I-7ab inhibited the growth of TNBC cells via targeting HDAC3 and promoting the acetylation of p53 - 21/02/18

Doi : 10.1016/j.biopha.2018.01.063

Mei Yang ^a,^{^{1
These authors contributed equally to the work.}}, Xuefei Dang ^a,^{^{1
These authors contributed equally to the work.}}, Yue Tan ^a, Meixing Wang ^a, Xiaojing Li ^b, Gang Li ^a,^⁎
^a Department of Medical Oncology, Brunch of MinHang, Fudan University Shanghai Cancer Hospital, Shanghai, 200240, China
^b Department of Medical Oncology, Fifth People’s Hospital Affiliated to Fudan University, Shanghai, 200240, China

^⁎Corresponding author at: Department of Medical Oncology, Brunch of MinHang, Fudan University Shanghai Cancer Hospital, 106 Ruili Road, Shanghai China.Department of Medical OncologyBrunch of MinHangFudan University Shanghai Cancer HospitalShanghai200240China

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Abstract

Triple negative breast cancer (TNBC) is a heterogenous disease with high aggressive and poor outcome. The lack of biomarkers and targeted therapies makes it a challenge for the treatment of TNBC. Histone deacetylase inhibitors (HDACis) are emerging as novel anti-tumor agents in many types of human cancers. In this study, we found that I-7ab, a novel HDACi, inhibited the cell viability of TNBC cells and induced the cell apoptosis. Mechanistically, I-7ab specifically decreased the expression of HDAC3 and promoted the acetylation of p53 at both Lys373 and Lys382 amino acids. The up-regulated acetylation of p53 promoted the transcriptional activity of p53 and induced the expression of p21, which consequently caused cell cycle arrest at G1 phase. Administration of I-7ab inhibited the colony formation of TNBC cells. Collectively, these results indicated I-7ab as a promising anti-cancer agent in the treatment of TNBC.

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Keywords : TNBC, I-7ab, HDAC3, p53, Cell cycle arrest, Cell apoptosis

Plan

Introduction

Materials and methods

Activity of caspase-3

Cell cycle analysis

Western blot

Quantitative real-time PCR

Statistical analysis

Results

I-7ab inhibits the growth of TNBC cells

I-7ab decreased the expression of HDAC3 and enhanced the acetylation of p53

I-7ab promoted the transcriptional activity of p53 and induced the expression of p21

I-7ab induced cell cycle arrest and inhibited the colony formation of TNBC cells

Discussion

Conflict of interest

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Vol 99

P. 220-226 - mars 2018 Retour au numéro

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I-7ab inhibited the growth of TNBC cells via targeting HDAC3 and promoting the acetylation of p53 - 21/02/18

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