HDAC1 triggers the proliferation and migration of breast cancer cells via upregulation of interleukin-8

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Abstract

Targeted inhibition of histone deacetylase (HDAC) is one of the potent anticancer therapy approaches. Our data showed that mRNA and protein levels of HDAC1 in breast cancer cells were greater than that in normal fibroblast 3T3 cells and normal epithelial breast MCF10A cells. The mRNA levels of HDAC1 in 75% of breast cancer tissues (18/24) were greater than that in their corresponding adjacent normal tissues. Knockdown of HDAC1 by specific siRNAs can suppress the proliferation and migration of breast cancer cells and inhibit the expression of interleukin-8 (IL-8), while not IL-6. While recombinant IL-8 (rIL-8) can attenuate the suppression effects of si-HDAC1 on the proliferation and migration of breast cancer cells. HDAC1 can positively regulate the transcription and promoter activities of IL-8. While NF-κB and MAPK, two important signals responsible for the transcription of IL-8, did not mediate HDAC1 regulated IL-8 expression. The expression and nuclear translocation of Snail were increased in HDAC1 over expressed breast cancer cells. Targeted inhibition of Snail can attenuate HDAC1 over expression induced cell proliferation and migration. Collectively, our data showed that HDAC1 can trigger the proliferation and migration of breast cancer cells via activation of Snail/IL-8 signals.

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