[Effect of HMGB1 on proliferation of human nasopharyngeal carcinoma cell line C666-1 in vitro]

Nan Fang Yi Ke Da Xue Xue Bao. 2015 Nov;35(11):1540-5.
[Article in Chinese]

Abstract

Objective: To observe the effect of high-mobility group box-1 protein (HMGB1) on the proliferation of human nasopharyngeal carcinoma cell line C666-1 and explore the possible underlying mechanisms.

Methods: Cultured C666-1 cells were treated with a siRNA targeting HMGB1 gene. The changes in the cell proliferation were detected by CCK8 analysis, the cell cycle distribution was assayed with flow cytometry, and the expressions of cyclin D1, CDK6 and related pathway proteins were detected with Western blotting. The effect of a HMGB1 plasmid carrying the reporter gene GFP on the proliferation of C666-1 cells was tested with CCK8 and EDU analysis.

Results: Compared with the control cells, the cells transfected with the siRNA targeting HMGB1 showed obviously suppressed cell proliferation (P<0.001), cell cycle arrest in G1 phase (P<0.001), and down-regulated expressions of cyclin D1, CDK6, STAT3 and P-STAT3. Overexpression of HMGB1 in cells transfected with the HMGB1 plasmid showed a significantly increased ratio of S phase cells (P<0.05) and obviously enhanced cell proliferation (P<0.001).

Conclusion: HMGB1 can promote the proliferation of human nasopharyngeal carcinoma cell line C666-1 by up- regulating cyclin D1 and CDK6 via the STAT3 signaling pathway.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Carcinoma
  • Cell Cycle
  • Cell Cycle Checkpoints
  • Cell Division
  • Cell Line, Tumor
  • Cell Proliferation*
  • Cyclin D1 / metabolism
  • Cyclin-Dependent Kinase 6 / metabolism
  • Down-Regulation
  • HMGB1 Protein / genetics*
  • Humans
  • Nasopharyngeal Carcinoma
  • Nasopharyngeal Neoplasms / pathology*
  • RNA, Small Interfering
  • STAT3 Transcription Factor / metabolism
  • Signal Transduction*
  • Transfection
  • Up-Regulation

Substances

  • CCND1 protein, human
  • HMGB1 Protein
  • RNA, Small Interfering
  • STAT3 Transcription Factor
  • STAT3 protein, human
  • Cyclin D1
  • CDK6 protein, human
  • Cyclin-Dependent Kinase 6