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Total 64 results found since Jan 2013.

Metabolic profiling of triple-negative breast cancer cells reveals metabolic vulnerabilities
ConclusionsSimilar to the genomic heterogeneity observed in TNBC, our results reveal metabolic heterogeneity among TNBC subtypes and demonstrate that understanding metabolic profiles and drug responses may prove valuable in targeting TNBC subtypes and identifying therapeutic susceptibilities in TNBC patients. Perturbation of metabolic pathways sensitizes TNBC to inhibition of receptor tyrosine kinases. Such metabolic vulnerabilities offer promise for effective therapeutic targeting for TNBC patients.
Source: Cancer and Metabolism - August 22, 2017 Category: Cancer & Oncology Source Type: research

Salinomycin acts through reducing AKT-dependent thymidylate synthase expression to enhance erlotinib-induced cytotoxicity in human lung cancer cells.
In this study, we showed that erlotinib (1.25 - 10μM) treatment down-regulating of TS expression in an AKT inactivation manner in two NSCLC cell lines, human lung squamous cell carcinoma H1703 and adenocarcinoma H1975 cells. Knockdown of TS using small interfering RNA (siRNA) or inhibiting AKT activity with PI3K inhibitor LY294002 enhanced the cytotoxicity and cell growth inhibition of erlotinib. A combination of erlotinib and salinomycin resulted in synergistic enhancement of cytotoxicity and cell growth inhibition in NSCLC cells, accompanied with reduced protein levels of phospho-AKT(Ser473), phospho-AKT(Thr308), and TS...
Source: Experimental Cell Research - April 25, 2017 Category: Cytology Authors: Tung CL, Chen JC, Wu CH, Peng YS, Chen WC, Zheng HY, Jian YJ, Wei CL, Cheng YT, Lin YW Tags: Exp Cell Res Source Type: research

In Vitro and In Vivo Synergistic Antitumor Activity of the Combination of BKM120 and Erlotinib in Head and Neck Cancer: Mechanism of Apoptosis and Resistance
This study investigated whether cotargeting of EGFR and PI3K has synergistic antitumor effects and apoptosis induction. We examined growth suppression, apoptosis, and signaling pathway modulation resulting from single and combined targeting of EGFR and PI3K with erlotinib and BKM120, respectively, in a panel of SCCHN cell lines and a xenograft model of SCCHN. In a panel of 12 cell lines, single targeting of EGFR with erlotinib or PI3K with BKM120 suppressed cellular growth without inducing significant apoptosis. Cotargeting of EGFR and PI3K synergistically inhibited SCCHN cell line and xenograft tumor growth, but induced v...
Source: Molecular Cancer Therapeutics - April 2, 2017 Category: Cancer & Oncology Authors: Anisuzzaman, A. S. M., Haque, A., Wang, D., Rahman, M. A., Zhang, C., Chen, Z., Chen, Z. G., Shin, D. M., Amin, A. R. M. R. Tags: Cancer Biology and Signal Transduction Source Type: research

YAP promotes erlotinib resistance in human non-small cell lung cancer cells.
Authors: Hsu PC, You B, Yang YL, Zhang WQ, Wang YC, Xu Z, Dai Y, Liu S, Yang CT, Li H, Hu B, Jablons DM, You L Abstract Yes-associated protein (YAP) is a main mediator of the Hippo pathway, which promotes cancer development. Here we show that YAP promotes resistance to erlotinib in human non-small cell lung cancer (NSCLC) cells. We found that forced YAP overexpression through YAP plasmid transfection promotes erlotinib resistance in HCC827 (exon 19 deletion) cells. In YAP plasmid-transfected HCC827 cells, GTIIC reporter activity and Hippo downstream gene expression of AREG and CTGF increased significantly (P<0.0...
Source: Oncotarget - July 15, 2016 Category: Cancer & Oncology Tags: Oncotarget Source Type: research

Mechanism of c-Met and EGFR tyrosine kinase inhibitor resistance through epithelial mesenchymal transition in non-small cell lung cancer.
Abstract According to Cancer Research UK currently available estimates, 14.1 million new lung cancer cases were diagnosed and a staggering 8.2 million people worldwide died from lung cancer in 2012. EGFR and c-Met are two tyrosine kinase receptors most commonly overexpressed or mutated in Non-small Cell Lung Cancer (NSCLC) resulting in increased proliferation and survival of lung cancer cells. Tyrosine kinase inhibitors (TKIs), such as Erlotinib, approved by the FDA as first/second line therapy for NSCLC patients have limited clinical efficacy due to acquired resistance. In this manuscript, we investigate and disc...
Source: Biochemical and Biophysical Research communications - July 6, 2016 Category: Biochemistry Authors: Rastogi I, Rajanna S, Webb A, Chhabra G, Foster B, Webb B, Puri N Tags: Biochem Biophys Res Commun Source Type: research

Interaction of the EGF Receptor and the Hippo Pathway in the Diabetic Kidney
Activation of the EGF receptor (EGFR) or the Hippo signaling pathway can control cell proliferation, apoptosis, and differentiation, and the dysregulation of these pathways can contribute to tumorigenesis. Previous studies showed that activation of EGFR signaling in renal epithelial cells can exacerbate diabetic kidney injury. Moreover, EGFR has been implicated in regulating the Hippo signaling pathway in Drosophila; thus, we examined this potential interaction in mammalian diabetic kidney disease. Yes-associated protein (YAP) is a transcriptional regulator regulated by the Hippo signaling pathway. We found YAP protein exp...
Source: Journal of the American Society of Nephrology : JASN - May 30, 2016 Category: Urology & Nephrology Authors: Chen, J., Harris, R. C. Tags: Basic Research Source Type: research

Autophagy inhibition facilitates erlotinib cytotoxicity in lung cancer cells through modulation of endoplasmic reticulum stress.
In this study, we found the sensitivity to erlotinib, a well-used EGFR-TKI, was correlated with basal autophagy level. Erlotinib was able to induce autophagy not only in TKI-sensitive, but also TKI-resistant cancer cells. Inhibition of autophagy significantly enhanced cytotoxicity of erlotinib in TKI-resistant cancer cells via modulation of endoplasmic reticulum (ER) stress induced apoptosis. In this process, CCAAT/enhancer binding protein homologous protein (CHOP) acted as an executioner. Downregulation of CHOP with siRNA blocked the autophagy inhibition and erlotinib co-treatment induced apoptosis and prevented cancer ce...
Source: International Journal of Oncology - March 31, 2016 Category: Cancer & Oncology Authors: Wang Z, Du T, Dong X, Li Z, Wu G, Zhang R Tags: Int J Oncol Source Type: research

MAPK1E322K mutation increases head and neck squamous cell carcinoma sensitivity to erlotinib through enhanced secretion of amphiregulin.
In this study, we investigated the mechanism of MAPK1E322K-mediated EGFR activation in the context of erlotinib sensitivity. We demonstrated increased AREG secretion in HNSCC cell lines harboring endogenous or exogenous MAPK1E322K compared to wild type MAPK1. We found inhibition or knockdown of MAPK1 with siRNA resulted in reduced secretion of AREG and decreased sensitivity to erlotinib in the setting of MAPK1E322K. MAPK1E322K was associated with increased AREG secretion leading to an autocrine feedback loop involving AREG, EGFR and downstream signaling. Knockdown of AREG in HNSCC cells harboring MAPK1E322K abrogated EGFR ...
Source: Oncotarget - March 25, 2016 Category: Cancer & Oncology Tags: Oncotarget Source Type: research

Targeting non-canonical autophagy overcomes erlotinib resistance in tongue cancer
In this report, we found that autophagy prior to or induced by erlotinib treatment plays an important role in erlotinib resistance in tongue cancer cells. Using LC3 transfection, we observed that autophagy is upregulated and further induced when treated with erlotinib. Moreover, we found that autophagy plays a cytoprotective role by MTT analysis of the cell viability in TSCCs when treated with rapamycin or hydroxychloroquine (HCQ) in combination with erlotinib. However, 3-methyladenine (3-MA) did not influence the autophagy. Then, through siRNA technology and WB, we found that erlotinib-induced autophagy is mediated by ATG...
Source: Tumor Biology - January 21, 2016 Category: Cancer & Oncology Source Type: research

Abstract A65: A novel regulatory mechanism involving Ras-mediated activation of the zinc-finger transcription factor, SAF-1/MAZ induces EGFR/HER1 expression in breast cancer cells
Tumor microenvironment (TME) plays a critical role in tumor growth, invasion and metastasis. In TME, epidermal growth factor receptor (EGFR) family members, including HER1, HER2, HER3 and HER4, are involved in determining aggressive growth of breast cancer due to their ability to transduce the growth promoting functions of growth factors. This activity is potentiated by the over-expression of these receptor molecules in cancer cells. To reduce the activity of EGFR molecules, various inhibitors have been developed. EGFR/HER1 tyrosine kinase inhibitors (TKIs), gefitinib and erlotinib, show antitumor activity but these drugs ...
Source: Molecular Cancer Therapeutics - January 7, 2016 Category: Cancer & Oncology Authors: Ray, A., Havis, B., Ray, B. Tags: EGFR / Her2: Poster Presentations - Proffered Abstracts Source Type: research

Effects of kinase insert domain receptor (KDR) gene silencing on the sensitivity of A549 cells to erlotinib.
Abstract We investigated the effects of kinase insert domain receptor (KDR) gene silencing on the proliferation of A549 cells and their sensitivity to erlotinib. A KDR small interfering RNA (siRNA) sequence was designed and synthesized; then, it was transfected into A549 cells using Lipofectamine(TM) 2000. KDR mRNA and protein expression after KDR gene silencing was detected by reverse transcription polymerase chain reaction and western blotting; the A549 cell cycle was detected by flow cytometry. A 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay and colony formation assay were performed to dete...
Source: Cell Research - December 7, 2015 Category: Cytology Authors: Zhu WL, Liu YH Tags: Genet Mol Res Source Type: research

Inhibition of the effect of epidermal growth factor (EGF) on lung cancer cells. The use of plasmids encoding specific siRNA molecules
Conclusions: The inhibition of EGF system blockade with siRNA technique appears to be more effective strategy in cancer treatment in vitro, as compared to erlotinib, since this effect is probably EGFR gene mutation-independent. However, we have not definitively proved if it resulted in increased tumor cell immunogenicity.
Source: European Respiratory Journal - October 30, 2015 Category: Respiratory Medicine Authors: Gawronski, M., Kopinski, P., Jankowski, M., Goede, A., Szpechcinski, A., Chorostowska, J. Tags: 11.1 Lung Cancer Source Type: research

Quantitative proteomics unveiled: Regulation of DNA double strand break repair by EGFR involves PARP1.
CONCLUSION: We have established a powerful, quantitative phosphoproteomic approach to investigate regulatory mechanisms in DSB repair, dependent on protein phosphorylation after irradiation. Using this approach we have identified PARP1 as a mediator of EGFR/MEK-dependent regulation of DSB repair. PMID: 26422459 [PubMed - as supplied by publisher]
Source: Radiotherapy and Oncology : journal of the European Society for Therapeutic Radiology and Oncology - September 25, 2015 Category: Radiology Authors: Myllynen L, Kwiatkowski M, Gleißner L, Riepen B, Hoffer K, Wurlitzer M, Petersen C, Dikomey E, Rothkamm K, Schlüter H, Kriegs M Tags: Radiother Oncol Source Type: research

Nuclear EGFR renders cells radio-resistant by binding mRNA species and triggering a metabolic switch to increase lactate production.
CONCLUSIONS: We showed that nuclear EGFR selectively binds and stabilizes mRNA involved in the Warburg effect in response to irradiation. As a consequence, cells switch from aerobic to anaerobic glucose metabolism, which can be prevented by HIF1α inhibitor BAY87-2243, Dasatinib, Erlotinib or EGFR siRNA. PMID: 26320552 [PubMed - as supplied by publisher]
Source: Radiotherapy and Oncology : journal of the European Society for Therapeutic Radiology and Oncology - August 27, 2015 Category: Radiology Authors: Dittmann K, Mayer C, Paasch A, Huber S, Fehrenbacher B, Schaller M, Rodemann HP Tags: Radiother Oncol Source Type: research