2005
DOI: 10.1158/0008-5472.can-05-0058
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Inhibition of the Phosphatidylinositol 3-Kinase/Akt/Mammalian Target of Rapamycin Pathway but not the MEK/ERK Pathway Attenuates Laminin-Mediated Small Cell Lung Cancer Cellular Survival and Resistance to Imatinib Mesylate or Chemotherapy

Abstract: The fact that small cell lung cancer (SCLC) is commonly incurable despite being initially responsive to chemotherapy, combined with disappointing results from a recent SCLC clinical trial with imatinib, has intensified efforts to identify mechanisms of SCLC resistance. Adhesion to extracellular matrix (ECM) is one mechanism that can increase therapeutic resistance in SCLC cells. To address whether adhesion to ECM increases resistance through modulation of signaling pathways, a series of SCLC cell lines were pl… Show more

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Cited by 112 publications
(86 citation statements)
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“…This small effect on apoptosis is in keeping with previous data published on the use of LY294002. 18,35 Integrins and growth factors in untransformed cells only regulate cell cycle progression at the G1/S checkpoint. 11 Current evidence suggests a central role for PI3-kinase signaling pathway in regulating cell cycle progression.…”
Section: Discussionmentioning
confidence: 99%
“…This small effect on apoptosis is in keeping with previous data published on the use of LY294002. 18,35 Integrins and growth factors in untransformed cells only regulate cell cycle progression at the G1/S checkpoint. 11 Current evidence suggests a central role for PI3-kinase signaling pathway in regulating cell cycle progression.…”
Section: Discussionmentioning
confidence: 99%
“…Many lung cancers, especially SCLCs express high levels of Bcl-2 and activated Akt. 48,49 Downregulation of hASH1 by siRNAs lead to increased apoptosis which resulted in potentially compensatory increase in Bcl-2 in the pulmonary carcinoid cells, which normally express hASH1. On the other hand, enforced expression of hASH1 in the immortalized human bronchial epithelial BEAS2B cells which normally lack hASH1 was associated with increased expression of p-Akt and p-mTOR, a downstream target of Akt and significant drop in apoptosis.…”
Section: Discussionmentioning
confidence: 99%
“…Accumulating evidence supports this role for the PI3K/AKT pathway. [389][390][391][392] The PI3K-AKT pathway was important in actions of tobacco carcinogens and in transformation-related characteristics of lung cells. 393,394 The JAK-STAT pathway may also be involved in NRG stimulation of proliferation of lung cells mediated by ERBB3.…”
Section: Erbb3 In Lung Cancermentioning
confidence: 99%
“…Some lung cancer cell lines with wildtype EGFR show responsiveness to gefitinib or erlotinib. ERBB3 is high in those that are responsive, 392,416 in association with an epithelial as opposed to a de-differentiated mesenchymal phenotype. 417 Similarly, ERBB3, as well as epiregulin and amphiregulin, were expressed at higher levels in lung cancer cell lines that are highly (HCC827, H3255 and H4006) or moderately (H1819 and HCC2279) sensitive to gefitinib compared to the gefitinib resistant cell line H1299.…”
Section: Erbb3 Egfr Mutation and Clinical Responsiveness To Egfr Inhmentioning
confidence: 99%