5-Aza-2′-deoxycytidine induces growth inhibition and upregulation of epidermal growth factor receptor on human epithelial cancer cells

Caraglia, Michele; Pinto, Antonio; Correale, Pierpaolo; Zagonel, Vittorina; Genua, Geppino; Leardi, A.; Pepe, Stefano; Bianco, A. R.; Tagliaferri, Pierosandro

doi:10.1093/oxfordjournals.annonc.a058806

Cited by 25 publications

(13 citation statements)

References 26 publications

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“…We selected the relatively unresponsive MiaPaCa2 cell line, as well as the PaCa44 and CFPAC1 cell lines, which show strong inhibition of cell proliferation associated with arrest or delay in S or G2/M phases. Low rates of induction of apoptosis confirmed that 5-aza-CdR treatment produces a predominantly cytostatic effect in these pancreatic cancer cell lines, as observed for other cancer cell lines (Davidson et al, 1992;Caraglia et al, 1994;Karpf et al, 1999;Sato et al, 2003a).…”

Section: Discussionsupporting

confidence: 69%

Growth delay of human pancreatic cancer cells by methylase inhibitor 5-aza-2′-deoxycytidine treatment is associated with activation of the interferon signalling pathway

et al. 2005

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Section: Discussionsupporting

confidence: 69%

Growth delay of human pancreatic cancer cells by methylase inhibitor 5-aza-2′-deoxycytidine treatment is associated with activation of the interferon signalling pathway

et al. 2005

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“…The triggering of protective response to anticancer activity of biological agents is not an occasional event and several preclinical findings support the hypothesis that a reactive response can be induced in cancer cells that is translated in an overactivation of other signaling pathways [65,66].…”

Section: Reviewmentioning

confidence: 77%

Anaplastic lymphoma kinase: a glimmer of hope in lung cancer treatment?

Franco¹,

Rocco

Marino

et al. 2013

Expert Review of Anticancer Therapy

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Anaplastic lymphoma kinase (ALK) rearrangements (ALK-Rs) have been identified in 3-7% of all non-small-cell lung cancers (NSCLCs) and represent an important molecular target for NSCLC treatment. The authors discuss the role of ALK-Rs in the prediction of clinical-pathological features of NSCLCs and the technical problems related to their determination in specimens. The authors also describe the preclinical and clinical results derived from the use of ALK inhibitors. ALK-R is generally detected in patients with specific clinical-pathological features: never-smokers, young males, adenocarcinoma histotype and EGF receptor/KRAS wild-type. The diagnosis of ALK-R remains a challenge, implicating the need of a careful filtering of patients. NSCLC patients harboring ALK-R have shown sensitivity to ALK inhibitors even if their activity is limited at the time by the occurrence of mechanisms of resistance. The authors summarize the strategies that in the future could overcome these mechanisms of escape.

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“…Our results together with previously reported data on increased EGFR mRNA in a glioblastoma cell line [46] and the presence of the IFN-regulatory factor-1 in the EGFR promoter region [47] all support the hypothesis that IFNα can directly regulate EGFR expression.The supra-additive anti-proliferative effect achieved by combining gefitinib with IFNα may indicate that the process of HER1/EGFR up-regulation itself has the potential to enhance sensitivity to its inhibitors. However, an equally plausible hypothesis is that this is a secondary effect via changes in the cell growth status [48,49,50,51]. Thus, increased receptor expression could be part of a homeostatic cellular response to the strong anti-proliferative stimuli of the combined treatment.…”

Section: Discussionmentioning

confidence: 99%

Interferon-α Promotes the Anti-Proliferative Effect of Gefitinib (ZD1839) on Human Colon Cancer Cell Lines

Yang

Qu²,

Russell³

et al. 2005

Oncology

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Objective: Interferon-α (IFNα) treatment is associated with up-regulation of epidermal growth factor receptor (HER1/EGFR) expression and marked growth inhibition of colon cancer cell lines in vitro.We aimed to determine the effect of combining IFNα and gefitinib on colon cancer cell line growth. Methods: A panel of nine colon cancer cell lines were characterised for expression of HER1/EGFR and then treated with gefitinib alone, or IFNα alone, or IFNα plus gefitinib, following a pre-treatment using vehicle or IFNα. Crystal violet staining and flow cytometry were used to assess cell proliferation and expression of HER1/EGFR. The indexes and statistical assays were used to evaluate significant differences between treatment groups against vehicle control. Results: All cell lines except SW620 were HER1/EGFR positive. IFNα treatment was associated with significant up-regulation of cell surface HER1/EGFR expression in all HER1/EGFR-positive cell lines except KM12SM. Concurrent treatment with IFNα and gefitinib, or IFNα pre-treatment followed by gefitinib, or IFNα pre-treatment followed by a combination of IFNα plus gefitinib, additively or supra-additively/synergistically enhanced the sensitivity of the seven HER1/EGFR-up-regulated cell lines. Conclusion: IFNα improves the anti-proliferative effect of EGFR inhibition in colorectal cancer cell lines. This approach may have clinical implications for improving treatment based on targeting of HER1/EGFR.

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5-Aza-2′-deoxycytidine induces growth inhibition and upregulation of epidermal growth factor receptor on human epithelial cancer cells

Abstract: We suggest a role for 5azaCdR in enhancing the efficacy of therapeutic approaches involving the use of anti-EGF-R immunoconjugated for the imaging and the treatment of human epithelial neoplasias.

Cited by 25 publications

References 26 publications

Growth delay of human pancreatic cancer cells by methylase inhibitor 5-aza-2′-deoxycytidine treatment is associated with activation of the interferon signalling pathway

Growth delay of human pancreatic cancer cells by methylase inhibitor 5-aza-2′-deoxycytidine treatment is associated with activation of the interferon signalling pathway

Anaplastic lymphoma kinase: a glimmer of hope in lung cancer treatment?

Interferon-α Promotes the Anti-Proliferative Effect of Gefitinib (ZD1839) on Human Colon Cancer Cell Lines

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