Platelet-derived growth factor (PDGF)-signaling mediates radiation-induced apoptosis in human prostate cancer cells with loss of p53 function

Kim, Harold E.; Han, Sunkyu; Kasza, T.; Han, Richard C.; Choi, Hyeong Seon; Palmer, Kenneth C.; Kim, Hyeong Reh C

doi:10.1016/s0360-3016(97)00358-1

Cited by 19 publications

(11 citation statements)

References 22 publications

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“…Platelet‐derived growth factors (PDGF) exist as dimers formed from A and B chains that bind with differing affinities to the PDGFα receptor and the PDGFβ receptor. PDGFs signal through their receptors to elicit a diversity of cellular responses in vitro, including cell proliferation, survival, transformation, and chemotaxis 1220. In vivo, contradictory studies have reported a lack of either form of ligand or receptor in BPH,1221 whereas others have observed limited expression of the PDGF‐β receptor in BPH 1222.…”

Section: 0 Goalsmentioning

confidence: 99%

Human prostate cancer risk factors

Bostwick

Burke

Djakiew

et al. 2004

Cancer

516

359

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Section: 0 Goalsmentioning

confidence: 99%

Human prostate cancer risk factors

Bostwick

Burke

Djakiew

et al. 2004

Cancer

516

359

View full text Add to dashboard Cite

“…Growth factor production by prostate cancer cells is thought to be important in tumor progression [67,68]. PDGF is a major autocrine factor for prostate cancer cells [69,70] and signals a diversity of cellular responses in vitro, including cell proliferation, survival, transformation, and chemotaxis. These genes implicate Egr1 as an important regulator of growth factor and receptor genes in prostate cancer.…”

Section: Does Egr1 Regulate the Epidermal Growth Factor Receptor-ligamentioning

confidence: 99%

Egr1 Transcription Factor: Multiple Roles in Prostate Tumor Cell Growth and Survival

2002

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The transcription factor, Egr1, so-called because it is encoded by the immediate early growth response gene, Egr1, is rapidly induced by growth factors to transduce the proliferative signal. The induction of Egr1 by external stimuli is generally transient but appears to be sustained in some prostate tumor cell lines and tumors, suggesting that Egr1 stimulates tumor cell growth. In contradiction, in breast, lung and brain tumors, Egr1 expression is often absent or reduced and when re-expressed, results in growth suppression. Re-expression of Egr1 in tumor cells also leads to antiapoptotic activity, which would encourage tumor cell survival. Egr1 is also required for, or stimulates, the differentiation of several cell types. Another contradiction is that after stress stimuli to some cell types, Egr1 is required for programmed cell death or apoptosis in both normal and tumor cells. Egr1 also plays a role in tumor progression, through the hypoxic signal generated in growing tumors. Egr1 is highly induced under these conditions and its activities stimulate angiogenesis and improved survival of tumor cells. How this large agenda can be achieved lies in the choice of Egr1 target genes, and varying patterns of coordinated expression have been described, but the mechanisms for this choice are not clear. This review points to areas where research should be focussed.

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“…PDGFs signal through their receptors to elicit a diversity of cellular responses in vitro, including cell proliferation, survival, transformation, and chemotaxis [127]. In vivo, contradictory studies have reported a complete lack of either form of ligand or receptor in BPH [128], while others have observed limited expression of the PDGF␤ receptor in BPH [129].…”

Section: Platelet-derived Growth Factors and Receptorsmentioning

confidence: 99%