Fig. 6: MiR-26a overexpression positively correlates with HIF-1α, Bax, and Bad levels, and poor prognosis in GBM receiving temozolomide therapy. | Cell Death & Disease

Fig. 6: MiR-26a overexpression positively correlates with HIF-1α, Bax, and Bad levels, and poor prognosis in GBM receiving temozolomide therapy.

From: Hypoxia-mediated mitochondria apoptosis inhibition induces temozolomide treatment resistance through miR-26a/Bad/Bax axis

Fig. 6

a The expression levels of miR-26a, Bax and Bad in normal brain and glioma tissues. b Spearman′s correlation analysis determined the correlation between expression levels of Bax, Bad, and miR-26a in human GBM specimens. c qRT-PCR analysis of miR-26a expression levels in primary and recurrent glioma tissues from 10 patients who are treated with TMZ therapy regularly. d Representative images of IHC staining of HIF-1α and ISH staining of miR-26a expression in a pair of primary and recurrent GBM tumors (×200 and ×400 magnification). Scale bar: 100 μm. e Based on TCGA public datasets, Kaplan–Meier curves showed the negative correlation between miR-26a and clinical outcome. f The diagram summarizes our findings: hypoxia induces activation of miR-26a by HIF-1α. HIF-1α/ miR-26a axis rescues Bax/Bad-driven mitochondrial membrane dysfunction and subsequently, suppresses cytochrome c release and activation of caspase-3, which helps the GBM cell survive under TMZ treatment. Asterisk indicates significant difference at p < 0.05 compared with primary glioma tissue or normal tissue and double asterisk indicates significant difference at p < 0.01 compared with primary glioma tissue or normal tissue

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