The ?6?1 and ?6?4 integrins in human prostate cancer progression

Cress, Anne E.; Rabinovitz, Isaac; Zhu, Weiguo; Nagle, Ray B.

doi:10.1007/bf00690293

Cited by 181 publications

(170 citation statements)

References 51 publications

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“…Loss of the 6 4 integrin may give a less-stable attachment to the ECM, while the continued expression of the 6 1 integrin may provide enough attachment for the cells to become mobile. This may also explain why prostate cancer cells favor to move along laminin-5 coated nerves (Cress et al 1995).…”

Section: Integrinsmentioning

confidence: 99%

New experimental markers for early detection of high-risk prostate cancer: role of cell–cell adhesion and cell migration

Mól

Geldof

Meijer

et al. 2007

J Cancer Res Clin Oncol

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Today's treatment and diagnosis of prostate cancer still exhibit major limitations. The search for new and additional prognostic markers is therefore still an actual Weld of interest. Potential markers involved in numerous biological processes in the tumor cell have been investigated intensively. For therapeutic interventions it is important to distinguish between harmless and aggressive disease in an early stage. Therefore the subject of this review is limited to markers associated with those functional processes, which discriminate early stage aggressive, metastatic cancer from harmless disease. Important processes in this respect are: altered cell adhesion and cellular migration. E-cadherin, N-cadherin, -catenin, integrins, focal adhesion kinase, connexins and matrix metalloproteinases all appear promising biological markers associated with the early stage metastatic process in prostate cancer. Here we discuss their potential to become valid biological markers based on literature data. Thus far, none of these markers proved to be a valid individual marker by itself due to prostate cancer heterogeneity and transient expression. Analyzing a combination of the potential markers discussed in this review is expected to be a better approach toward discriminating high-from low-risk tumors in an early stage of prostate cancer.

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Section: Integrinsmentioning

confidence: 99%

New experimental markers for early detection of high-risk prostate cancer: role of cell–cell adhesion and cell migration

Mól

Geldof

Meijer

et al. 2007

J Cancer Res Clin Oncol

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“…Changes in several adhesion and motility associated proteins have been identified. Differential expression of transmembrane integrin receptor subtypes, in prostate cancer as compared to normal prostate, has been reported by a number of investigators (Cress et al, 1995;Fornaro et al, 1996Fornaro et al, , 1999Meredith et al, 1995;Nagle et al, 1994). Integrins are transmembrane proteins, which form heterodimers of a and b subunits, thus forming unique receptors which bind specific extracellular matrix proteins (Giancotti and Ruoslahti, 1999;Yamada, 1997).…”

Section: Introductionmentioning

confidence: 98%

Over expression of endoglin in human prostate cancer suppresses cell detachment, migration and invasion

et al. 2002

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The regulation of cell adhesion and motility in human prostate is not well understood. We have previously shown that the endoglin gene is differently expressed during changes in prostate cell adhesion. Endoglin is a transmembrane transforming growth factor b binding protein typically expressed by endothelial cells. In this report we demonstrate that endoglin over expression increases prostate cell attachment, while decreasing migration and invasion. Engineered decreases in endoglin expression have opposite effects. While endoglin exerted only relatively small effects upon cell adhesion, large effects upon cell migration and invasion were observed. Endoglin was shown to localize to focal adhesion plaques, consistent with its role in regulating cell adhesion and motility. Loss of endoglin expression in cancer, as compared to normal prostate, was seen in human prostate cell lines. Suppression of endoglin expression in a panel of normal human prostate cell lines led to cell detachment. Endoglin is identified as a regulator of cell adhesion, motility and invasion in human prostate. Loss of endoglin expression appears to be associated with prostate cancer progression, at least in vitro.

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“…Limited understanding is available concerning the development and progression of prostate cancer despite its prevalence. Neoplastic changes are first apparent in prostatic intraepithelial neoplasia (PIN) and it is thought that PIN may be a precursor to prostate cancer [3][4][5][6][7][8][9]. PIN lesions are characterized by an attenuated basal lamina, enlarged nuclei, and an increased number of luminal type cells.…”

Section: Introductionmentioning

confidence: 99%

“…Laminin 5 is downregulated or lost in several squamous and epithelial carcinomas including the prostate [10,[21][22][23][24]. In our previous studies, we have found that the loss of laminin 5 and the α6β4 integrin (laminin receptor) was a characteristic feature accompanying the transition of normal prostate epithelial glands to PIN lesions to invasive prostate cancer [4,6,7].…”

Section: Introductionmentioning

confidence: 99%

Integrin‐dependent amplification of the G2 arrest induced by ionizing radiation

2005

Self Cite

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The progressive loss of laminin 5 and the α6β4 integrin is a characteristic of the transition of prostatic intraepithelial neoplasia (PIN) to invasive human prostate cancer. Our objective was to determine if the loss of the interaction with laminin 5 would influence the ability of human epithelial cells to respond to DNA damage. Three cellular damage responses to ionizing radiation (IR) were analyzed including G2 progression, cdc2 phosphorylation, and cell survival. The adhesion of normal human prostate epithelial cells to laminin 5 amplified the G2 arrest induced by IR, and depends on a known cell binding domain of laminin 5. The alteration of G2 arrest was confirmed by an inhibition of phospho-cdc2 nuclear translocation. In contrast, a prostate epithelial cancer cell line blocked in G2 independent of adhesion to laminin 5. The survival of these cell lines in response to IR was unaffected by adhesion to laminin 5. These results suggest that cell adhesion to laminin 5 in normal cells will amplify the IR induced G2 cell cycle progression block without altering cell survival. The loss of laminin 5 and the α6β4 integrin in PIN lesions may contribute to the selection and progression of genetically unstable cell types via attenuation of a DNA damage induced G2 arrest.

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The ?6?1 and ?6?4 integrins in human prostate cancer progression

Cited by 181 publications

References 51 publications

New experimental markers for early detection of high-risk prostate cancer: role of cell–cell adhesion and cell migration

New experimental markers for early detection of high-risk prostate cancer: role of cell–cell adhesion and cell migration

Over expression of endoglin in human prostate cancer suppresses cell detachment, migration and invasion

Integrin‐dependent amplification of the G2 arrest induced by ionizing radiation

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