The 3′ Untranslated Region of Prohibitin and Cellular Immortalization

Er, Jupe; Xt, Liu; Kiehlbauch, JL; Jk, McClung; Rt, Dell'Orco

doi:10.1006/excr.1996.0120

Cited by 80 publications

(58 citation statements)

References 0 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Since the last decade of the 20 th century, several 3'untranslated regions of eukaryotic mRNAs were found to have in vitro tumor suppressor activity. They caused phenotypic reversion (lowering of tumorigenicity) in cultured tumor cells or malignant cells [1][2][3][4][5][6]. However, the molecular mechanisms of these tumor suppressor effects remain elusive.…”

Section: Introductionmentioning

confidence: 99%

Gene expression profile favoring phenotypic reversion: a clue for mechanism of tumor suppression by NF-IL6 3′UTR

et al. 2003

View full text Add to dashboard Cite

Transfection of cDNA in 3'untranslated region of human nuclear factor for interleukin-6 (NF-IL6 3'UTR) induced tumor suppression in a human hepatoma cell line. cDNA array analysis was used to reveal changes in gene expression profile leading to tumor suppression The results indicate that this suppression was not due to activation of dsRNA-dependent protein kinase, nor to inactivation of oncogenes; rather, all the changes in expression of known genes, induced by NF-IL6 3'UTR cDNA may be ascribed to the suppression of cellular malignancy. Therefore, our results imply that this 3'untranslated region may have played role of a regulator of gene expression profile.

show abstract

Section: Introductionmentioning

confidence: 99%

Gene expression profile favoring phenotypic reversion: a clue for mechanism of tumor suppression by NF-IL6 3′UTR

et al. 2003

View full text Add to dashboard Cite

show abstract

“…In particular, we found that several proteins of interest were more highly expressed in resting B cells than in lymphoma cells, including factors that are involved in cell cycle regulation, such as leukemia inhibitory factor (Lif), which is an autocrine/paracrine B cell regulator that me- diates B cell arrest through the Ras and Jak/Stat pathways, 26 prohibitin, a tumor suppressor and cell cycle regulator that plays role in growth regulation of fibroblasts, 27,28 which our group has previously shown is an important negative regulator of E2Fs, 29 and matrin-3 (p130), a cell cycle regulator that mediates cell cycle arrest by p130 and regulates Cdk2. 30 We also identified heat shock cognate 71 kd protein (Hsp70), which is a chaperone protein associated with growth inhibition in lymphoid cells 31 and was more highly expressed in resting B cells than in lymphoma cells.…”

Section: Dlbcl-associated Proteomementioning

confidence: 99%

Development of a Malignancy-Associated Proteomic Signature for Diffuse Large B-Cell Lymphoma

Romesser

Perlman

Faller

et al. 2009

The American Journal of Pathology

View full text Add to dashboard Cite

The extreme pathological diversity of non-Hodgkin's lymphomas has made their accurate histological assessment difficult. New diagnostics and treatment modalities are urgently needed for these lymphomas, particularly in drug development for cancer-specific targets. Previously, we showed that a subset of B cell lymphoma, diffuse large B cell lymphoma, may be characterized by two major, orthogonal axes of gene expression: one set of transcripts that is differentially expressed between resting and proliferating, nonmalignant cells (ie, a "proliferative signature") and another set that is expressed only in proliferating malignant cells (ie, a "cancer signature"). A differential proteomic analysis of B cell proliferative states, similar to previous transcriptional profiling analyses, holds great promise either to reveal novel factors that participate in lymphomagenesis or to define biomarkers of onset or progression. Here, we use a murine model of diffuse large B cell lymphoma to conduct unbiased two-dimensional gel electrophoresis and mass spectrometry-based comparative proteomic analyses of malignant proliferating B cells and tissue-matched, normal resting, or normal proliferating cells. We show that the expression patterns of particular proteins or isoforms across these states fall into eight specific trends that provide a framework to identify malignancy-associated biomarkers and potential drug targets , a signature proteome. Our results support the central hypothesis that clusters of proteins of known function represent a panel of expression markers uniquely associated with malignancy and not normal proliferation.

show abstract

“…The cell-cycle function of prohibitin is less well understood and there is some dispute over the precise role of the protein (Coates et al, 2001). Injection of the mRNA results in cell-cycle arrest in some cell types (McClung et al, 1989;Nuell et al, 1991), and this may in part be due to the 3 0 untranslated region (3 0 UTR) of the mRNA (Jupe et al, 1996). Even the localization of the protein is not clear, with some groups maintaining that the protein is purely mitochondrial (Coates et al, 2001), and others demonstrating a secondary localization in the nucleus (Thompson et al, 2001;Wang et al, 2002b).…”

Section: Introductionmentioning

confidence: 99%

Androgens target prohibitin to regulate proliferation of prostate cancer cells

et al. 2004

View full text Add to dashboard Cite

Proteins involved in the growth response of prostate cancer cells to androgen were investigated by comparing the proteomes of LNCaP cells treated with vehicle or androgen. Whole-cell lysates were separated by twodimensional PAGE, and HPLC-MS/MS was used to identify androgen-regulated proteins. Prohibitin, a protein with cell-cycle regulatory activity, was shown to be downregulated by 50% following androgen stimulation. Western blot and reverse transcription-PCR experiments confirmed the result and showed that regulation occurs at the level of transcription. To determine the importance of prohibitin in androgen-stimulated growth, we used transient transfection to overexpress the protein and RNA interference to knock down the protein. Subsequent FACS analysis showed that cells with reduced levels of prohibitin showed a slight but reproducible increase in the percentage of population in cell cycle, while cells with increased prohibitin levels showed a clear reduction in the percentage entering cell cycle, following dihydrotestosterone stimulation, when compared to untransfected controls. Confocal microscopy showed localization of prohibitin in the nucleus as well as the mitochondria of LNCaP cells. It therefore seems that the regulation of prohibitin is a vital part of the cellular growth response to androgen stimulation in LNCaPs and prohibitin may have a nuclear regulatory role in cell-cycle progression.

show abstract

The 3′ Untranslated Region of Prohibitin and Cellular Immortalization

Cited by 80 publications

References 0 publications

Gene expression profile favoring phenotypic reversion: a clue for mechanism of tumor suppression by NF-IL6 3′UTR

Gene expression profile favoring phenotypic reversion: a clue for mechanism of tumor suppression by NF-IL6 3′UTR

Development of a Malignancy-Associated Proteomic Signature for Diffuse Large B-Cell Lymphoma

Androgens target prohibitin to regulate proliferation of prostate cancer cells

Contact Info

Product

Resources

About