Molecular Cloning and Characterization of STAMP1, a Highly Prostate-specific Six Transmembrane Protein that Is Overexpressed in Prostate Cancer

Korkmaz, Kemal; Elbi, Cem; Korkmaz, Ceren; Loda, Massimo; Hager, Gordon L.; Saatcioglu, Fahri

doi:10.1074/jbc.m202414200

Cited by 91 publications

(162 citation statements)

References 41 publications

Supporting

Mentioning

136

Contrasting

Unclassified

Order By: Relevance

“…(27) STAMP1 is highly restricted to prostate for expression and is overexpressed in prostate cancer compared with benign prostate tissue. (28,29) STAMP1 expression is correlated with the presence of functional AR, even though it appears not to be androgen regulated. (28) STAMP2 has a more general tissue distribution.…”

Section: Stamp Familymentioning

confidence: 97%

“…(28,29) STAMP1 expression is correlated with the presence of functional AR, even though it appears not to be androgen regulated. (28) STAMP2 has a more general tissue distribution. One of the major sites of its expression is the prostate, and it is strongly androgen regulated.…”

Section: Stamp Familymentioning

confidence: 97%

“…Live cell imaging and colocalization studies indicate that STAMPs reside predominantly in the Golgi and shuttle to and from the plasma membrane suggesting that they are involved in the endocytic or exocytic pathways. (25,28) STAMP3/pHyde, when expressed ectopically, causes apoptosis in prostate cancer cell lines and xenografts through a caspase 3-dependent pathway. (31) Consistent with this, TSAP6 knockdown in cell lines inhibited p53-induced apoptosis and this appears to be due to TSAP6 association with Nix, a proapoptotic Bcl-2-related protein and the Myt1 kinase, a negative regulator of the G 2 /M transition.…”

Section: Stamp Familymentioning

confidence: 99%

See 2 more Smart Citations

Androgen signaling and its interactions with other signaling pathways in prostate cancer

2007

Self Cite

View full text Add to dashboard Cite

SummaryProstate cancer is the most frequently diagnosed nonskin cancer and the third leading cause of cancer mortality in men. In the initial stages, prostate cancer is dependent on androgens for growth, which is the basis for androgen ablation therapy. However, in most cases, prostate cancer progresses to a hormone refractory phenotype for which there is no effective therapy available at present. The androgen receptor (AR) is required for prostate cancer growth in all stages, including the relapsed, ''androgen-independent'' tumors in the presence of very low levels of androgens. This review focuses on AR function and AR-target genes and summarizes the major signaling pathways implicated in prostate cancer progression, their crosstalk with each other and with AR signaling. This complex network of interactions is providing a deeper insight into prostate carcinogenesis and may form the basis for novel diagnostic and therapeutic strategies. IntroductionProstate adenocarcinoma is the most frequently diagnosed non-cutaneous male malignancy and the third leading cause of cancer-related death in men in most western industrialized countries. (1) It is estimated that around 660,000 men worldwide will be diagnosed with prostate cancer and 250,000 men will die from it in 2010; thus, it will remain a major health problem in the future. (1) It was more than 60 years ago that the important role of male sex hormones (androgens) for the development and growth of prostate cancer was demonstrated. (2) Accordingly, androgen ablation therapy has been the main line of therapy for prostate cancer. Therefore, much of the focus in prostate cancer research to date has naturally been on androgens, how to decrease the androgens in the circulation and how to inhibit the androgen receptor (AR).In addition to AR signaling, it has now become evident that other signaling pathways, as well as non-genomic and genomic alterations, are involved in prostate cancer development and progression. Furthermore, recent studies indicated that signaling through AR has a critical role even after androgen ablation and disease progression (for review see Ref.3). In the following sections, we give an overview of androgen signaling in prostate cancer, with a special focus on recent findings about AR function and AR target genes. We then review the involvement of other central signaling pathways in prostate cancer, with a special focus on their cross-talk with the AR signaling pathway. Clinical implications of these findings and potential directions for future research are also outlined.

show abstract

Section: Stamp Familymentioning

confidence: 97%

Section: Stamp Familymentioning

confidence: 97%

Section: Stamp Familymentioning

confidence: 99%

See 1 more Smart Citation

Androgen signaling and its interactions with other signaling pathways in prostate cancer

2007

Self Cite

View full text Add to dashboard Cite

show abstract

“…While searching for genes that are similar to STAMP1 (Korkmaz et al, 2002), we identified a BAC clone (GenBank Accession # AC003991) on human Chr7q21 that showed significant sequence similarity to STAMP1 cDNA ( Figure 1a). Computational exon/intron junction analysis of this locus and alignment of the full-length cDNA sequence revealed that there is a gene at this locus that is composed of five exons and four introns which is similar to STAMP1 cDNA along its whole sequence (Figure 1a).…”

Section: Isolation and Characterization Of The Stamp2 Gene And Mrnamentioning

confidence: 99%

“…While searching for genes that are differentially expressed during early stages of prostate cancer (Korkmaz et al, 2000), we have cloned a novel gene, six transmembrane protein of prostate 2 (STAMP2), named for its high sequence similarity to STAMP1, a highly prostate-enriched gene that is overexpressed in prostate cancer (Korkmaz et al, 2002). We show that STAMP2 is a highly androgen-regulated gene in androgen receptor-positive prostate cancer cells, but not in androgen receptor-negative cells.…”

Section: Introductionmentioning

confidence: 99%

Molecular cloning and characterization of STAMP2, an androgen-regulated six transmembrane protein that is overexpressed in prostate cancer

et al. 2005

Self Cite

View full text Add to dashboard Cite

We have identified a novel gene, six transmembrane protein of prostate 2 (STAMP2), named for its high sequence similarity to the recently identified STAMP1 gene. STAMP2 displays a tissue-restricted expression with highest expression levels in placenta, lung, heart, and prostate and is predicted to code for a 459-amino acid six transmembrane protein. Using a form of STAMP2 labeled with green flourescent protein (GFP) in quantitative time-lapse and immunofluorescence confocal microscopy, we show that STAMP2 is primarily localized to the Golgi complex, trans-Golgi network, and the plasma membrane. STAMP2 also localizes to vesicular-tubular structures in the cytosol and colocalizes with the Early Endosome Antigen1 (EEA1) suggesting that it may be involved in the secretory/endocytic pathways. STAMP2 expression is exquisitely androgen regulated in the androgen-sensitive, androgen receptor-positive prostate cancer cell line LNCaP, but not in androgen receptornegative prostate cancer cell lines PC-3 and DU145. Analysis of STAMP2 expression in matched normal and tumor samples microdissected from prostate cancer specimens indicates that STAMP2 is overexpressed in prostate cancer cells compared with normal prostate epithelial cells. Furthermore, ectopic expression of STAMP2 in prostate cancer cells significantly increases cell growth and colony formation suggesting that STAMP2 may have a role in cell proliferation. Taken together, these data suggest that STAMP2 may contribute to the normal biology of the prostate cell, as well as prostate cancer progression.

show abstract

Human pHyde is not a classical tumor suppressor gene in prostate cancer

Porkka

Nupponen

Tammela

et al. 2003

Intl Journal of Cancer

View full text Add to dashboard Cite

A novel putative tumor suppressor gene, pHyde, was recently cloned from rat prostate. The rat gene has been shown to inhibit prostate cancer cell proliferation both in vitro and in vivo. However, the role of human pHyde in prostate cancer has not been studied before. Here Prostate cancer is the most common malignancy among men in many Western industrialized countries. 1 In spite of the common nature of the disease, the molecular mechanisms of prostate cancer initiation, development and progression are still unclear. At the chromosomal level, though, the genetic alterations of prostate cancer are quite well-characterized by comparative genomic hybridization (CGH) and loss of heterozygosity (LOH) analyses. 2 According to these studies, loss of genetic material is more common in early prostate cancer than gains or amplifications, 3 which indicates the critical role of tumor suppressor genes in the carcinogenesis of prostate epithelial cells. Although major efforts have been made to reveal the tumor suppressor genes harboring the frequently deleted regions, only a few target genes have been identified. Many commonly deleted genes, e.g., NKX3.1, MXI1, and CDH1 (alias E-cadherin), have been identified, but only a few mutations in the remaining alleles of these genes have been found. 2 According to the "two-hit" model originally proposed by Knudson, 4 classical tumor suppressor genes are inactivated by a mutation in one allele and subsequently, by a loss of the remaining allele. Therefore, the genes mentioned above cannot be considered as classical tumor suppressor genes. Of the presently known classical tumor suppressor genes, only mutations of TP53 and PTEN have been found in substantial fraction of prostate carcinomas, and those being mainly late stage cancers. 2,5 Recently, Rinaldy and Steiner 6 isolated a novel cDNA, named as pHyde, from a non-metastatic Dunning rat prostate cancer cell line using a competitive hybridization strategy between non-metastatic and metastatic sublines. Subsequently, a transfection with a recombinant adenovirus that contained the rat pHyde was shown to inhibit proliferation of human prostate cancer cell lines LNCaP and DU145. In addition, a single injection of the pHyde construct into DU145 xenograft tumors was reported to reduce the tumor size in nude mice. 7 In further studies, the rat pHyde was shown to function as an intrinsic apoptotic factor by inducing apoptosis through a caspase-3 dependent pathway. 8,9 The biological function of pHyde makes it an attractive candidate for being a novel prostate cancer tumor suppressor gene. However, since no data about the human pHyde have been published so far, the significance of pHyde as a tumor suppressor gene has remained unclear.The aim of our study was to find out whether the human pHyde meets the criteria of a classical tumor suppressor gene. We screened prostate cancer cell lines, xenografts and clinical tumors for mutations by denaturing high-pressure liquid chromatography (DHPLC), and sequencing and gene copy number alterations by FIS...

show abstract

Molecular Cloning and Characterization of STAMP1, a Highly Prostate-specific Six Transmembrane Protein that Is Overexpressed in Prostate Cancer

Cited by 91 publications

References 41 publications

Androgen signaling and its interactions with other signaling pathways in prostate cancer

Androgen signaling and its interactions with other signaling pathways in prostate cancer

Molecular cloning and characterization of STAMP2, an androgen-regulated six transmembrane protein that is overexpressed in prostate cancer

Human pHyde is not a classical tumor suppressor gene in prostate cancer

Contact Info

Product

Resources

About