion of carcinoma cells.",
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High-mobility group box 1 (HMGB1) protein regulates tumor-associated cell migration through the interaction with BTB domain. / Ko, Young Bok; Kim, Boh Ram; Nam, Sang Lyun; Yang, Jung Bo; Park, Sang Yoon; Rho, Seung Bae.

In: Cellular Signalling, Vol. 26, No. 4, 01.04.2014, p. 777-783.

Research output: Contribution to journalArticleResearchpeer-review

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AU - Rho, Seung Bae

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