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Stress stimuli induce cancer-stemness gene expression via Sp1 activation leading to therapeutic resistance in glioblastoma.

Abstract：

:It has been suggested that stress stimuli from the microenvironment maintain a subset of tumor cells with stem-like properties, including drug resistance. Here, we investigate whether Sp1, a stress-responsive factor, regulates stemness gene expression and if its inhibition sensitizes cancer cells to chemotherapy. Hydrogen peroxide- and serum deprivation-induced stresses were performed in glioblastoma (GBM) cells and patient-derived cells, and the effect of the Sp1 inhibitor mithramycin A (MA) on these stress-induced stem cells and temozolomide (TMZ)-resistant cells was evaluated. Sp1 and stemness genes were not commonly overexpressed in clinical GBM samples. However, their expression was highly induced by stress stimuli. Using MA, we demonstrated Sp1 as a critical stemness-related transcriptional factor protecting GBM cells against stress- and TMZ-induced death. Thus, Sp1 inhibition may prevent recurrence of malignant cells persisting after primary therapy.

journal_name

Biochem Biophys Res Commun

journal_title

Biochemical and biophysical research communications

authors

Chang KY,Huang CT,Hsu TI,Hsu CC,Liu JJ,Chuang CK,Hung JJ,Chang WC,Tsai KK,Chuang JY

doi

10.1016/j.bbrc.2017.09.095

subject

Has Abstract

pub_date

2017-11-04 00:00:00

pages

14-19

issue

1

eissn

0006-291X

issn

1090-2104

pii

S0006-291X(17)31866-1

journal_volume

493

pub_type

杂志文章

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