We are analyzing https://link.springer.com/article/10.1007/s00432-004-0581-8.

Title:
Gefitinib (‘IRESSA’, ZD1839) inhibits EGF-induced invasion in prostate cancer cells by suppressing PI3 K/AKT activation | Journal of Cancer Research and Clinical Oncology
Description:
Androgen-independent prostate cancer (AI-PC) is characterized by a higher invasive potential compared to hormone-responsive prostate cancer. A therapeutic option for AI-PC should thus be targeted to suppress not only cell proliferation, but also the invasive ability of the cells. Here, we investigated the effect of the epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor gefitinib (‘IRESSA’, ZD1839) on EGF-stimulated invasion and proliferation in two androgen-independent prostate cancer cell lines PC3 and DU145. In addition, we determined the effect of the compound on EGF-stimulated PI3 K/AKT pathway activation, in view of the key role exerted by this pathway in carcinoma cell invasion. Cell proliferation was determined by thymidine incorporation in the nuclei. Cell cycle analysis was performed by flow cytometry. Invasion through matrigel in vitro was measured by using Boyden chambers. PI3 K activity was measured by immunokinase assay and AKT phosphorylation was evaluated by Western blot analysis. Gefitinib inhibits invasion through matrigel and collagen in response to EGF in both cell lines. In addition, we confirm the inhibitory effect of the compound on basal and EGF-induced cell proliferation. Such an effect was accompanied by accumulation of the cells in the G0/G1 phase of the cell cycle. The effect of the compound is due, as expected, to suppression of EGF-induced autotransphosphorylation of EGFR. In addition, we demonstrate here that gefitinib inhibits EGF-induced activation of PI3 K/AKT pathway in both cell lines. Overall, our results demonstrate that gefitinib is able to suppress invasion and proliferation of AI-PC cells by suppressing EGF-stimulated activation of the PI3 K/AKT pathway and support a possible use of the drug in the treatment of advanced PC to limit not only proliferation but also invasion to other districts.
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Keywords {🔍}

cancer, google, scholar, cas, pubmed, article, cell, prostate, growth, cells, factor, receptor, kinase, invasion, res, human, forti, baldi, proliferation, epidermal, gefitinib, muratori, bonaccorsi, pathway, clin, journal, research, lines, carcinoma, protein, privacy, cookies, content, egfinduced, kakt, activation, androgenindependent, effect, access, signaling, induces, expression, maggi, university, florence, analysis, publish, search, clinical, iressa,

Topics {✒️}

anti-egf receptor therapy month download article/chapter dna-fragmented human sperm egf-induced cell proliferation inhibits egf-induced invasion hormone-responsive prostate cancer mitogen-activated protein kinase platelet-activating factor mediates egf-egfr transduction system suppressing egf-stimulated activation gianni forti & elisabetta baldi related subjects pten/mmac/tep1 expression carcinoma cell invasion human prostate cancer human cell lines protein tyrosine kinase ivermectin suppresses growth prostate cancer invasion growth factor involvement platelet-activating factor hec-1a cells prostate cancer cells egf-stimulated invasion androgen receptor mediates /akt pathway activation kif15 suppresses proliferation full article pdf prostate cancer epidemiology egf-induced autotransphosphorylation privacy choices/manage cookies phosphoinositide 3-kinase pathway targeted alpha6beta4 integrin reduced tumor growth androgen receptor expression promotes enhanced motility colonic cancer cells constitutively active akt tumor-induced angiogenesis egf-stimulated pi3 pten induces chemosensitivity pten/mmac1/tep ai-pc cells cell cycle analysis enhanced androgen responsiveness target-based agents induces g1 arrest european economic area clinical oncology aims

Questions {❓}

Baldi E, Bonaccorsi L, Forti G (2003) Androgen receptor: good guy or bad guy in prostate cancer invasion?

Schema {🗺️}

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         description: Androgen-independent prostate cancer (AI-PC) is characterized by a higher invasive potential compared to hormone-responsive prostate cancer. A therapeutic option for AI-PC should thus be targeted to suppress not only cell proliferation, but also the invasive ability of the cells. Here, we investigated the effect of the epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor gefitinib (‘IRESSA’, ZD1839) on EGF-stimulated invasion and proliferation in two androgen-independent prostate cancer cell lines PC3 and DU145. In addition, we determined the effect of the compound on EGF-stimulated PI3 K/AKT pathway activation, in view of the key role exerted by this pathway in carcinoma cell invasion. Cell proliferation was determined by thymidine incorporation in the nuclei. Cell cycle analysis was performed by flow cytometry. Invasion through matrigel in vitro was measured by using Boyden chambers. PI3 K activity was measured by immunokinase assay and AKT phosphorylation was evaluated by Western blot analysis. Gefitinib inhibits invasion through matrigel and collagen in response to EGF in both cell lines. In addition, we confirm the inhibitory effect of the compound on basal and EGF-induced cell proliferation. Such an effect was accompanied by accumulation of the cells in the G0/G1 phase of the cell cycle. The effect of the compound is due, as expected, to suppression of EGF-induced autotransphosphorylation of EGFR. In addition, we demonstrate here that gefitinib inhibits EGF-induced activation of PI3 K/AKT pathway in both cell lines. Overall, our results demonstrate that gefitinib is able to suppress invasion and proliferation of AI-PC cells by suppressing EGF-stimulated activation of the PI3 K/AKT pathway and support a possible use of the drug in the treatment of advanced PC to limit not only proliferation but also invasion to other districts.
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