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Total 64 results found since Jan 2013.

Combination Therapy with PIK3R3-siRNA and EGFR-TKI Erlotinib Synergistically Suppresses Glioblastoma Cell Growth In Vitro
CONCLUSIONS: Our data propose that suppression of PIK3R3 can effectively triggers apoptosis and enhances the sensitivity of the glioblastoma cells to EGFR-TKI erlotinib. Thus, PIK3R3 can be a potential therapeutic target in glioblastoma patients.<br />.PMID:34967581 | DOI:10.31557/APJCP.2021.22.12.3993
Source: Cancer Control - December 30, 2021 Category: Cancer & Oncology Authors: Razieh Amini Hadi Karami Mohammad Bayat Source Type: research

Abstract 5323: Integrated computational cell-line modeling of drug sensitivity and high-throughput siRNA screening reveals novel molecular biomarkers for conventional chemotherapy
Conclusions: We present an integrated approach that combines a novel Bayesian multi-task learning model with high-throughput siRNA screens. Our approach aims to uncover sets of important aberrations and allows for the subtyping of drugs based on similarities in targets and mechanisms of action. We integrate our results with high-throughput RNAi experiments to identify synthetic lethal events in specific therapeutic context. Citation Format: Olga H. Nikolova, Mehmet Gönen, Rodrigo Dienstmann, In Sock Jang, Russell Moser, Silvia Cermelli, Chang Xu, Ryan M. Mitchell, Eduardo Mendez, Carla Grandori, Christopher Kemp, Stephen ...
Source: Cancer Research - September 30, 2014 Category: Cancer & Oncology Authors: Nikolova, O. H., Gonen, M., Dienstmann, R., Jang, I. S., Moser, R., Cermelli, S., Xu, C., Mitchell, R. M., Mendez, E., Grandori, C., Kemp, C., Friend, S., Guinney, J., Margolin, A. Tags: Molecular and Cellular Biology 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

Antitumor activity of kinetochore-associated protein 2 siRNA against lung cancer patient-derived tumor xenografts.
Authors: Makita Y, Teratani M, Murata S, Hoashi Y, Matsumoto S, Kawamata Y Abstract It has been widely reported that patient-derived tumor xenografts (PDXs) are more similar to tumor tissues than conventional cancer cell lines. Kinetochore-associated protein 2 (KNTC2) is known to be upregulated specifically in tumor tissues of cancer patients and is recognized as a potential target for cancer therapy. Previously, in vivo antitumor activities of KNTC2 short interfering RNA encapsulated into a lipid nanoparticle (KNTC2-LNP) were reported in orthotopic hepatocellular carcinoma mouse models. However, it remains unclear...
Source: Oncology Letters - March 16, 2018 Category: Cancer & Oncology Tags: Oncol Lett Source Type: research

Inhibition of SMYD2 Sensitized Cisplatin to Resistant Cells in NSCLC Through Activating p53 Pathway
In conclusion, the present study elucidated that the activity of SMYD2 in NSCLC may affect the cell sensitivity to chemotherapeutic agents, especially to CDDP. The elevated SMYD2 mediated CDDP resistance and malignant phenotype in NSCLC, indicating that SMYD2 may be a useful biomarker of CDDP resistance in NSCLC. Inhibition of SMYD2 contributes to the methylation-related activation of p53 and thus results in cell apoptosis. Furthermore, combination treatment with CDDP and an SMYD2 inhibitor had a synergistically antitumor effects in a xenograft model in vivo. Given that SMYD2 has reversible effects and is a targetable prot...
Source: Frontiers in Oncology - April 25, 2019 Category: Cancer & Oncology 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

Neurokinin-1 activation affects EGFR related signal transduction in triple negative breast cancer.
Abstract Breast cancers bear overexpression of neurokinin-1 (NK-1). The aim of this study was to investigate the relationship between NK-1 and EGFR in triple negative breast cancers (TNBCs). Immunohistochemistry was performed to investigate NK-1 and EGFR expressions in TNBCs. [Sar(9),Met(O2)(11)] substance P (SMSP) was used to activate NK-1 in two TNBC cell lines, MDA-MB-231 and MDA-MB-468. L-733060 and siRNA against NK-1 was used to inhibit NK-1. The in vitro regulatory effect of NK-1 was determined using CCK-8 proliferation assay. The effects of NK-1 activation and inhibition on EGFR and its downstreaming pathwa...
Source: Cellular Signalling - March 25, 2015 Category: Cytology Authors: Wang JG, Juan Y, Hu JL, Yang WL, Ren H, Ding D, Zhang L, Liu XP Tags: Cell Signal Source Type: research

Inhibition of Hedgehog signaling sensitizes NSCLC cells to standard therapies through modulation of EMT-regulating miRNAs
Conclusions: We demonstrate that Hh pathway, through EMT-induction, leads to reduced sensitivity to EGFR-TKIs in NSCLCs. Therefore, targeting Hh pathway may lead to the reversal of EMT phenotype and improve the therapeutic efficacy of EGFR-TKIs in NSCLC patients.
Source: Journal of Hematology and Oncology - October 7, 2013 Category: Hematology Authors: Aamir AhmadMa¿in MaitahKevin GinnebaughYiwei LiBin BaoShirish GadgeelFazlul Sarkar Source Type: research

AXL and MET Inhibition in Resistance to EGFR Inhibitor
In this study, we investigated the antitumor activity of NPS-1034, a newly developed drug that targets both MET and AXL, in NSCLC cells with acquired resistance to gefitinib or erlotinib (HCC827/GR and HCC827/ER, respectively). Characterization of H820 cells and evaluation of NPS-1034 efficacy in these cells were also performed. The resistance of HCC827/GR was mediated by MET activation, whereas AXL activation led to resistance in HCC827/ER. The combination of gefitinib or erlotinib with NPS-1034 synergistically inhibited cell proliferation and induced cell death in both resistant cell lines. Accordingly, suppression of Ak...
Source: Cancer Research - January 5, 2014 Category: Cancer & Oncology Authors: Rho, J. K., Choi, Y. J., Kim, S. Y., Kim, T. W., Choi, E. K., Yoon, S.-J., Park, B. M., Park, E., Bae, J. H., Choi, C.-M., Lee, J. C. Tags: Therapeutics, Targets, and Chemical Biology Source Type: research

Synthetic Lethality Screen Identifies RPS6KA2 as Modifier of Epidermal Growth Factor Receptor Activity in Pancreatic Cancer.
Abstract Pancreatic cancer is characterized by a high degree of resistance to chemotherapy. Epidermal growth factor receptor (EGFR) inhibition using the small-molecule inhibitor erlotinib was shown to provide a small survival benefit in a subgroup of patients. To identify kinases whose inhibition acts synergistically with erlotinib, we employed a kinome-wide small-interfering RNA (siRNA)-based loss-of-function screen in the presence of erlotinib. Of 779 tested kinases, we identified several targets whose inhibition acted synergistically lethal with EGFR inhibition by erlotinib, among them the S6 kinase ribosomal p...
Source: Neoplasia - December 1, 2013 Category: Cancer & Oncology Authors: Milosevic N, Kühnemuth B, Mühlberg L, Ripka S, Griesmann H, Lölkes C, Buchholz M, Aust D, Pilarsky C, Krug S, Gress T, Michl P Tags: Neoplasia Source Type: research

Effect of simvastatin on the resistance to EGFR tyrosine kinase inhibitors in a non-small cell lung cancer with the T790M mutation of EGFR.
This study investigated overcoming resistance to EGFR-TKI using simvastatin. We demonstrated that addition of simvastatin to gefitinib enhanced caspase-dependent apoptosis in T790M mutant NSCLC cells. Simvastatin also strongly inhibited AKT activation, leading to suppression of β-catenin activity and the expression of its targets, survivin and cyclin D1. Both insulin treatment and AKT overexpression markedly increased p-β-catenin and survivin levels, even in the presence of gefitinib and simvastatin. However, inhibition of AKT by siRNA or LY294002 treatment decreased p-β-catenin and survivin levels. To determine the rol...
Source: Experimental Cell Research - March 12, 2014 Category: Cytology Authors: Hwang KE, Kwon SJ, Kim YS, Park DS, Kim BR, Yoon KH, Jeong ET, Kim HR Tags: Exp Cell Res Source Type: research

Abstract 856: Combination of crizotinib and radiation in the treatment of ALK-positive and cetuximab-resistant lung cancer
We examined the effect of crizotinib in combination with radiation on ALK signaling, cell proliferation, cell cycle distribution and radiosensitivity in ALK-positive NSCLC cell lines H3122 and H2228 in vitro. We also examined the in-vivo effects of crizotinib in combination with radiation in H3122 and H2228 xenograft models. Crizotinib blocked phosphorylation of ALK and its downstream effectors and inhibited cell proliferation in a dose-dependent manner. The combination of crizotinib and radiation resulted in increased inhibition of cell growth. Although cells were sensitized to radiation by crizotinib, molecular knockdown...
Source: Cancer Research - September 30, 2014 Category: Cancer & Oncology Authors: Li, C., Huang, S., Walters, N., Armstrong, E. A., Harari, P. M. Tags: Clinical Research (Excluding Clinical Trials) Source Type: research