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Cancer: Non-Small Cell Lung Cancer

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Total 1077 results found since Jan 2013.

SHP1-mediated cell cycle redistribution inhibits radiosensitivity of non-small cell lung cancer
Conclusions: SHP1 decreases the radiosensitivity of NSCLC cells through affecting cell cycle distribution. This finding could unravel the molecular mechanism involved in NSCLC radioresistance.
Source: Radiation Oncology - July 10, 2013 Category: Cancer & Oncology Authors: Rubo CaoQian DingPindong LiJun XueZhenwei ZouJing HuangGang Peng Source Type: research

PTTG1 promotes migration and invasion of human non-small cell lung cancer cells and is modulated by miR-186
This study identified both PTTG1 and miR-186 as potential anti-invasion targets for therapeutic intervention in NSCLC.
Source: Carcinogenesis - September 6, 2013 Category: Cancer & Oncology Authors: Li, H., Yin, C., Zhang, B., Sun, Y., Shi, L., Liu, N., Liang, S., Lu, S., Liu, Y., Zhang, J., Li, F., Li, W., Liu, F., Sun, L., Qi, Y. Tags: Original Manuscript 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

Combating Resistance to Anti-IGFR Antibody by Targeting the Integrin {beta}3-Src Pathway
Conclusions Increased Src activation through integrin αβ3 confers considerable resistance against anti–IGF-1R mAb-based therapies in HNSCC and NSCLC cells. Dual targeting of the IGF-1R pathway and collateral integrin β3–Src signaling module may override this resistance.
Source: JNCI - October 15, 2013 Category: Cancer & Oncology Authors: Shin, D. H., Lee, H.-J., Min, H.-Y., Choi, S. P., Lee, M.-S., Lee, J. W., Johnson, F. M., Mehta, K., Lippman, S. M., Glisson, B. S., Lee, H.-Y. Tags: Article 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

miR‐138 inhibits proliferation by targeting 3‐phosphoinositide‐dependent protein kinase‐1 in non‐small cell lung cancer cells
ConclusionsThese findings suggest miR‐138 as a potential tumor suppressor could inhibit cell proliferation by targeting PDK1 in NSCLC cells, which could be employed as a potential therapeutic target for miRNA‐based NSCLC therapy.
Source: The Clinical Respiratory Journal - January 9, 2014 Category: Respiratory Medicine Authors: Xian‐wei Ye, Hong Yu, Yan‐kun Jin, Xiao‐ting Jing, Mei Xu, Zi‐fen Wan, Xiang‐yan Zhang Tags: Original Article 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

Upregulation of COX-2 in the lung cancer promotes overexpression of multidrug resistance protein 4 (MRP4) via PGE2-dependent pathway.
In conclusion, the present study suggests that overexpression of MRP4 in lung cancer may be attributable to COX-2 upregulation via a PGE2-dependent pathway. PMID: 24909729 [PubMed - as supplied by publisher]
Source: European Journal of Pharmaceutical Sciences - June 5, 2014 Category: Drugs & Pharmacology Authors: Maeng HJ, Lee WJ, Jin QR, Jang J, Shim WS Tags: Eur J Pharm Sci Source Type: research

Repression of phosphoinositide-dependent protein kinase 1 expression by ciglitazone via Egr-1 represents a new approach for inhibition of lung cancer cell growth
Conclusion: Collectively, our results demonstrate that ciglitazone inhibits PDK1 expression through AMPKalpha-mediated induction of Egr-1 and Egr-1 binding to the specific DNA site in the PDK1 gene promoter, which is independent of PPARgamma. Activation of AMPKalpha by metformin enhances the effect of ciglitazone. In turn, this leads to inhibition of NSCLC cell proliferation.
Source: Epidemiologic Perspectives and Innovations - June 13, 2014 Category: Epidemiology Authors: SWei Sunny HannQing TangFang ZhengShunyu ZhaoJianping ChenZhiYu Wang Source Type: research

Nicotine-mediated invasion and migration of non-small cell lung carcinoma cells by modulating STMN3 and GSPT1 genes in an ID1-dependent manner
Conclusions: Collectively, our data suggests that nicotine and EGF induce genes such as STMN3 and GSPT1 to promote the proliferation, invasion and migration of NSCLC, thus enhancing their tumorigenic properties. These studies thus reveal a central role for ID1 and its downstream targets in facilitating lung cancer progression.
Source: Molecular Cancer - July 16, 2014 Category: Cancer & Oncology Authors: Sajitha NairNamrata Bora-SinghalDeepak PerumalSrikumar Chellappan Source Type: research

Btbd7 contributes to reduced E-cadherin expression and predicts poor prognosis in non-small cell lung cancer
Conclusions: Btbd7 contributes to reduced expression of E-cadherin and may be a promising cancer marker in non-small cell lung cancer.
Source: BMC Cancer - September 24, 2014 Category: Cancer & Oncology Authors: Chuifeng FanYuan MiaoXiupeng ZhangDi LiuGuiyang JiangXuyong LinQiang HanLan LuanZhonghai XuEnhua Wang 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 2332: Oncogenic mutant KRAS modulates EZH2 expression through MEK-ERK signaling by remodeling gene expression in NSCLC
In this study, we investigated whether pharmacological disruption of signaling MEK-ERK pathway would affect EZH2 expression in a panel of NSCLC cell lines with and without KRAS mutation. Moreover, we analyzed the transcriptome expression following knockdown of EZH2 expression in NSCLC cell lines with different types of KRAS mutations. Methods. NSCLC cell lines were treated with different doses of MEK inhibitor AZD6244 (0, 0.5 and 1μM) and the expressions of EZH2, MEK and MAPK were determined by Western-blots. Cell lines were transfected with gene-specific EZH2 siRNA and control siRNA. Gene expression profiling was perform...
Source: Cancer Research - September 30, 2014 Category: Cancer & Oncology Authors: Riquelme, E. M., Shen, L., Wang, J., Behrens, C., Minna, J. D., Wistuba, I. I. Tags: Molecular and Cellular Biology Source Type: research

Abstract 2485: Secretome signature associated with TITF1/NKX2-1-negative non-small cell lung cancer
Conclusion: Our findings suggest functional relevance of SRGN in tumor microenvironment and tumor aggressiveness in TITF1/NKX2-1-negative NSCLC. Validation study for plasma levels of CXCL1 and CXCL5 in NSCLC subjects is now on-going. Citation Format: Ayumu Taguchi, Muge Celiktas, Dhillon Dilsher, Qing Zhang, Chee-Hong Wong, Alice Chin, Adi Gazdar, Samir Hanash. Secretome signature associated with TITF1/NKX2-1-negative non-small cell lung cancer. [abstract]. In: Proceedings of the 105th Annual Meeting of the American Association for Cancer Research; 2014 Apr 5-9; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2014;74(19...
Source: Cancer Research - September 30, 2014 Category: Cancer & Oncology Authors: Taguchi, A., Celiktas, M., Dilsher, D., Zhang, Q., Wong, C.-H., Chin, A., Gazdar, A., Hanash, S. Tags: Cancer Chemistry Source Type: research

Abstract 2622: New therapeutic strategies in neuroblastoma: combined targeting of a novel tyrosine kinase inhibitor and liposomal siRNAs against ALK
The anaplastic lymphoma kinase (ALK), a tyrosine kinase receptor involved in the genesis of several human cancers, is a promising therapeutic target in Neuroblastoma (NB). Many studies on sporadic cases with advanced NB have shown ALK mutated or highly expressed independently of its genetic status (mutated, amplified, wild-type) and its pivotal role in NB growth and survival. As ALK is currently considered a master driver of NB oncogenesis, the use of therapies inhibiting ALK represents a suitable treatment option. The ALK inhibitor Crizotinib was recently approved for the treatment of advanced NSCLC patient. However, as o...
Source: Cancer Research - September 30, 2014 Category: Cancer & Oncology Authors: Paolo, D. D., Emionite, L., Liu, G., Cilli, M., Fiore, A. D., Brignole, C., Liang, C., Pastorino, F., Gibbons, J., Ponzoni, M., Perri, P. Tags: Experimental and Molecular Therapeutics Source Type: research