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Total 33 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
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
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
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
Mistletoe (viscum album) extract targets Axl to suppress cell proliferation and overcome cisplatin- and erlotinib-resistance in non-small cell lung cancer cells.
Conclusion : Taken together, our data provide that VAE targets Axl to suppress cell proliferation and to circumvent cisplatin- and erlotinib-resistance in NSCLC cells. Graphical abstract
Source: Phytomedicine - September 29, 2017 Category: Drugs & Pharmacology Source Type: research
Abstract 774: EGFR-regulated RGS expression contributes to paclitaxel resistance in human lung cancer cells
Lung cancer is one of the main causes of cancer-related death worldwide, and the 5-year survival of lung cancer is less than 20%. Paclitaxel is a widely used chemotherapeutic agent to treat a variety of cancers, but its therapeutic efficacy tends to be limited due to the development of drug resistance, raising the need to understand the molecular mechanisms underlying paclitaxel resistance. In the current study, we investigated the mechanisms of paclitaxel resistance in non-small cell lung cancers (NSCLCs). First, we established paclitaxel-resistant NSCLC cell lines, including H460 TxR and SK-MES TxR, by pulse- or prolonge...
Source: Cancer Research - September 30, 2014 Category: Cancer & Oncology Authors: Park, S.-H., Sung, M.-A., Lee, H.-Y. Tags: Experimental and Molecular Therapeutics Source Type: research
Abstract 2269: Combination of erlotinib and epigallocatechin-3-gallate induces apoptosis of squamous cell carcinoma of the head and neck through posttranslational regulation of Bim and Bcl-2
Conclusion: Our results strongly suggest that the combination of erlotinib and EGCG induces apoptosis of SCCHN cells by regulating Bim and Bcl-2 at the post-translational level. Currently, a clinical trial is underway at Winship Cancer Institute of Emory University to inhibit or reverse the progression of oral premalignant lesions using this combination. (This study is supported by R03CA159369, P50CA128613 and Robbins Scholar Award of Winship Cancer Institute).
Citation Format: Abedul Haque, Mohammad A. Rahman, Zhuo G. Chen, Dong M. Shin, A.R.M. Ruhul Amin. Combination of erlotinib and epigallocatechin-3-gallate induces ap...
Source: Cancer Research - September 30, 2014 Category: Cancer & Oncology Authors: Haque, A., Rahman, M. A., Chen, Z. G., Shin, D. M., Amin, A. R. M. R. Tags: Molecular and Cellular Biology Source Type: research
Abstract 2762: Akt kinase-interacting protein1, a novel therapeutic target for lung cancer with EGFR-activating and gatekeeper mutations
Epidermal growth factor receptor (EGFR) tyrosine kinase inhibitors (TKIs), such as gefitinib and erlotinib, show favorable effects in EGFR mutant lung cancer. However, responders eventually develop acquired resistance almost without exception, and secondary T790M mutations in EGFR account for approximately 50% of the acquired resistance. Recent studies indicated that EGFR mutant lung cancer cells are dependent on EGFR/Akt signaling for survival even after acquired T790M secondary mutation. Akt kinase-interacting protein1 (Aki1) is a scaffold protein that binds to wild-type EGFR after EGF ligand stimulation, maintains signa...
Source: Cancer Research - September 30, 2014 Category: Cancer & Oncology Authors: Yamada, T., Carbone, D. P., Takeuchi, S., Fujita, N., Yano, S. Tags: Experimental and Molecular Therapeutics Source Type: research
Abstract 2558: The mechanistic study on the effect of platinum-based chemotherapy efficacy imposed by EGFR-TKI regulated ERCC1 in non-small cell lung cancer (NSCLC)
Platinum-based chemotherapy is conventionally the first line treatment for EGFR wild type patients while EGFR-TKI is the standard for patients with mutation. Subgroup biomarker studies conducted in FASTACT-2 (Wu et al Lancet Oncology 2013) indicated that patients with positive ERCC1 attained longer overall survival and progression free survival under intercalated chemotherapy and EGFR-TKI, in comparison with solely chemotherapy. EGFR-TKI is postulated to down-regulate ERCC1 expression in EGFR wild type NSCLC cells, hence enhancing the Chemo efficacy. The study aims to investigate the missing link between EGFR and ERCC1 in ...
Source: Cancer Research - August 2, 2015 Category: Cancer & Oncology Authors: Cheong, H. T., Hui, C. W. C., Xu, F., Mok, T. S. K., Wong, C. H. Tags: Experimental and Molecular Therapeutics Source Type: research
