Autocrine Motility Factor-Receptor in Human Bladder-Carcinoma - Gene-Expression, Loss of Cell-Contact Regulation and Chromosomal Mapping

Silletti, Steve; Yao, Ji Ping; Sanford, Julie Anne; Mohammed, Abdulmajid; Otto, Tobias; Wolman, Sandra R.; A, Raz

doi:10.3892/ijo.3.5.801

Cited by 12 publications

(16 citation statements)

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“…The results indicated that the AMFR mRNA was expressed differentially in normal and tumor tissues, and this expression was regulated by cell density in normal but not in cancer cells. These ISH data closely correlate with the results obtained from immunofluorescence and Western blot analyses using anti-AMFR (anti-gp78) antibody [12].…”

Section: Introductionsupporting

confidence: 74%

“…Meanwhile, the J82 carcinoma cells maintained a high level of surface gp78 expression even at a cell-cell contact density. Western blot analysis of total cellular gp78 protein content revealed the same expression pattern in these cell types [12]. All these data indicate that firstly the enhanced level of AMF receptor protein is associated with the malignancy of the cells or tissues, and secondly, cell-cell contact markedly down-regulates the expression of AMFR in the normal but not in the carcinoma cells.…”

Section: Discussionsupporting

confidence: 48%

“…For instance, it was shown that enhanced expression of gp78, accompanied by a concomitant decrease in E-cadherin expression, was correlated with higher grade disease, recurrence and incidence of metastasis in invasive and non-invasive clinical human bladder cancer specimens, as revealed by the immunofluorescence staining [13]. Moreover, Silletti et al [12] investigated the regulation and pattern of AMFR protein expression in human bladder cells of different malignant phenotypes, i.e., the normal (FHs738BL), papilloma (RT4) and carcinoma (J82) cells. They found that all the three types of bladder cells expression the gp78 receptor protein at a similar level in subconfluent cultures though the distribution of the protein on cell surface differed among the cell types.…”

Section: Discussionmentioning

confidence: 99%

“…These ISH data are closely consistent with that of the AMFR protein expression detected by immunofluorescence techniques. Furthermore, previous experiments using quantitative Southern blot hybridization demonstrated that all the three different cell phenotypes (i.e., the normal FHs738BL, papilloma RT4 and carcinoma J82) had a roughly equivalent AMFR gene copy number and identical DNA restriction pattern [12]. In addition, a comparison of the complete nucleotide sequences between the AMFR gene from human HT-1080 fibrosarcoma and that from normal human placenta failed to detect any point mutations in the coding region of the gene (data not shown).…”

Section: Discussionmentioning

confidence: 99%

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Differential expression of autocrine motility factor receptor (AMFR) mRNA in normal and cancer cells detected by in situ hybridization

Huangbaiqu

Avrahamraz

1995

Cell Res

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The receptor for autocrine motility factor (AMFR) is known to be involved in the process of AMF-mediated cell migration and metastasis. This paper describes the procedures of non-radioactive in situ hybridization (ISH) detection of AMFR mRNA in both paraffin-embedded surgical sections and cultured cells using either biotinylated oligonucleotide probes or digoxigenin-labeled RNA probes. The results showed that the AMFR mRNA was expressed at an enhanced level in hyperplastic and malignant tissues of breast and prostate cancer patient surgical specimens, indicating that the elevated AMFR expression was associated with the tissue malignancy. Moreover, AMFR mRNA was detected in both normal and carcinoma cells when cultured at a subconfluent density. However, AMFR expression was inhibited in confluent normal (3T3-A31 murine fibroblast and FHs738BL human bladder) cells while it continued to express in carcinoma (J82 human bladder) and metastatic (3T3-M murine fibroblast) cells irrespective of cell density. This suggested a cell-cell contact downregulation of AMFR mRNA expression in normal but not in cancer cells. The ISH data obtained in this study are closely consistent with the AMFR protein expression pattern previously reported, implying that the differential expression of AMFR gene may be regulated and controlled at the transcriptional level. 222In situ hybridization detection of AMFR mRNA

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Section: Introductionsupporting

confidence: 74%

Section: Discussionsupporting

confidence: 48%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

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Differential expression of autocrine motility factor receptor (AMFR) mRNA in normal and cancer cells detected by in situ hybridization

Huangbaiqu

Avrahamraz

1995

Cell Res

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“…Furthermore, it was suggested that retinoic acid-induced differentiation and suppression of invasion of melanoma cells is related, at least in part, to down-regulation of autocrine motility factor receptor expression [40]. The monoclonal antibody against the receptor for AMF (anligp78 mAb) was found to mimic the physiological effect of AMF, and the enhanced motility induced by anti-gp78 mAb was mediated by a pertussis toxin-sensitive G-protein pathway, as has been described for other motility factors [41]. We found a different expression pattern of gp78hAMFR in various bladder cancer cell lines.…”

Section: Cell Adhesionmentioning

confidence: 99%

Parameters of Tumor Progression and Metastases in Bladder Carcinomas

Otto¹,

Goepel²,

Krege³

et al. 1996

Oncol Res Treat

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Histopathological parameters are insufficient predictors for the individual course of disease in bladder cancer patients. In the past decade, however, other criteria have been developed as a possible prognostic aid to a better disease management, such as expression of specific cell surface antigens, DNA content, chromosomal aberrations, cell proliferation, tumor cell-associated antigens, angiogenesis, gene rearrangements, and point mutations. Since most tumors of the bladder are carcinomas and are associated with dedifferentiation and high metastatic capability, we investigated whether reduced expression of so-called differentiation factors in combination with increased cell motility might be correlated with tumor progression.

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Gp78 involvement in cellular proliferation: Can act as a promising modulator for cell cycle regulatory proteins?

Joshi

Upadhyay

Chhangani

et al. 2018

Journal Cellular Physiology

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In cells, protein synthesis and degradation are normal processes, which are tightly regulated by various cellular metabolic pathways. Cellular protein quality control (PQC) mechanisms always present a continuous and rigorous check over all intracellular proteins before they can participate in various cellular physiological processes with the help of PQC pathways like autophagy and ubiquitin proteasome system (UPS). The UPS employs few selective E3 ubiquitin ligases for the intracellular degradation of cyclin-dependent kinase inhibitor 1B (p27 ) that tightly controls cell cycle progression. But, the complex mechanistic interactions and the interplay between E3 ubiquitin ligases involved in the functional regulation as well as expression of p27 are not well known. Here, we demonstrate that cell surface glycoprotein Gp78, a putative E3 ubiquitin ligase, is involved in the stabilization of intracellular steady-state levels of p27. Transient overexpression of Gp78 increases the accumulation of p27 in cells in the form of massive inclusions like structures, which could be due to its cumulative increased stability in cells. We have also monitored how under stress condition, E3 ubiquitin ligase Gp78 regulates endogenous levels of p27 in cells. ER stress treatment generates a marginal increase in Gp78 endogenous levels, and this elevation effect was prominent for intracellular accumulation of p27 in cells. Taken together, our current findings suggest a valuable multifactorial regulatory mechanism and linkage of p27 with UPS pathway.

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Autocrine Motility Factor-Receptor in Human Bladder-Carcinoma - Gene-Expression, Loss of Cell-Contact Regulation and Chromosomal Mapping

Cited by 12 publications

References 0 publications

Differential expression of autocrine motility factor receptor (AMFR) mRNA in normal and cancer cells detected by in situ hybridization

Differential expression of autocrine motility factor receptor (AMFR) mRNA in normal and cancer cells detected by in situ hybridization

Parameters of Tumor Progression and Metastases in Bladder Carcinomas

Gp78 involvement in cellular proliferation: Can act as a promising modulator for cell cycle regulatory proteins?

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