Arsenic trioxide regulates the apoptosis of glioma cell and glioma stem cell via down-regulation of stem cell marker Sox2.

Hui Sun, Shaojun Zhang
Author Information
  1. Hui Sun: Department of Neurosurgery, The First Affiliated Hospital, Bengbu Medical College, Bengbu, Anhui 233004, People's Republic of China. huisun_bmc@yahoo.com.cn

Abstract

Knowledge of the mechanism by which arsenic trioxide exerts the anti-tumor effects may help in designing a more effective regimen for therapy. Transcription factor Sox2, a key gene implicated in maintaining the "stemness" of embryonic and adult stem cells, plays an important role in the carcinogenesis and maintenance of glioblastoma. Here, we found that the expression of Sox2 at transcriptional level was decreased during As(2)O(3)-induced glioma cell apoptosis. And, the ectopic expression of Sox2 attenuated the apoptotic effect of As(2)O(3) on glioma cell. Furthermore, As(2)O(3) inhibited the self-renewal of glioma stem cells, and efficiently induces the apoptosis of glioma stem cells, at least, partly through down-regulation of Sox2. These data identify a previously unrecognized mechanism of the anti-tumor effects of arsenic trioxide.

MeSH Term

Antineoplastic Agents
Apoptosis
Arsenic Trioxide
Arsenicals
Biomarkers
Brain Neoplasms
Cell Line, Tumor
Down-Regulation
Glioblastoma
Humans
Neoplastic Stem Cells
Oxides
SOXB1 Transcription Factors
Transcription, Genetic

Chemicals

Antineoplastic Agents
Arsenicals
Biomarkers
Oxides
SOX2 protein, human
SOXB1 Transcription Factors
Arsenic Trioxide

Word Cloud

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