We are analyzing https://link.springer.com/article/10.1007/s00240-002-0282-1.

Title:
Rapamycin induces Smad activity in prostate cancer cell lines | Urolithiasis
Description:
Rapamycin inhibits the FK506-binding protein 12 (FKBP12)/mammalian target of rapamycin (mTOR) complex and causes cell cycle arrest in G1. The precise mechanism of growth inhibition by rapamycin is only partly understood. Rapamycin led to growth inhibition in the human prostate cancer cell lines LNCaP and PC3 cells after 72 h, ID50: 93 and 50 nM, respectively. Filter cDNA array analysis showed down-regulation by more than 0.75× by rapamycin in PC3 cells and LNCaP cells of the following genes: follistatin, eukaryotic initiation factor-4E (eIF4E), glucose-6-phosphate dehydrogenase (GAPDH), lactate dehydrogenase (LDH)-A, ATP synthase, heat shock protein (HSP)-1. Upregulation by more than 1.5× was found for: bone morphogenetic protein (BMP)-4, FKBP12, carcinoma embryonic antigen (CEA) precursor, eukaryotic initiation factor (eIF)-3 p36 subunit, latent transforming growth factor (TGF) beta binding protein (LTBP)1. Rapamycin induced BMP4 and reduced follistatin expression in PC3 cells. This resulted in a dose-dependent nuclear expression of Smad4 and activated the SBE4 Smad-reporter, indicating activation of TGFbeta/BMP signaling. Combining rapamycin with PI3K inhibition (LY294002) increased growth inhibition. These findings illustrate that Smad signaling plays a role in the anticancer effects of rapamycin and show that combination with PI3K inhibition improves growth inhibition.
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Keywords {🔍}

article, rapamycin, cancer, growth, inhibition, privacy, cookies, content, research, smad, prostate, cell, protein, access, information, publish, search, van, cells, factor, analysis, data, log, journal, lines, poel, hanrahan, zhong, follistatin, discover, signalling, department, oncology, usa, springer, optional, personal, parties, policy, find, track, urological, induces, activity, cite, simons, explore, target, mtor, mechanism,

Topics {✒️}

month download article/chapter eukaryotic initiation factor-4e bone morphogenetic protein winship cancer institute dose-dependent nuclear expression rapamycin induced bmp4 eukaryotic initiation factor increased growth inhibition full article pdf van der poel reduced follistatin expression privacy choices/manage cookies sbe4 smad-reporter smad signaling plays cell cycle arrest fk506-binding protein 12 heat shock protein beta binding protein related subjects growth inhibition european economic area scope submit manuscript carcinoma embryonic antigen inhibiting smad3 phosphorylation tak1 promotes emt conditions privacy policy glucose-6-phosphate dehydrogenase accepting optional cookies tgfbeta/bmp signaling article log main content log journal finder publish usage analysis article cite pi3k inhibition information check access instant access lncap cells tgf privacy policy personal data books a rapamycin inhibits rapamycin led combining rapamycin optional cookies manage preferences follistatin data protection

Schema {🗺️}

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         headline:Rapamycin induces Smad activity in prostate cancer cell lines
         description: Rapamycin inhibits the FK506-binding protein 12 (FKBP12)/mammalian target of rapamycin (mTOR) complex and causes cell cycle arrest in G1. The precise mechanism of growth inhibition by rapamycin is only partly understood. Rapamycin led to growth inhibition in the human prostate cancer cell lines LNCaP and PC3 cells after 72 h, ID50: 93 and 50 nM, respectively. Filter cDNA array analysis showed down-regulation by more than 0.75× by rapamycin in PC3 cells and LNCaP cells of the following genes: follistatin, eukaryotic initiation factor-4E (eIF4E), glucose-6-phosphate dehydrogenase (GAPDH), lactate dehydrogenase (LDH)-A, ATP synthase, heat shock protein (HSP)-1. Upregulation by more than 1.5× was found for: bone morphogenetic protein (BMP)-4, FKBP12, carcinoma embryonic antigen (CEA) precursor, eukaryotic initiation factor (eIF)-3 p36 subunit, latent transforming growth factor (TGF) beta binding protein (LTBP)1. Rapamycin induced BMP4 and reduced follistatin expression in PC3 cells. This resulted in a dose-dependent nuclear expression of Smad4 and activated the SBE4 Smad-reporter, indicating activation of TGFbeta/BMP signaling. Combining rapamycin with PI3K inhibition (LY294002) increased growth inhibition. These findings illustrate that Smad signaling plays a role in the anticancer effects of rapamycin and show that combination with PI3K inhibition improves growth inhibition.
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            Urology
            Nephrology
            Medical Biochemistry
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      headline:Rapamycin induces Smad activity in prostate cancer cell lines
      description: Rapamycin inhibits the FK506-binding protein 12 (FKBP12)/mammalian target of rapamycin (mTOR) complex and causes cell cycle arrest in G1. The precise mechanism of growth inhibition by rapamycin is only partly understood. Rapamycin led to growth inhibition in the human prostate cancer cell lines LNCaP and PC3 cells after 72 h, ID50: 93 and 50 nM, respectively. Filter cDNA array analysis showed down-regulation by more than 0.75× by rapamycin in PC3 cells and LNCaP cells of the following genes: follistatin, eukaryotic initiation factor-4E (eIF4E), glucose-6-phosphate dehydrogenase (GAPDH), lactate dehydrogenase (LDH)-A, ATP synthase, heat shock protein (HSP)-1. Upregulation by more than 1.5× was found for: bone morphogenetic protein (BMP)-4, FKBP12, carcinoma embryonic antigen (CEA) precursor, eukaryotic initiation factor (eIF)-3 p36 subunit, latent transforming growth factor (TGF) beta binding protein (LTBP)1. Rapamycin induced BMP4 and reduced follistatin expression in PC3 cells. This resulted in a dose-dependent nuclear expression of Smad4 and activated the SBE4 Smad-reporter, indicating activation of TGFbeta/BMP signaling. Combining rapamycin with PI3K inhibition (LY294002) increased growth inhibition. These findings illustrate that Smad signaling plays a role in the anticancer effects of rapamycin and show that combination with PI3K inhibition improves growth inhibition.
      datePublished:
      dateModified:
      pageStart:380
      pageEnd:386
      sameAs:https://doi.org/10.1007/s00240-002-0282-1
      keywords:
         Bone morphogenetic protein Follistatin Rapamycin Prostate cancer Transforming growth factor (TGF) Mammalian target of rapamycin (mTOR)
         Urology
         Nephrology
         Medical Biochemistry
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