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Cancer: Non-Small Cell Lung Cancer
Drug: Tarceva

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Total 29 results found since Jan 2013.

The combination of osimertinib with Raf inhibitor overcomes osimertinib resistance induced by KRAS amplification in EGFR-mutated lung cancer cells
Exp Cell Res. 2023 Jul 11:113722. doi: 10.1016/j.yexcr.2023.113722. Online ahead of print.ABSTRACTOsimertinib is a third-generation epidermal growth factor receptor (EGFR)1 tyrosine kinase inhibitor (TKI) approved for the treatment of EGFR-positive patients exhibiting a T790 M resistance mutation after treatment with an earlier generation of EGFR TKIs. However, resistance to osimertinib inevitably develops despite its efficacy, and the resistance mechanisms are complex and not fully understood. We established cell lines with acquired resistance to osimertinib from gefitinib- or erlotinib-resistant NSCLC cells using a dose-...
Source: Experimental Cell Research - July 13, 2023 Category: Cytology Authors: Tae-Gul Lee Hye-Min Kang Seo Yun Kim Hye-Ryoun Kim Cheol Hyeon Kim Source Type: research

Heat shock protein 90 inhibitor 17-AAG down-regulates thymidine phosphorylase expression and potentiates the cytotoxic effect of tamoxifen and erlotinib in human lung squamous carcinoma cells
Biochem Pharmacol. 2022 Aug 9:115207. doi: 10.1016/j.bcp.2022.115207. Online ahead of print.ABSTRACTElevated thymidine phosphorylase (TP) levels, a key enzyme in the pyrimidine nucleoside salvage pathway, in cancer cells, are related to a poor prognosis in a variety of cancers. Heat shock protein 90 (Hsp90) is a ubiquitous molecular chaperone that is involved in the stabilization and maturation of many oncogenic proteins. The aim of this study is to elucidate whether Hsp90 inhibitor 17-AAG could enhance tamoxifen- and erlotinib-induced cytotoxicity in nonsmall cell lung cancer (NSCLC) cells via modulating TP expression in ...
Source: Biochemical Pharmacology - August 12, 2022 Category: Drugs & Pharmacology Authors: Jen-Chung Ko Jyh-Cheng Chen Jou-Min Hsieh Pei-Yu Tseng Chen-Shan Chiang Li-Ling Liu Chin-Cheng Chien I-Hsiang Huang Qiao-Zhen Chang Bo-Cheng Mu Yun-Wei Lin Source Type: research

GLI1 activation is a key mechanism of erlotinib resistance in human non-small cell lung cancer.
Authors: Dong Z, Wang Y, Ding V, Yan X, Lv Y, Zhong M, Zhu F, Zhao P, He C, Ding F, Shi H Abstract Lung cancer is the leading cause of cancer-associated death worldwide. In recent years, the advancement of epidermal growth factor receptor-tyrosine kinase inhibitor (EGFR-TKI) targeted therapies has provided clinical benefits for lung cancer patients with EGFR mutations. The response to EGFR-TKI varies in patients with lung cancer, and resistance typically develops during the course of the treatment. Therefore, understanding biomarkers which can predict resistance to EGFR-TKI is important. Overexpression of GLI cause...
Source: Oncology Letters - September 1, 2020 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

YM155 sensitizes non-small cell lung cancer cells to EGFR-tyrosine kinase inhibitors through the mechanism of autophagy induction
In this study, we showed that YM155 markedly enhanced the sensitivity of erlotinib to EGFR-TKI resistant NSCLC cell lines H1650 (EGFR exon 19 deletion and PTEN loss) and A549 (EGFR wild type and KRAS mutation) through inducing autophagy-dependent apoptosis and autophagic cell death. The effects of YM155 combined with erlotinib on apoptosis and autophagy inductions were more obvious than those of YM155 in combination with survivin knockdown by siRNA transfection, suggesting that YM155 induced autophagy and apoptosis in the NSCLC cells partially depend on survivin downregulation. Meanwhile, we found that the AKT/mTOR pathway...
Source: Biochimica et Biophysica Acta (BBA) Molecular Basis of Disease - October 11, 2018 Category: Molecular Biology Source Type: research

Novel drug-resistance mechanisms of pemetrexed-treated non-small cell lung cancer.
In this study, we explored new drug resistance mechanisms of PEM-treated NSCLC using two combinations of parental and PEM-resistant NSCLC cell lines from PC-9 and A549. PEM increased the apoptosis cells in parental PC-9 and the senescent cells in parental A549. However, such changes were not observed in the respective PEM-resistant cell lines. Quantitative RT-PCR analysis revealed that, besides an increased gene expression of thymidylate synthase in PEM-resistant PC-9 cells, the solute carrier family 19 member1 (SLC19A1) gene expression was markedly decreased in PEM-resistant A549 cells. The siRNA-mediated knockdown of SLC...
Source: Oncotarget - April 25, 2018 Category: Cancer & Oncology Tags: Oncotarget Source Type: research

Inositol trisphosphate receptor type 3-mediated enhancement of EGFR and MET co-targeting efficacy in non-small cell lung cancer detected by 18F-fluorothymidine.
CONCLUSIONS: Our findings indicate that 18F-FLT PET/CT is able to detect the enhanced efficacy of EGFR and MET inhibitors in oncogene-driven NSCLC and that such enhancement is mediated by IP3R3 through its interaction with K-Ras. PMID: 29618618 [PubMed - as supplied by publisher]
Source: Clinical Cancer Research - April 4, 2018 Category: Cancer & Oncology Authors: Iommelli F, De Rosa V, Terlizzi C, Monti M, Panico M, Fonti R, Del Vecchio S Tags: Clin Cancer Res Source Type: research

Estrogen receptor β1 activation accelerates resistance to epidermal growth factor receptor-tyrosine kinase inhibitors in non-small cell lung cancer.
In conclusion, ERβ1 was activated in EGFR-TKI secondary resistance. The downregulation of ERβ1 sensitized the cells to EGFR-TKIs. ERβ1 may be a key molecule in EGFR-TKI therapy. In addition, anti-ERβ1 treatment may reverse TKI resistance. PMID: 29328407 [PubMed - as supplied by publisher]
Source: Oncology Reports - January 14, 2018 Category: Cancer & Oncology Tags: Oncol Rep Source Type: research

Comparison of epithelial mesenchymal transition mediated tyrosine kinase inhibitor resistance in non-small cell lung cancer cell lines with wild type EGFR and mutant type EGFR.
This study investigates the role of epithelial-mesenchymal transition (EMT) in the development of resistance against TKIs in NSCLC. Currently, the role of p120-catenin, Kaiso factor and PRMT-1 in reversal of EMT in T790M mutated and TKI-resistant NSCLC cells is a new line of study. In this investigation we found upregulation of cytoplasmic p120-catenin, and it was co-localized with Kaiso factor. In the nucleus, binding of p120-catenin to Kaiso factor initiates transcription by activating EMT-transcription factors such as Snail, Slug, Twist, and ZEB1. PRMT-1 was also found to be upregulated, which induces methylation of Twi...
Source: Biochemical and Biophysical Research communications - January 11, 2018 Category: Biochemistry Authors: Iderzorig T, Kellen J, Osude C, Singh S, Woodman JA, Garcia C, Puri N Tags: Biochem Biophys Res Commun 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

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