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Cancer: Non-Small Cell Lung Cancer

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Total 1077 results found since Jan 2013.

Identification of microRNAs involved in gefitinib resistance of non-small-cell lung cancer through the insulin-like growth factor receptor 1 signaling pathway.
Authors: Ma W, Kang Y, Ning L, Tan J, Wang H, Ying Y Abstract Multiple clinical and experimental studies have suggested that epidermal growth factor receptor tyrosine kinase inhibitors (EGFR-TKIs) may be effective at treating advanced non-small cell lung cancer (NSCLC), however, the molecular basis of primary resistance to EGFR-TKIs in NSCLC remains unclear. In the current study, the insulin-like growth factor 1 receptor (IGF-1R) gene in the gefitinib-resistant human lung adenocarcinoma epithelial cell line A549 (A549/GR) was silenced using small interfering RNA (siRNA) in order to determine the role of microRNA (m...
Source: Experimental and Therapeutic Medicine - September 17, 2017 Category: General Medicine Tags: Exp Ther Med Source Type: research

Synergistic effect of targeting dishevelled-3 and the epidermal growth factor receptor-tyrosine kinase inhibitor on mesothelioma cells in vitro.
Authors: Moriyama G, Tanigawa M, Sakai K, Hirata Y, Kikuchi S, Saito Y, Kyoyama H, Matsuda K, Seike M, Gemma A, Uematsu K Abstract It was previously revealed that Wnt signaling is activated in mesothelioma cells. Although epidermal growth factor receptor (EGFR) is expressed in mesothelioma cells, EGFR-tyrosine kinase inhibitors (TKIs) are not effective for mesothelioma treatment. However, in non-small cell lung cancer, the blocking of Wnt signaling has been identified to enhance the anticancer effect of EGFR-TKIs. To confirm the anticancer effect of blocking Wnt signaling in combination with EGFR-TKI treatment in m...
Source: Oncology Letters - February 7, 2018 Category: Cancer & Oncology Tags: Oncol Lett Source Type: research

CDK16 overexpressed in non-small cell lung cancer and regulates cancer cell growth and apoptosis via a p27-dependent mechanism
Publication date: July 2018 Source:Biomedicine & Pharmacotherapy, Volume 103 Author(s): Hongtao Wang, Hongli Liu, Shengping Min, Yuanbing Shen, Wei Li, Yuqing Chen, Xiaojing Wang Cyclin-dependent kinase 16 (CDK16, PCTAIRE1) expression is upregulated in a wide variety of human malignancies. However, the function(s) of CDK16 in non-small cell lung cancer (NSCLC) remain unknown. Therefore, here we investigated the role of CDK16 in NSCLC. From 43 NSCLC tumors and matching healthy control lung tissues, immunohistochemistry revealed significantly greater CDK16 and phospho-p27Ser10 staining levels in NSCLC samples relati...
Source: Biomedicine and Pharmacotherapy - May 14, 2018 Category: Drugs & Pharmacology Source Type: research

Self-targeted knockdown of CD44 improves cisplatin sensitivity of chemoresistant non-small cell lung cancer cells
ConclusionsThese results suggest that self-targeted downregulation of chemoresistance-associated cell surface proteins during chemotherapy is an effective therapeutic strategy for overcoming the chemoresistance of NSCLC cells.
Source: Cancer Chemotherapy and Pharmacology - December 4, 2018 Category: Cancer & Oncology Source Type: research

Downregulation of basic fibroblast growth factor increases cisplatin sensitivity in A549 non-small cell lung cancer cells
Conclusion: bFGF decreased NSCLC sensitivity to cisplatin in vitro, while it enhanced colony formation ability and increased OCT-4 expression of A549 cells, which might account for its involved mechanisms of cisplatin resistance.
Source: Journal of Cancer Research and Therapeutics - December 19, 2018 Category: Cancer & Oncology Authors: Long He Yousheng Meng Zhihui Zhang Yanguo Liu Xiuwen Wang Source Type: research

Molecules, Vol. 25, Pages 1994: Nanoparticle-Mediated Gene Silencing for Sensitization of Lung Cancer to Cisplatin Therapy
M. Merkel Platinum-based chemotherapy remains a mainstay treatment for the management of advanced non-small cell lung cancer. A key cellular factor that contributes to sensitivity to platinums is the 5′-3′ structure-specific endonuclease excision repair cross-complementation group 1 (ERCC1)/ xeroderma pigmentosum group F (XPF). ERCC1/XPF is critical for the repair of platinum-induced DNA damage and has been the subject of intense research efforts to identify small molecule inhibitors of its nuclease activity for the purpose of enhancing patient response to platinum-based chemotherapy. As an ...
Source: Molecules - April 23, 2020 Category: Chemistry Authors: Daniel P. Feldmann Joshua Heyza Christoph M. Zimmermann Steve M. Patrick Olivia M. Merkel Tags: Brief Report Source Type: research

Silencing tumor-intrinsic CD73 enhances the chemosensitivity of NSCLC and potentiates the anti-tumoral effects of cisplatin: An in vitro study
Biomed Pharmacother. 2021 Nov 30:112370. doi: 10.1016/j.biopha.2021.112370. Online ahead of print.ABSTRACTAIMS: Besides suppressing anti-tumoral immune responses, tumor-intrinsic inhibitory immune checkpoints have been implicated in tumor development. Herein, we aimed to investigate the significance of tumor-intrinsic CD73, as an inhibitory immune checkpoint, in non-small cell lung cancer (NSCLC) development and propose a novel therapeutic approach.MAIN METHODS: We investigated the cell viability, chemosensitivity, apoptosis, migration, and the cell cycle of A-549 and NCI-H1299 following treatment with cisplatin and CD73-s...
Source: Biomedicine and pharmacotherapy = Biomedecine and pharmacotherapie - December 4, 2021 Category: Drugs & Pharmacology Authors: Elham Baghbani Saeed Noorolyai Shima Rahmani Dariush Shanehbandi Mahdi Abdoli Shadbad Leili Aghebati-Maleki Ahad Mokhtarzadeh Oronzo Brunetti Rossella Fasano Nicola Silvestris Behzad Baradaran Source Type: research

Abstract 573: BRG1-inactivating mutations as potential predictive markers for Aurora kinase A-targeted therapies in non-small cell lung cancers (NSCLCs)
Conclusions: BRG1-inactivating mutations make cells dependent to RAN/TPX2-mediated mitotic spindle assembly machinery and create targetable mitotic vulnerabilities in NSCLCs. BRG1-mutant NSCLCs are sensitive to Aurora kinase A-targeted treatments due to its crucial role on RAN/TPX2-dependent mitotic spindle formation. Our current data, thus far, suggest that wild-type BRG1-expressing cells tolerate the inhibition of AURKA due to properly regulated and, therefore, functionally normal centrosomes whereas BRG1 loss leads to centrosomal defects. Citation Format: Vural Tagal, Shuguang Wei, Wei Zhang, Bruce A. Posner, John D. Mi...
Source: Cancer Research - September 30, 2014 Category: Cancer & Oncology Authors: Tagal, V., Wei, S., Zhang, W., Posner, B. A., Minna, J. D., Gazdar, A. F., Roth, M. G. Tags: Molecular and Cellular Biology 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

Effects of targeted silencing of FOXC1 gene on proliferation and in vitro migration of human non-small-cell lung carcinoma cells.
CONCLUSION: Silencing FOXC1 may evidently inhibit the migration of these cells by reversing the EMT process through suppressing cadherin, being associated with the expressions of extracellular MMPs. PMID: 27648121 [PubMed - as supplied by publisher]
Source: American Journal of Translational Research - September 22, 2016 Category: Research Tags: Am J Transl Res Source Type: research

MicroRNA-183 Acts as a Tumor Suppressor in Human Non-Small Cell Lung Cancer by Down-Regulating MTA1
Conclusion: Our study indicates that miR-183 down-regulates MTA1 to inhibit the proliferation, EMT, migration and invasion of human NSCLC cells.Cell Physiol Biochem 2018;46:93 –106
Source: Cellular Physiology and Biochemistry - March 23, 2018 Category: Cytology Source Type: research

Knockdown of TRIM66 inhibits malignant behavior and epithelial-mesenchymal transition in non-small cell lung cancer.
CONCLUSION: Silence TRIM66 expression suppressed NSCLC cell proliferation, invasion, and migration. The siRNA-mediated TRIM66 silencing could block the occurrence of EMT. TRIM66 could be a promising novel target for future NSCLC treatments. PMID: 29929749 [PubMed - as supplied by publisher]
Source: Pathology, Research and Practice - June 18, 2018 Category: Pathology Authors: Dai HY, Ma Y, Da Z, Hou XM Tags: Pathol Res Pract Source Type: research

Knockdown of TRIM66 inhibits malignant behavior and epithelial-mesenchymal transition in non-small cell lung cancer
ConclusionSilence TRIM66 expression suppressed NSCLC cell proliferation, invasion, and migration. The siRNA-mediated TRIM66 silencing could block the occurrence of EMT. TRIM66 could be a promising novel target for future NSCLC treatments.
Source: Pathology Research and Practice - July 5, 2018 Category: Pathology Source Type: research