Cellular expression of beta-microseminoprotein (β-MSP) mRNA and its protein in untreated prostate cancer

Tsurusaki, Toshifumi; Koji, Takehiko; Sakai, Hideki; Kanetake, Hiroshi; Nakane, Paul K.; Saito, Yutaka

doi:10.1002/(sici)1097-0045(19980501)35:2<109::aid-pros4>3.0.co;2-e

Cited by 42 publications

(22 citation statements)

References 27 publications

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“…For ISH, cells were seeded into wells of 8-well Lab-Tek chamber glass slides (Nalge Nunc International, Naperville, IL, USA) and cultured overnight. ISH of these cells was performed according to the method described previously (Koji et al, 1996;Tsurusaki et al, 1998). Briefly, cells grown on glass slides were sequentially incubated with 0.2 N HCl for 20 min, 0.2% Triton X-100 in phosphate-buffered saline (PBS) for 10 min, and 2 µg ml -1 proteinase K at 37°C for 20 min.…”

Section: Ish For Cultured Cellsmentioning

confidence: 99%

“…The cells were washed with 50% formamide in 2 × SSC for 5 h followed by washing with PBS, and were then incubated with anti-T-T dimer monoclonal antibody followed by the incubation with peroxidase-conjugated antimouse IgG. Peroxidase bound to tissue sections was visualized as described previously (Koji et al, 1996;Tsurusaki et al, 1998). Hybridization signals were considered positive when accumulated black deposits were seen in individual cells.…”

Section: Ish For Cultured Cellsmentioning

confidence: 99%

“…To evaluate the specificity of VEGF-C mRNA signals, a panel of control experiments were conducted on sections adjacent to the malignant area (Koji et al, 1996;Tsurusaki et al, 1998). A number of consecutive tissue sections were hybridized with T-T dimerized oligo-DNA complementary to 28S rRNA as a positive control (Yoshii et al, 1995) and also T-T dimerized VEGF-C sense oligo-DNA as a negative control in every run.…”

Section: Control Experiments For Ishmentioning

confidence: 99%

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Vascular endothelial growth factor-C expression in human prostatic carcinoma and its relationship to lymph node metastasis

et al. 1999

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Lymph node dissemination is a major prognostic factor in human cancer. However, the molecular mechanisms underlying lymph node metastasis are poorly understood. Recently, vascular endothelial growth factor-C (VEGF-C) was identified as a ligand for VEGF receptor-3 (VEGFR-3/Flt-4) and the expression of VEGFR-3 was found to be highly restricted to the lymphatic endothelial cells. In this report, we investigated the expression of VEGF-C and VEGFR-3 in human prostatic carcinoma tissue by using in situ hybridization and immunohistochemical staining respectively. Expression of VEGF-C mRNA in prostatic carcinoma was significantly higher in lymph node-positive group than in lymph node-negative group. In addition, the number of VEGFR-3-positive vessels was increased in stroma surrounding VEGF-C-positive prostatic carcinoma cells. These results suggest that the expression of VEGF-C in prostatic carcinoma cells is implicated in the lymph node metastasis. © 1999 Cancer Research Campaign

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Section: Ish For Cultured Cellsmentioning

confidence: 99%

Section: Ish For Cultured Cellsmentioning

confidence: 99%

Section: Control Experiments For Ishmentioning

confidence: 99%

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Vascular endothelial growth factor-C expression in human prostatic carcinoma and its relationship to lymph node metastasis

et al. 1999

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“…It has been reported that MSMB mRNA and protein expression is reduced in malignant prostatic epithelia compared with benign epithelia. 5 In prostate cancer, the MSMB gene may be subjected to transcriptional silencing by methylation, mediated by enhancer of zeste homologue-2 (EZH2), a Polycomb group member which is often overexpressed in castration-resistant prostate cancer (CRPC). 6,7 MSMB expression has been reported by several groups to be negatively associated with disease-free survival 8 and outcome.…”

Section: Introductionmentioning

confidence: 99%

Effect of androgen deprivation therapy on the expression of prostate cancer biomarkers MSMB and MSMB-binding protein CRISP3

Dahlman

Edsjö

Halldén

et al. 2010

Prostate Cancer Prostatic Dis

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We have investigated the effects of short-term neoadjuvant and long-term androgen deprivation therapies (ADTs) on b-microseminoprotein (MSMB) and cysteine-rich secretory protein-3 (CRISP3) expression in prostate cancer patients. We also studied if MSMB expression was related to genotype and epigenetic silencing. Using an Affymetrix cDNA microarray analysis, we investigated the expression of MSMB, CRISP3, androgen receptor (AR), KLK3 and Enhancer of Zeste Homologue-2 (EZH2) in tissue from prostate cancer patients receiving (n ¼ 17) or not receiving (n ¼ 23) ADT before radical prostatectomy. MSMB, CRISP3 and AR were studied in tissue from the same patients undergoing TURP before and during ADT (n ¼ 16). MSMB genotyping of these patients was performed by TaqMan PCR. MSMB and KLK3 expression levels decreased during ADT. Expression levels of AR and CRISP3 were not affected by short-term ADT but were high in castration-resistant prostate cancer (CRPC) and metastases. Levels of EZH2 were also high in metastases, where MSMB was low. Genotyping of the MSMB rs10993994 polymorphism showed that the TT genotype conveys poor MSMB expression. MSMB expression is influenced by androgens, but also by genotype and epigenetic silencing. AR and CRISP3 expression are not influenced by short-term ADT, and high levels were found in CRPC and metastases.

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“…It suppresses the growth of human prostate cells, 28 and is high in normal prostate epithelial cells, decreased in prostate cancer. 29,30 The second is hepsin which is a cell surface serine protease. Hepsin expression promotes prostate cancer metastasis, 31 and is high in prostate cancer as compared to normal prostate epithelial cells.…”

Section: Gene Profiling Of Prostate Epithelial Cells Isolated From Inmentioning

confidence: 99%

Characterization of a method for profiling gene expression in cells recovered from intact human prostate tissue using RNA linear amplification

Ding

Xu²,

Chen³

et al. 2006

Prostate Cancer Prostatic Dis

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Coupling array technology to laser capture microdissection (LCM) has the potential to yield gene expression profiles of specific cell populations within tissue. However, remaining problems with linear amplification preclude accurate expression profiling when using the low nanogram amounts of RNA recovered after LCM of human tissue. We describe a novel robust method to reliably amplify RNA after LCM, allowing direct probing of 12K gene arrays. The fidelity of amplification was demonstrated by comparing the ability of amplified RNA (aRNA) versus that of native RNA to identify differentially expressed genes between two different cell lines, demonstrating a 99.3% concordance between observations. Array findings were validated by quantitative polymerase chain reaction analysis of a randomly selected subset of 32 genes. Using LCM to recover normal (N ¼ 5 subjects) or cancer (N ¼ 3) cell populations from intact human prostate tissue, three differentially expressed genes were identified. Independent investigators have previously identified differential expression of two of these three genes, hepsin and beta-microseminoprotein, in prostate cancer. Taken together, the current study demonstrates that accurate gene expression profiling can readily be performed on specific cell populations present within complex tissue. It also demonstrates that this approach efficiently identifies biologically relevant genes.

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Cellular expression of beta-microseminoprotein (β-MSP) mRNA and its protein in untreated prostate cancer

Cited by 42 publications

References 27 publications

Vascular endothelial growth factor-C expression in human prostatic carcinoma and its relationship to lymph node metastasis

Vascular endothelial growth factor-C expression in human prostatic carcinoma and its relationship to lymph node metastasis

Effect of androgen deprivation therapy on the expression of prostate cancer biomarkers MSMB and MSMB-binding protein CRISP3

Characterization of a method for profiling gene expression in cells recovered from intact human prostate tissue using RNA linear amplification

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