Genetic and small molecule inhibition of arylamine N-acetyltransferase 1 reduces anchorage-independent growth in human breast cancer cell line MDA-MB-231

Molecular Carcinogenesis
Marcus W SteppDavid W Hein

Abstract

Arylamine N-acetyltransferase 1 (NAT1) expression is reported to affect proliferation, invasiveness, and growth of cancer cells. MDA-MB-231 breast cancer cells were engineered such that NAT1 expression was elevated or suppressed, or treated with a small molecule inhibitor of NAT1. The MDA-MB-231 human breast cancer cell lines were engineered with a scrambled shRNA, a NAT1 specific shRNA or a NAT1 overexpression cassette stably integrated into a single flippase recognition target (FRT) site facilitating incorporation of these different genetic elements into the same genomic location. NAT1-specific shRNA reduced NAT1 activity in vitro by 39%, increased endogenous acetyl coenzyme A levels by 35%, and reduced anchorage-independent growth (sevenfold) without significant effects on cell morphology, growth rates, anchorage-dependent colony formation, or invasiveness compared to the scrambled shRNA cell line. Despite 12-fold overexpression of NAT1 activity in the NAT1 overexpression cassette transfected MDA-MB-231 cell line, doubling time, anchorage-dependent cell growth, anchorage-independent cell growth, and relative invasiveness were not changed significantly when compared to the scrambled shRNA cell line. A small molecule (5E)-[5-(...Continue Reading

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Citations

Sep 18, 2018·Pharmacogenetics and Genomics·David W HeinSotiria Boukouvala
Jun 13, 2020·Molecular Carcinogenesis·Michelle El KawakMona Aoun
Mar 20, 2019·Tumour Biology : the Journal of the International Society for Oncodevelopmental Biology and Medicine·Hikaru NakashimaHideki Nakayama
Dec 3, 2020·Drug Metabolism Reviews·Philip G Board, M W Anders
Jan 14, 2021·International Journal of Molecular Sciences·Han Yeoung LeeJong Kook Park
Oct 22, 2020·Toxicology Reports·Kyung U HongDavid W Hein

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