Retinoic acid responsive genes in the murine hepatocyte cell line AML 12

Mamoon, Abulkhair; Ventura-Holman, Tereza; Maher, Joseph F.; Subauste, José S.

doi:10.1016/j.gene.2007.10.020

Cited by 14 publications

(17 citation statements)

References 46 publications

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“…RNA isolation and preparation for microarray analysis have been previously described (Mamoon et al, 2008). The Affymetrix GeneChip Mouse Genome 430 2.0 array consisting of over 39,000 transcripts representing wellknown genes was used for these studies.…”

Section: Microarraysmentioning

confidence: 99%

“…Quantitative PCR reactions were performed in a DNA Engine Opticon 2 System (MJ Research Inc., Waltham, MA) as previously described (Mamoon et al, 2008). Samples were prepared using the DyNAmo™ SYBR® Green qPCR kit from Finnzymes (New England Biolabs, Beverly, MA).…”

Section: Quantitative Real-time Pcr (Qpcr)mentioning

confidence: 99%

“…We have previously demonstrated that AML12 cells constitutively express adequate amounts of RARs and RXRs to mediate liganddependent activation of RA-responsive genes (Mamoon et al, 2008). In order to study the effect of v-erbA on the regulation of RAdependent genes in this system, AML12 cells were stably transfected with the gag-v-erbA fusion protein cloned into a pcDNA vector containing the hygromycin-resistance gene.…”

Section: Expression Of V-erba In Aml12 Cellsmentioning

confidence: 99%

“…Previous microarray analyses in our laboratory have identified RAresponsive genes and analyzed their importance in the context of liver metabolism using the AML12 cell line as a model system (Mamoon et al, 2008). The aim of the present study is to contribute to the understanding of nuclear receptor-mediated transcriptional regulation by investigating the effect of v-erbA on the expression of RAresponsive genes.…”

Section: Introductionmentioning

confidence: 99%

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Modulation of expression of RA-regulated genes by the oncoprotein v-erbA

Ventura-Holman

Mamoon

Subauste

2008

Gene

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Section: Microarraysmentioning

confidence: 99%

Section: Quantitative Real-time Pcr (Qpcr)mentioning

confidence: 99%

Section: Expression Of V-erba In Aml12 Cellsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Modulation of expression of RA-regulated genes by the oncoprotein v-erbA

Ventura-Holman

Mamoon

Subauste

2008

Gene

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“…It has been shown that retinoic acid could inhibit the expression of MEF2D in murine hepatocytes (27). Retinoic acid has a key function in the control of cell proliferation, differentiation, and apoptosis and retinoic acid may play a role in the prevention and treatment of tumors (28).…”

Section: Introductionmentioning

confidence: 99%

Overexpression of the Transcription Factor MEF2D in Hepatocellular Carcinoma Sustains Malignant Character by Suppressing G2–M Transition Genes

Liu

et al. 2014

Cancer Research

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The underlying molecular pathogenesis in hepatocellular carcinoma remains poorly understood. The transcription factor MEF2D promotes survival in various cell types and it seems to function as an oncogene in leukemia. However, its potential contributions to solid cancers have not been explored. In this study, we investigated MEF2D expression and function in hepatocellular carcinoma, finding that MEF2D elevation in hepatocellular carcinoma clinical specimens was associated with poor prognosis. MEF2D-positive primary hepatocellular carcinoma cells displayed a faster proliferation rate compared with MEF2D-negative cells, and silencing or promoting MEF2D expression in these settings limited or accelerated cell proliferation, respectively. Notably, MEF2D-silencing abolished hepatocellular carcinoma tumorigenicity in mouse xenograft models. Mechanistic investigations revealed that MEF2D-silencing triggered G 2 -M arrest in a manner associated with direct downregulation of the cell-cycle regulatory genes RPRM, GADD45A, GADD45B, and CDKN1A. Furthermore, we identified MEF2D as an authentic target of miR-122, the reduced expression of which in hepatocellular carcinoma may be responsible for MEF2D upregulation. Together, our results identify MEF2D as a candidate oncogene in hepatocellular carcinoma and a potential target for hepatocellular carcinoma therapy. Cancer Res; 74(5);

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