Variations of Proline-Rich Kinase Pyk2 Expression Correlate with Prostate Cancer Progression

Stanzione, Rosita; Picascia, Antonietta; Chieffi, Paolo; Imbimbo, Ciro; Palmieri, Alessandro; Mirone, Vincenzo; Staibano, Stefania; Franco, Renato; Rosa, Gaetano De; Schlessinger, Joseph; Tramontano, Donatella

doi:10.1038/labinvest.3780211

Cited by 42 publications

(42 citation statements)

References 57 publications

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“…Stanzione and coworkers first reported the expression of PYK2 in benign and malignant prostate tissues (Stanzione et al 2001). However, in contrast to our observations, Stanzione's works showed that PYK2 is expressed only in benign prostate tissues, whereas its expression progressively reduces with an increasing grade of malignancy of PCa.…”

Section: :8contrasting

confidence: 55%

PYK2 via S6K1 regulates the function of androgen receptors and the growth of prostate cancer cells

Hsiao¹,

Huang²,

Hung³

et al. 2016

Endocrine-Related Cancer

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Androgen receptor (AR) is a steroid hormone receptor that functions as a transcription factor for regulating cell growth and survival. Aberrant AR function becomes a risk factor for promoting the progression of prostate cancer (PCa). In this study, we examined the roles of proline-rich tyrosine kinase 2 (PYK2) and ribosomal S6 kinase 1 (S6K1) in regulating AR expression and activity and growth properties in PCa cells. Compared with normal prostate tissues, PCa tumors exhibited high levels of PYK2 and S6K1 expression. Furthermore, the expression levels of PYK2 and S6K1 were significantly correlated with nuclear AR expression in PCa tissues. We further found the association between PYK2, S6K1, and AR in their protein expression and phosphorylation levels among normal prostate PZ-HPV-7 cells and prostate cancer LNCaP and 22Rv1 cells. Overexpression of the wild-type PYK2 in PZ-HPV-7 and LNCaP cells promoted AR and S6K1 expression and phosphorylation as well as enhanced cell growth. In contrast, expression of the mutated PYK2 or knockdown of PYK2 expression in LNCaP or 22Rv1 cells caused reduced expression or phosphorylation of AR and S6K1 as well as retarded cell growth. Under an androgen-deprived condition, PYK2-promoted AR expression and phosphorylation and PSA production in LNCaP cells can be abolished by knocking down S6K1 expression. In summary, our data suggested that PYK2 via S6K1 activation modulated AR function and growth properties in PCa cells. Thus, PYK2 and S6K1 may potentially serve as therapeutic targets for PCa treatment.

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Section: :8contrasting

confidence: 55%

PYK2 via S6K1 regulates the function of androgen receptors and the growth of prostate cancer cells

Hsiao¹,

Huang²,

Hung³

et al. 2016

Endocrine-Related Cancer

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“…41 In contrast, other studies reported rather decreased Pyk2 expression in advanced osteosacroma 42 and in high-grade prostate cancer compared with normal epithelial prostate tissue and benign prostatic hyperplasia. 23 These reports used small numbers of tissue cases and did not address the context of overexpression of the prognostic marker ErbB-2.…”

Section: Discussionmentioning

confidence: 99%

Focal Adhesion Kinase-Related Proline-Rich Tyrosine Kinase 2 and Focal Adhesion Kinase Are Co-Overexpressed in Early-Stage and Invasive ErbB-2-Positive Breast Cancer and Cooperate for Breast Cancer Cell Tumorigenesis and Invasiveness

Behmoaram

Bijian

Shi

et al. 2008

The American Journal of Pathology

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Malignant tumor cells invade surrounding normal tissue and disseminate to distant organs through a multistep and multifactorial process. In general, the acquisition of early autonomous motile property involves cell polarization toward blood and lymphatic vessels in response to chemotactic signals, cell cytoskeleton remodeling, and formation of cell plasma membrane protrusions. The latter are the site of dynamic turnover of multiple focal adhesion molecules, which allow formation of stable cellmatrix attachments near the leading edge of the protrusions, forward movement of the cell body, and disassembly of focal-matrix adhesions and retraction at the trailing edge. These processes are the driving force for early cancer cell migration and invasion.Central to the regulation of the cell migration cycle is the focal adhesion kinase (FAK) and its homologous FAKrelated proline-rich tyrosine kinase 2 (Pyk2).1 FAK and Pyk2 share 45% amino acid sequence homology with a

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“…PYK2 thus seems to have multiple ways to mediate ARA55-enhanced AR transcriptional activity. PYK2 is expressed in neurons, bone marrow, smooth muscles, and prostate (79,80). Tissue staining showed that PYK2 was decreased with increased malignancy of prostate cancers (80), indicating a regulatory role of PYK2 on ARA55-enhanced AR-mediated growth of cancer cells.…”

Section: Ar Coactivators In Prostate Cancermentioning

confidence: 99%

Androgen Receptor Coregulators in Prostate Cancer

Rahman

Miyamoto

Chang

2004

Clinical Cancer Research

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Variations of Proline-Rich Kinase Pyk2 Expression Correlate with Prostate Cancer Progression

Cited by 42 publications

References 57 publications

PYK2 via S6K1 regulates the function of androgen receptors and the growth of prostate cancer cells

PYK2 via S6K1 regulates the function of androgen receptors and the growth of prostate cancer cells

Focal Adhesion Kinase-Related Proline-Rich Tyrosine Kinase 2 and Focal Adhesion Kinase Are Co-Overexpressed in Early-Stage and Invasive ErbB-2-Positive Breast Cancer and Cooperate for Breast Cancer Cell Tumorigenesis and Invasiveness

Androgen Receptor Coregulators in Prostate Cancer

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