The effect of the anticancer drug doxorubicin on cytomegalovirus-infected human fibroblasts

Федорова, Н. Е.; Emelianova, Svetlana S.; Vinogradskaya, G. R.; Chichev, E. V.; Murzakova, Anastasia; Kirichenko, A. A.; Verbenko, V. N.; Кущ, А А

doi:10.1134/s1990519x15050053

Cited by 1 publication

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“…P73 is a p53 family member that generates two groups of isoforms, either containing a complete transactivation domain (TAp73, also named P73α) or exhibiting a truncated TA domain ( 10 ). Inhibition of cell proliferation or induction of cell apoptosis is induced by P73α in response to treatment with anti-cancer agents, including doxorubicin (DOX) ( 11 ). However, in contrast to p53, failure of tumor-formation in p73 knockout mice and observations of p73 overexpression in tumor cells, do not support p73 as a classical tumor suppressor ( 12 , 13 ).…”

Section: Introductionmentioning

confidence: 99%

Tan IIA inhibits H1299 cell viability through the MDM4‑IAP3 signaling pathway

Wang

Wei

et al. 2017

Mol Med Report

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Tanshinone IIA (Tan IIA), as a bioactive compound extracted from the dried roots of Salvia miltiorrhiza (also known as Danshen), is known to inhibit cancer cell proliferation and induce apoptosis. However, the mechanisms underlying the function of Tan IIA in cancer cell apoptosis remain to be elucidated The aim of the present study was to identify the molecular mechanisms underlying the anti-cancer effects of Tan IIA in p53-deficient H1299 cells. Tan IIA was demonstrated to suppress murine double minute 4 (MDM4) expression in a time- and dose-dependent manner through the inhibition of MDM4 mRNA synthesis. Tan IIA-induced downregulation of MDM4 resulted in an increase of P73α and a decrease of inhibitor of apoptosis 3 (IAP3). However, P73α was not activated as two P73α target genes, BCL2 binding component 3 and phorbol-12-myristate-13-acetate-induced protein 1, were not significantly induced. Tan IIA-induced inhibition of IAP3 expression may be involved in Tan IIA-induced apoptosis and inhibition of H1299 cell viability. Notably, a combination of Tan IIA and doxorubicin (DOX) exposure resulted in further MDM4 overexpression in H1299 cells, indicating that Tan IIA sensitized p53-deficient and MDM4-overexpressing H1299 cells to DOX-induced apoptosis.

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Section: Introductionmentioning

confidence: 99%