Gene expression of PMP22 is an independent prognostic factor for disease-free and overall survival in breast cancer patients

Tong, Dan; Heinze, Georg; Pils, Dietmar; Wolf, Andrea; Singer, Christian F.; Concin, Nicole; Hofstetter, Gerda; Schiebel, Ingrid; Rudas, Margaretha; Zeillinger, Robert

doi:10.1186/1471-2407-10-682

Cited by 24 publications

(11 citation statements)

References 18 publications

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“…increased p23 expression, significantly altered the expression of several such genes (Figure 8B) suggesting p23 may act by reprogramming gene expression profiles into more aggressive phenotypes. KYNU, CTSD and PMP22 are known to be up‐regulated in advanced metastatic cancers and correlate with poor prognosis whereas LAMB1 encodes a laminin‐1 protein shown to have reduced expression in breast cancer (Minn et al., 2005; Pruitt et al., 2013; Simpson et al., 2010; Tong et al., 2010).…”

Section: Resultsmentioning

confidence: 99%

The co‐chaperone p23 promotes prostate cancer motility and metastasis

et al. 2014

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Prostate cancer is an androgen receptor (AR)-dependent malignancy at initiation and progression, therefore hormone therapy is the primary line of systemic treatment. Despite initial disease regression, tumours inevitably recur and progress to an advanced castration-resistant state a major feature of which is metastasis to the bone. Up-regulation of AR cofactors and chaperones that overcome low hormone conditions to maintain basal AR activity has been postulated as a mechanism of therapy relapse.p23, an essential component of the apo-AR complex, acts also after ligand binding to increase AR transcriptional activity and target gene expression, partly by increasing chromatin-loaded holo-receptor-complexes. Immunohistochemical studies have demonstrated increased p23 expression in advanced prostate cancer. Here, we further characterise p23 roles in AR signalling and show that it modulates cytosolic AR levels in the absence of hormone, confirming a chaperoning function in the aporeceptor complex and suggesting p23 upregulates AR signalling at multiple stages. Moreover, p23 protein levels significantly increased upon treatment with not only androgen but also clinically relevant anti-androgens. This was in contrast to the HSP90 inhibitor 17-AAG, which did not modulate expression of the cochaperone – important given the HSP90-independent roles we and others have previously described for p23.Further, we demonstrate p23 is implicated in prostate cancer cell motility and in acquisition of invasiveness capacity through the expression of specific genes known to participate in cancer progression. This may drive metastatic processes in vivo since analysis of prostate tumour biopsies revealed that high nuclear p23 significantly correlated with shorter survival times and with development of metastases in patients with lower grade tumours. We propose that increased p23 expression may allow cells to acquire a more aggressive phenotype, contributing to disease progression, and that p23 is a plausible secondary target in combination with HSP90 inhibition as a potential therapy for advanced prostate cancer.

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Section: Resultsmentioning

confidence: 99%

The co‐chaperone p23 promotes prostate cancer motility and metastasis

et al. 2014

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“…Moreover, PMP22 is proved to be frequently amplified in osteosarcomas and may be involved in cell cycle to aberrant regulate cell growth in osteosarcoma tumorigenesisn [8,9]. Besides, PMP22 is observed to be differentially expressed in breast cell lines and is defined as an independent prognostic factor for overall survival in patients with breast cancer [10]. Irshad et al also have confirmed that PMP22 is a molecular signature in newly diagnosed prostate cancer with independent prognostic value [11].…”

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confidence: 94%

Suppression of peripheral myelin protein 22 (PMP22) expression by miR29 inhibits the progression of lung cancer

Qu¹,

Zhu²,

Tao³

et al. 2015

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PMP22 is recently recognized as a key player in a variety of prevalent cancers. In this study, we sought to explore the correlation of peripheral myelin protein 22 (PMP22) expression with cell proliferation, invasion and apoptosis in lung cancer cell line. miR29 was transfected into Anip973 lung adenocarcinoma cell line to interfere the expression of PMP22 using Lipofectamine ® 2000 reagent. Real-time polymerase chain reaction (RT-PCR) and Western blot were performed to determine the expression level of PMP22 at mRNA and protein level. Then MTT, Matrigel transwell assay and flow cytometry were respectively used to explore the proliferation, invasion and apoptosis in Anip973 lung adenocarcinoma cell line in vitro. miR29 could significantly down-regulate the expression level of PMP22 in Anip973 cells not only at mRNA level but also at protein level. Moreover, the proliferation rate, invasive cell number and apoptosis rate of Anip973 cells in miR29 transfected group significantly decreased compared with blank group, while no significant difference existed between control group and blank group. Our study found that suppression of PMP22 expression could inhibit cell proliferation, invasion and apoptosis in lung cancer cells. All these findings suggest that PMP22 may be involved in progression of lung cancer and could be a new therapeutic target for this disease.

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“…Regulation of Pmp22 mRNA by G3bp1 affects the cellular proliferation in breast cancer (Winslow et al, 2013). Pmp22 gene expression is a novel independent prognostic factor for disease free survival and overall survival for breast cancer patients and including it into a model with established prognostic factors will increase the accuracy of prognosis (Tong et al, 2010).…”

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confidence: 99%