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GSE146975 EGFR activity addiction facilitates anti-ERBB based combination treatment of squamous bladder cancer
Contributors : Michael Rose ; Bernd Denecke ; Nadine T GaisaSeries Type : Expression profiling by arrayOrganism :Recent findings suggested a benefit of anti-EGFR therapy for basal-like muscle invasive bladder cancer (MIBC). However, impact on bladder cancer with substantial squamous differentiated (Sq-BLCA) and especially pure squamous cell carcinoma (SCC) remains unknown. Therefore, we comprehensively characterized pure and mixed Sq-BLCA (n=125) on genetic and protein expression level, and performed functional pathway and drug-response analyses with cell line models and isolated primary SCC (p-SCC) cells of the human urin...
Source: GEO: Gene Expression Omnibus - March 12, 2023 Category: Genetics & Stem Cells Tags: Expression profiling by array 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

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

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

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

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 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

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

HRAS mutations and resistance to the epidermal growth factor receptor tyrosine kinase inhibitor erlotinib in head and neck squamous cell carcinoma cells
Conclusion: Activating HRAS mutations can confer erlotinib resistance in an HRAS mutant HNSCC cell line. Head Neck, 2013.
Source: Head and Neck - September 30, 2013 Category: ENT & OMF Authors: J. Hun Hah, Mei Zhao, Curtis R. Pickering, Mitchell J. Frederick, Genevieve A. Andrews, Samar A. Jasser, David R. Fooshee, Zvonimir L. Milas, Chad Galer, Daisuke Sano, William N. William, Edward Kim, John Heymach, Lauren A. Byers, Vali Papadimitrakopoulou Tags: Research Article Source Type: research