We are analyzing https://link.springer.com/article/10.1007/bf03401823.

Title:
Suberoylanilide Hydroxamic Acid as a Potential Therapeutic Agent for Human Breast Cancer Treatment | Molecular Medicine
Description:
Background Suberoylanilide hydroxamic acid (SAHA) is a prototype of the newly developed, second-generation, hybrid polar compounds. It is a novel histone deacetylase inhibitor with high potency for inducing cell differentiation of cultured murine erythroleukemia cells. Studies with SAHA have primarily been performed with hematopoietic tumor cells. Here we extent these studies with SAHA to human breast cancer cell lines in an attempt to find better therapeutic agents for breast cancer treatment. Materials and Methods Human breast cancer cell lines, MCF7, MDA-MB-231, and MDA-MB-435, as well as normal cells, including the normal breast epithelial cell line MCF-10A, and fibroblasts, were treated with SAHA. Cells assayed for cell survival by using trypan blue exclusion assay, colony formation assay, and cell cycle and apoptosis analysis. The effects of SAHA on cell cycle and apoptosis regulatory proteins were examined by Western blots analysis. The identification of additional target genes was carried out by differential display (DD) and reverse transcription-polymerase chain reaction (RT-PCR). Results SAHA inhibited clonogenic growth of MCF7, MDA-MB-231, and MDA-MB-435 breast cancer cells. These cells were more sensitive to SAHA-mediated cytotoxic effects than normal breast epithelial cells and fibroblasts. The cytotoxic effects of SAHA on breast cancer cells were manifested by G1 and G2/M cell cycle arrest and eventual apoptosis. The pan-caspase inhibitor, Z-VAD.fmk, blocked SAHA-induced cell death, DNA laddering, and cleavage of poly(ADP-ribose) polymerase, indicating the involvement of caspases in SAHA-mediated apoptosis. In addition, SAHA modulated cell cycle and apoptosis regulatory proteins. For example, cyclin-dependent kinase (CDK) inhibitors p21WAF1/Cip1 and p27Kip1 were induced, and retinoblastoma protein pRb was hypophosphorylated. Moreover, SAHA induced several genes associated with differentiation and/or growth inhibition. These genes encode gelsolin, isopentenyl-diphosphate delta isomerase (IDI1), and 1,25-dihydroxyvitamin D-3 up-regulated protein 1 (VDUP1), the last two of which were identified by DD. Induction of these genes may contribute to SAHA-mediated pro-differentiating and antiproliferative effects. Conclusions SAHA induced growth inhibition, cell cycle arrest, and eventual apoptosis in human breast cancer cells, possibly by modulating cell cycle and apoptosis regulatory proteins, such as CDK inhibitors p21 and p27, pRb, and other differentiation and/or growth inhibition-associated genes, including gelsolin, IDI1 and VDUP1. This, together with the low toxicity in normal cells, suggests that SAHA might have therapeutic potential for the treatment of human breast cancers.
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pubmed, google, scholar, cas, article, cell, cancer, human, cells, breast, histone, apoptosis, deacetylase, saha, res, expression, protein, gelsolin, acid, differentiation, central, biol, usa, nature, inhibitor, proteins, growth, chem, thioredoxin, cycle, genes, richon, sci, gene, asch, suberoylanilide, hydroxamic, effects, death, induced, retinoblastoma, inhibition, natl, acad, pardee, hybrid, polar, access, proc, transcriptional,

Topics {✒️}

epstein-barr virus-transformed lymphocytes month download article/chapter suberoylanilide hydroxamic acid n-methyl-n-nitrosourea dana-farber cancer institute radiation-induced g1 arrest hybrid polar compounds carcinogen-induced mammary tumorigenesis inappropriate s-phase entry g1 cyclin-dependent kinases cyclin-dependent kinase activities di-methylallyl diphosphate isomerase thioredoxin-binding protein-2/vitamin butyrate-mediated growth inhibition waf1/cip1 gene promoter isopentenyl-diphosphate delta isomerase phorbol ester-induced differentiation saha-mediated pro-differentiating cytodifferentiation agent-induced pathways atl-derived factor trans retinoic acid growth-promoting effect full article pdf tpa-induced monocytic differentiation vitamin d-regulated gene hybrid polar inducers programmed cell death janicke ru breast cancer cells autocrine growth factor cyclin-dependent kinase human breast cancers saha-mediated cytotoxic effects human isopentenyl diphosphate mammalian histone deacetylase breast cancer treatment normal human keratinocytes privacy choices/manage cookies cdk inhibitors p21 human myeloma cells anti-tumour activity hematopoietic tumor cells human bladder cancer histone deacetylase inhibitor histone deacetylase activity plzf-rar-alpha human thioredoxin homologue advanced breast cancer cell cycle arrest acute myelogenous leukemia

Questions {❓}

(1997) What’s up and down with histone deacetylation and transcription?

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