Cell cycle activity and expression of prohibitin mRNA

Roskams, A. Jane; Friedman, Varda; Wood, Carla M.; Walker, Lucy; Owens, Garrison; Stewart, David A.; Altus, Michael S.; Danner, David B.; Liu, Xiao-Tie; Jk, McClung

doi:10.1002/jcp.1041570211

Cited by 73 publications

(54 citation statements)

References 22 publications

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“…21,22 However, there is also study reported that PHB could contribute to the control of the S to G2 transition in the prostate cancer cells and cells containing PHB siRNA had an increase in cell population entering the S/G2 M phase. 23 Specifically 2% of these cells were detected in this phase when compared with control cells, which increased to 10% after the stimulation of dihydrotestosterone (DHT).…”

Section: Discussionmentioning

confidence: 99%

Prohibitin promotes androgen receptor activation in ER-positive breast cancer

Liu

Zhang

et al. 2017

Cell Cycle

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Prohibitin (PHB) is an evolutionarily conserved protein with multiple functions in both normal and cancer cells. Androgen receptor (AR) was reported to act as a different role in the ER-positive and ER-negative breast cancer. However, little is known about the role of PHB and whether PHB could regulate AR expression in the ER-positive breast cancer. Here, we determined the expression and clinical outcomes of PHB in breast cancer samples using 121 breast cancer tissues and published databases, and investigated the role of PHB in breast cancer cell growth, apoptosis and cell cycle arrest in the ER-positive breast cancer cells. We obtained the expression of PHB is significantly low in breast cancer samples, and low PHB expression positively correlated with poor prognosis of breast cancer. We detected that PHB could inhibit breast cancer cell proliferation, change cell cycle distribution and promote cell apoptosis in the ER-positive breast cancer cells. Moreover, we found PHB could significantly increase AR expression in both mRNA and protein levels in the ER-positive breast cancer cells. Additionally, a significant positive correlation between PHB and AR expression was identified in the 121 breast cancer tissues. PHB and AR expression are associated with prognosis in the ER-positive breast cancer patients. Our results indicate that PHB promotes AR activation in ER-positive breast cancer, making PHB and AR potential molecular targets for ER-positive breast cancer therapy.

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Section: Discussionmentioning

confidence: 99%

Prohibitin promotes androgen receptor activation in ER-positive breast cancer

Liu

Zhang

et al. 2017

Cell Cycle

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“…When microinjected into normal human fibroblasts, Phb1 mRNA attenuated DNA synthesis, however, this effect was subsequently shown to be mediated by the 3Ј-untranslated region rather than the coding region of the cDNA (52,53). The mechanism of cell cycle regulation was determined by Wang et al (54,55) who showed Phb1 could bind Rb as well as E2F1 to repress their transcriptional activity (56).…”

Section: Discussionmentioning

confidence: 99%

The PHB1/2 Phosphocomplex Is Required for Mitochondrial Homeostasis and Survival of Human T Cells

Ross

Nagy

Kirken

2008

Journal of Biological Chemistry

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Many immune pathologies are the result of aberrant regulation of T lymphocytes. A functional proteomics approach utilizing two-dimensional gel electrophoresis coupled with mass spectrometry was employed to identify differentially expressed proteins in response to T cell activation. Two members of the prohibitin family of proteins, Phb1 and Phb2, were determined to be up-regulated 4 -5-fold upon activation of primary human T cells. Furthermore, their expression was dependent upon CD3 and CD28 signaling pathways that synergistically led to the upregulation (13-15-fold) of Phb1 and Phb2 mRNA levels as early as 48 h after activation. Additionally, orthophosphate labeling coupled with phosphoamino acid analysis identified Phb1 to be serine and Phb2 serine and tyrosine phosphorylated. Tyrosine phosphorylation of Phb2 was mapped to Tyr 248 using mass spectrometry and confirmed by mutagenesis and phosphospecific antibodies. In contrast to previous reports of Phb1 and Phb2 being nuclear localized, subcellular fractionation, immunofluorescent, and electron microscopy revealed both proteins to localize to the mitochondrial inner membrane of human T cells. Accordingly, small interfering RNA-mediated knockdown of Phbs in Kit225 cells resulted in disruption of mitochondrial membrane potential. Additionally, Phb1 and Phb2 protein levels were up-regulated 2.5-fold during cytokine deprivation-mediated apoptosis of Kit225 cells, suggesting this complex plays a protective role in human T cells. Taken together, Phb1 and Phb2 are novel phosphoproteins up-regulated during T cell activation that function to maintain mitochondrial integrity and thus represent previously unrecognized therapeutic targets for regulating T cell activation, differentiation, viability, and function.

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“…Tumor suppressor genes are known to regulate both cell proliferation and cell death (9,40). Prohibitins act as negative regulators of cell proliferation in mammals and are implicated in tumor suppression (7).…”

Section: Discussionmentioning

confidence: 99%

“…7). Prohibitins negatively control the cell cycle in the early G 1 phase and specifically inhibit initiation of DNA synthesis (8,9). Prohibitin genes appear to be expressed in many tissues and organisms, but with some modulation of expression consistent with a role in the cell cycle (7,8,10).…”

mentioning

confidence: 99%

Prohibitins, Stomatins, and Plant Disease Response Genes Compose a Protein Superfamily That Controls Cell Proliferation, Ion Channel Regulation, and Death

Nadimpalli

Yalpani

Johal

et al. 2000

Journal of Biological Chemistry

151

155

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Prohibitins, stomatins, and a group of plant defense response genes are demonstrated to belong to a novel protein superfamily. This superfamily is bound by similar primary and secondary predicted protein structures and hydropathy profiles. A PROSITE-formatted regular expression was generated that is highly predictive for identifying members of this superfamily using PHI-BLAST. The superfamily is named PID (proliferation, ion, and death) because prohibitins are involved in proliferation and cell cycle control, stomatins are involved in ion channel regulation, and the plant defenserelated genes are involved in cell death. The plant defense gene family is named HIR (hypersensitive induced reaction) because its members are associated with hypersensitive reactions involving cell death and pathogen resistance. For this study, eight novel maize genes were introduced: four closely related to prohibitins (Zmphb1, Zm-phb2, Zm-phb3, and Zm-phb4), one to stomatins (Zm-stm1), and three to a gene implicated in plant disease responses (Zm-hir1, Zm-hir2, and Zm-hir3). The maize Zm-hir3 gene transcript is up-regulated in a disease lesion mimic mutation (Les9), supporting a role in maize defense responses. Members of this gene superfamily are involved in diverse functions, but their structural similarity suggests a conserved molecular mechanism, which we postulate to be ion channel regulation.

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Cell cycle activity and expression of prohibitin mRNA

Cited by 73 publications

References 22 publications

Prohibitin promotes androgen receptor activation in ER-positive breast cancer

Prohibitin promotes androgen receptor activation in ER-positive breast cancer

The PHB1/2 Phosphocomplex Is Required for Mitochondrial Homeostasis and Survival of Human T Cells

Prohibitins, Stomatins, and Plant Disease Response Genes Compose a Protein Superfamily That Controls Cell Proliferation, Ion Channel Regulation, and Death

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