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Literature summary for 3.4.24.86 extracted from

  • Lin, P.; Sun, X.; Feng, T.; Zou, H.; Jiang, Y.; Liu, Z.; Zhao, D.; Yu, X.
    ADAM17 regulates prostate cancer cell proliferation through mediating cell cycle progression by EGFR/PI3K/AKT pathway (2012), Mol. Cell. Biochem., 359, 235-243.
    View publication on PubMed
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Application

Application Comment Organism
medicine ectopic over-expression of ADAM17 results in increased cell proliferation. ADAM17 promotes G1 to S phase transition concomitantly with upregulation of cyclin E, CDK2 and downregulation of p21 and p27 proteins. ADAM17 over-expression cells show more TGF-alpha released to the supernatant and activate the EGFR/PI3K/AKT pathway. Silencing ADAM17 leads to the opposite effect. Both siRNAs knockdown of ADAM17 and blocking the EGFR/PI3K/AKT pathway cause downregulation of cyclin E,CDK2,and upregulation of p21 and p27 in prostate cancer cells Homo sapiens

Organism

Organism UniProt Comment Textmining
Homo sapiens P78536
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Source Tissue

Source Tissue Comment Organism Textmining
DU-145 cell
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 Homo sapiens
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PC-3 cell
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 Homo sapiens
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placenta
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 Homo sapiens
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General Information

General Information Comment Organism
physiological function ectopic over-expression of ADAM17 results in increased cell proliferation. ADAM17 promotes G1 to S phase transition concomitantly with upregulation of cyclin E, CDK2 and downregulation of p21 and p27 proteins. ADAM17 over-expression cells show more TGF-alpha released to the supernatant and activate the EGFR/PI3K/AKT pathway. Silencing ADAM17 leads to the opposite effect. Both siRNAs knockdown of ADAM17 and blocking the EGFR/PI3K/AKT pathway cause downregulation of cyclin E,CDK2,and upregulation of p21 and p27 in prostate cancer cells Homo sapiens