2003
DOI: 10.1002/ijc.11171
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Synergistic antiproliferative and apoptotic effects induced by epidermal growth factor receptor and protein kinase a inhibitors in human prostatic cancer cell lines

Abstract: Our results revealed that the blockade of epidermal growth factor receptor (EGFR) tyrosine kinase and protein kinase A (PKA) signaling pathways by specific inhibitors (PD153035 and Rp-cAMPs) leads to a synergistic inhibition of EGF-and serum-stimulated growth of human prostatic cancer cells (LNCaP, DU145 and PC3) concomitant with an arrest in the G1 phase of cellular cycle. Of particular interest, the combination of PD153035 and Rp-cAMPs also caused a more substantial apoptotic/necrotic death of these prostati… Show more

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Cited by 28 publications
(34 citation statements)
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“…1a, 2a and 3a). This is consistent with other reports (32,(36)(37)(38)(39). We also found that EGF treatments inhibited the DU145 prostate cell line in vitro (Figs.…”
Section: Discussionsupporting
confidence: 94%
See 1 more Smart Citation
“…1a, 2a and 3a). This is consistent with other reports (32,(36)(37)(38)(39). We also found that EGF treatments inhibited the DU145 prostate cell line in vitro (Figs.…”
Section: Discussionsupporting
confidence: 94%
“…Our data are in line with other reports. For example, aromatic quinozoline molecules ZD1839 and PD153035 and specific tyrosine kinase inhibitors (36), have been found to have the mainly cytostatic effects on the LNCaP, DU145 and PC3 prostate cancer cells via G1 arrest with some mild apoptotic effects (32,(37)(38)(39).…”
Section: Discussionmentioning
confidence: 99%
“…During carcinogenesis, activation of pathways that drive proliferation can render cells resistant to apoptosis (28). To determine whether the rate of proliferation of primary prostate cells might influence the incidence of apoptosis in these cell lines, their relative rates of growth were measured by MTT assay.…”
Section: Acquisition and Characterization Of Prostatetissuementioning
confidence: 99%
“…27,29,[31][32][33]35,36 It has also been reported that the blockade of either HH or EGF-EGFR signaling, by using a selective SMO or EGFR inhibitor, such as cyclopamine and gefitinib (also known as Iressa or ZD1839), respectively, leads to the growth inhibition and apoptotic death of many cancer cell types, including prostate tumor epithelial cells in vivo and in vitro. 17,21,33,35,[37][38][39][40][41] In addition, our previous work has also revealed that the combined use of low concentrations of EGFR inhibitor with the protein kinase A inhibitor (Rp-cAMPs) or sodium nitroprusside resulted in the growth arrest and a more substantial rate of PC cell death as compared to the drugs alone. 39,40 The present investigation was undertaken to determine whether the simultaneous blockade of SHH-GLI-1 and EGF-EGFR pathways might effectively counteract the PC cell growth and survival induced by different growth factors than single agents.…”
mentioning
confidence: 99%
“…17,21,33,35,[37][38][39][40][41] In addition, our previous work has also revealed that the combined use of low concentrations of EGFR inhibitor with the protein kinase A inhibitor (Rp-cAMPs) or sodium nitroprusside resulted in the growth arrest and a more substantial rate of PC cell death as compared to the drugs alone. 39,40 The present investigation was undertaken to determine whether the simultaneous blockade of SHH-GLI-1 and EGF-EGFR pathways might effectively counteract the PC cell growth and survival induced by different growth factors than single agents. Therefore, the antiproliferative and cytotoxic effects induced by cyclopamine, alone or in combination with selective EGFR inhibitor gefitinib, were estimated on the androgen-responsive LNCaP-C33 and LNCaP-LN3 and androgen-independent LNCaP-C81, DU145 and PC3 PC lines in serum-free medium and stimulated by SHHNp, EGF and serum.…”
mentioning
confidence: 99%