Expression of a human cell adhesion molecule, MUC18, in prostate cancer cell lines and tissues

Wu, Guang-Jer; Varma, Vijay; Wu, Mei-Whey H.; Wang, Shur-Wern; Qu, Pengpeng; Yang, Hanfang; Petros, John A.; Lim, So Dug; Amin, Mahul B.

doi:10.1002/pros.1111

Cited by 59 publications

(89 citation statements)

References 28 publications

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“…35 We chose to use RNAi for a portion of the CD44v9 exon, since v7-v10 exons are usually expressed together, 25 as well as for another cell adhesion protein, Muc18. According to previous work, expression of Muc18 by prostate cancer cell lines 26,27 correlates with invasiveness and with in vivo metastasis in nude mice. 26 Muc18 interference gave a modest but significant decrease in invasion, consistent with this work.…”

Section: Discussionmentioning

confidence: 75%

“…30 Others have studied Muc18 in PC in some depth. Expression of Muc18 by prostate cancer cell lines 26,27 correlated with invasiveness and with in vivo metastasis in nude mice. 26 Also, Muc18 immunohistochemical expression was increased in prostate cancer acini and their precursor lesion, prostatic intraepithelial neoplasia (PIN), in 37 cases.…”

mentioning

confidence: 95%

“…Most other cell adhesion molecules are downregulated or unchanged in PC. The exceptions are increased expression of Muc18 (CD146, or MelCAM), 26,27 N-cadherin and cadherin-11, although expression was consistently seen only in the highest Gleason score cancer, 28 and d-catenin. 29 Muc18 was originally found to be overexpressed on the surface of melanoma cells where it mediates their metastasis.…”

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confidence: 99%

“…26 Also, Muc18 immunohistochemical expression was increased in prostate cancer acini and their precursor lesion, prostatic intraepithelial neoplasia (PIN), in 37 cases. 27 Thus, we chose to study the effect of expression and silencing of Muc18.…”

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confidence: 99%

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Prostate cancer invasion is influenced more by expression of a CD44 isoform including variant 9 than by Muc18

Omara-Opyene

Qiu

Shah

et al. 2004

Laboratory Investigation

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The standard form of cell adhesion glycoprotein CD44 is a metastasis suppressor in prostate cancer. However, we previously showed by RT-PCR and Western blotting that cancer overexpresses unique CD44 variant v7-v10 isoforms. Muc18 is another cell adhesion marker reportedly overexpressed by prostate cancer. Matched frozen section-confirmed tumor and benign tissues were harvested from 10 prostatectomy specimens and tumor was microdissected from two lymph node metastases. Tissues were homogenized for RNA preparations, and RT-PCR was performed for the CD44v7-v10 sequence. In cultured prostate cancer cells, we caused RNA interference against CD44v9 and/or Muc18. We used PC3M cells and a derivative cell line called G s a, that constitutively expresses this G-protein and is more invasive. Lipofection was performed for a green fluorescent protein plasmid and for two 22-mer DNA fragments, cloned into a plasmid expression vector to generate hairpin, interfering dsRNA. Assays for invasion into Matrigel, a basement membrane matrix, were performed in 4-5 experiments. RT-PCR demonstrated expression of a 608 bp band representing CD44v7-v10 or a 638 bp band of Prostate cancer remains a public health problem of enormous magnitude; it is the second most common cause of cancer fatality among North American men and the most common in Great Britain. Only a minority of all cases invade locally and metastasize, thus requiring altered expression of cell adhesion molecules to allow tumor cell detachment, migration through a stromal matrix, and lymphovascular invasion.CD44, a family of transmembrane glycoproteins involved in homotypic cell, cell-matrix, and cellcytoskeletal interaction, holds promise as a prostate tumor marker. The extracellular domain of CD44 binds numerous matrix substituents: hyaluronic acid, heparin-affinity growth factors, vascular endothelial growth factor, p185 HER2 , epidermal growth factor, and hepatocyte growth factor. Its intracellular domain binds to ezrin, radixin, moesin and merlin, which interact with the cytoskeleton; notably, neutral endopeptidase 24.11 competes with CD44 for this interaction. 1 CD44 also binds directly to the cytoskeletal substituent ankyrin, thus determining cell and tissue architectural form. 2 CD44 is an oncodevelopmental protein, with roles in

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Section: Discussionmentioning

confidence: 75%

mentioning

confidence: 95%

mentioning

confidence: 99%

mentioning

confidence: 99%

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Prostate cancer invasion is influenced more by expression of a CD44 isoform including variant 9 than by Muc18

Omara-Opyene

Qiu

Shah

et al. 2004

Laboratory Investigation

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“…Hypermethylation of the promoter sequence of the gene is responsible at least in part for lower expression in cancer cells. In contrast to high expression of the invasion suppressor, prostasin, in normal cells, MUC18, a cell adhesion molecule associated with metastatic ability, is expressed at low levels in normal prostatic cell cultures but at high levels in several prostate cancer cell lines (Wu et al 2001).…”

Section: Adhesion Migration and Invasionmentioning

confidence: 92%

Primary cell cultures as models of prostate cancer development

Peehl¹

2005

Endocr Relat Cancer

152

142

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This review focuses on primary cultures of human prostatic epithelial cells and their applications as models of normal and malignant biological behavior. Current abilities to culture cells from normal tissues, from premalignant dysplastic lesions (prostatic intraepithelial neoplasia), from primary adenocarcinomas, and from metastases are described. Evidence for representation of the interrelated cells of the normal prostatic epithelium -stem cells, basal epithelial cells, secretory epithelial cells, transit amplifying cells and neuroendocrine cells -in primary cultures is presented. Comparisons between normal and cancer-derived primary cultures are made regarding biological activities relevant to carcinogenesis, such as proliferation, apoptosis, differentiation, senescence, adhesion, migration, invasion, steroid hormone metabolism, other metabolic pathways and angiogenesis. Analyses of tumor suppressor activity, differential gene expression and cytogenetics in primary cultures have revealed changes relevant to prostate cancer progression. Preclinical studies with primary cultures have provided information useful for designing new strategies for chemoprevention, chemotherapy, cytotoxin therapy, radiation therapy, gene therapy and imaging. While the behavior of normal primary cultures is often used as a basis for comparison with established, immortal prostate cancer cell lines, the most informative studies are performed with donor-matched pairs of normal and malignant primary cultures, grown under identical conditions. Challenges that remain to be addressed if the full potential of primary cultures as a model system is to be realized include isolation, culture and characterization of stem cells, improved methodology to induce or maintain a fully differentiated, androgen-responsive phenotype, and identification of cell surface antigens or other markers with which to purify pure populations of live cancer or premalignant cells apart from non-malignant epithelial cells prior to culture.

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M‐CAM expression as marker of poor prognosis in epithelial ovarian cancer

Aldovini

Demichelis²,

Doglioni³

et al. 2006

Intl Journal of Cancer

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Currently available clinico–pathologic criteria provide an imperfect assessment of outcome for patients with advanced epithelial ovarian cancer (EOC). Identification of prognostic factors related to tumor biology might improve this assessment. We investigated the prognostic significance of the melanoma cell adhesion molecule (M‐CAM) in EOC. Using the same antibody, M‐CAM expression was tested by Western blotting in protein extracts and by immunohistochemestry in tissue microarrays generated from 133 consecutively resected, well characterized EOC samples. Fisher test, Kaplan–Meier method and Cox proportional hazards analysis were used to relate M‐CAM expression to clinico–pathological variables and to time to progression (TTP) and overall survival (OS). In vitro biochemical analysis showed a progressively increased M‐CAM expression from normal to malignant cells. M‐CAM protein, detected immunohistochemically, was significantly associated with advanced tumor stage, serous and undifferentiated histotype, extent of residual disease and p53 accumulation. Presence or absence of M‐CAM significantly divided patients according to their TTP (median, 22 vs. 79 months, respectively; log‐rank p = 0.001) and OS (median, 42 vs. 131 months, respectively; log‐rank p = 0.0003). In the subgroup of advanced stage patients who achieved complete response after front‐line treatment, M‐CAM expression and absence of residual disease were significantly associated with shorter TTP (p = 0.003, HR 5.25, 95% Cl 1.79–15.41 and p = 0.011, HR 3.77, 95% Cl 1.36–10.49 respectively) at the multivariate level. In the same sub‐group of patients, M‐CAM expression remained the only parameter significantly associated with OS (p = 0.005, HR 3.35, 95% Cl 1.42–6.88). M‐CAM is a marker of early relapse and poorer outcome in EOC. In particular, M‐CAM expression identifies a subgroup of front‐line therapy‐responding patients who undergo dramatic relapses, thus helping to better select patients who might benefit from new/alternative therapeutic modalities. © 2006 Wiley‐Liss, Inc.

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Expression of a human cell adhesion molecule, MUC18, in prostate cancer cell lines and tissues

Cited by 59 publications

References 28 publications

Prostate cancer invasion is influenced more by expression of a CD44 isoform including variant 9 than by Muc18

Prostate cancer invasion is influenced more by expression of a CD44 isoform including variant 9 than by Muc18

Primary cell cultures as models of prostate cancer development

M‐CAM expression as marker of poor prognosis in epithelial ovarian cancer

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