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Depletion of the human N^α^‐terminal acetyltransferase A induces p53‐dependent apoptosis and p53‐independent growth inhibition by Darina Gromyko; Thomas Arnesen; Anita Ryningen; Jan Erik Varhaug; Johan R. Lillehaug is a Medicine article available to read on EtoBox.

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## Abstract The human protein N^α^‐terminal acetyltransferase A complex (hNatA), composed of the catalytic hNaa10p (hArd1) and auxiliary hNaa15p (hNat1/NATH/Tubedown) subunits, was reported to be important for cell survival and growth of various types of cancer. However, little is known about the mechanisms mediating growth inhibition and apoptosis following loss of hNatA function. Here, we have screened 11 different thyroid cell lines for h__NAA10__ RNAi phenotypes and observed mostly growth inhibition, which was independent of __TP53__ functional status and developed by several different mechanisms involving (__i__) downregulation of cyclin D1, (__ii__) increase in p27/Kip1 and (__iii__) inactivation of Rb/E2F pathway. hNatA depletion in aggressive thyroid cancer cell lines (8305C, CAL‐62 and FTC‐133) with mutated __TP53__ increased sensitivity to drug‐induced cytotoxicity, but in a cell type specific manner: 8305C (TRAIL), CAL‐62 (daunorubicin) and FTC‐133 (troglitazone). Cells harboring wild‐type __TP53__ were also prone to apoptosis __via__ the p53 pathway after hNatA downregulation. Importantly, in hNatA‐depleted cells DNA‐damage signaling was activated in the absence of exog

Who reads Depletion of the human N^α^‐terminal acetyltransferase A induces p53‐dependent apoptosis and p53‐independent growth inhibition?

Author

Darina Gromyko; Thomas Arnesen; Anita Ryningen; Jan Erik Varhaug; Johan R. Lillehaug

Publisher

John Wiley and Sons; Wiley (John Wiley & Sons); John Wiley & Sons Inc.; Wiley; Research Square; Test accounts (ISSN 0020-7136)

Published

2010

Language

EN

Field

Medicine (Health Sciences)