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Source: Biochemical Pharmacology
Cancer: Lung Cancer

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Total 7 results found since Jan 2013.

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

Activation of notch 3/c-MYC/CHOP axis regulates apoptosis and promotes sensitivity of lung cancer cells to mTOR inhibitor everolimus.
Abstract The mammalian target of rapamycin (mTOR) pathway converges diverse environmental cues to support the lung cancer growth and survival. However, the mTOR-targeted mono-therapy does not achieve expected therapeutic effect. Here, we revealed that fangchinoline (FCL), an active alkaloid that purified from the traditional Chinese medicine Stephania tetrandra S. Moore, enhanced the anti-lung cancer effect of mTOR inhibitor everolimus (EVE). The combination of EVE and FCL was effective to activate Notch 3, and subsequently evoked its downstream target c-MYC. The blockage of Notch 3 signal by the molecular inhibit...
Source: Biochemical Pharmacology - March 18, 2020 Category: Drugs & Pharmacology Authors: Li T, Xu XH, Guo X, Yuan T, Tang ZH, Jiang XM, Xu YL, Zhang LL, Chen X, Zhu H, Shi JJ, Lu JJ Tags: Biochem Pharmacol Source Type: research

Hydrogen sulfide modulates epithelial-mesenchymal transition and angiogenesis in non-small cell lung cancer via HIF-1 α activation.
Hydrogen sulfide modulates epithelial-mesenchymal transition and angiogenesis in non-small cell lung cancer via HIF-1α activation. Biochem Pharmacol. 2019 Dec 20;:113775 Authors: Wang M, Yan J, Cao X, Hua P, Li Z Abstract Hydrogen sulfide (H2S) has been frequently implicated in tumor progression. However, the exact regulation mechanism of H2S in human non-small cell lung cancer (NSCLC) has not been fully elucidated. Here, analysis of NSCLC biopsies and adjacent non-tumor tissues revealed selectively high levels of endogenous H2S-producing enzymes, cystathionine-beta-synthase (CBS), cystathionine-gamm...
Source: Biochemical Pharmacology - December 19, 2019 Category: Drugs & Pharmacology Authors: Wang M, Yan J, Cao X, Hua P, Li Z Tags: Biochem Pharmacol Source Type: research

Salinomycin enhances cisplatin-induced cytotoxicity in human lung cancer cells via down-regulation of AKT-dependent thymidylate synthase expression.
In this study, we showed that salinomycin (0.5 - 2 μg/mL) treatment down-regulating of TS expression in an AKT inactivation manner in two NSCLC cell lines, human lung adenocarcinoma A549 and squamous cell carcinoma H1703 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 salinomycin. A combination of cisplatin and salinomycin resulted in synergistic enhancement of cytotoxicity and cell growth inhibition in NSCLC cells, accompanied with reduced activation of phospho-AKT, and TS expression. Overexpression ...
Source: Biochemical Pharmacology - September 21, 2016 Category: Drugs & Pharmacology Authors: Ko JC, Zheng HY, Chen WC, Peng YS, Wu CH, Wei CL, Chen JC, Lin YW Tags: Biochem Pharmacol Source Type: research

Cannabinoids increase lung cancer cell lysis by lymphokine-activated killer cells via upregulation of icam-1.
CANNABINOIDS INCREASE LUNG CANCER CELL LYSIS BY LYMPHOKINE-ACTIVATED KILLER CELLS VIA UPREGULATION OF ICAM-1. Biochem Pharmacol. 2014 Jul 25; Authors: Haustein M, Ramer R, Linnebacher M, Manda K, Hinz B Abstract Cannabinoids have been shown to promote the expression of the intercellular adhesion molecule 1 (ICAM-1) on lung cancer cells as part of their anti-invasive and antimetastatic action. Using lung cancer cell lines (A549, H460) and metastatic cells derived from a lung cancer patient, the present study addressed the impact of cannabinoid-induced ICAM-1 on cancer cell adhesion to lymphokine-activa...
Source: Biochemical Pharmacology - July 25, 2014 Category: Drugs & Pharmacology Authors: Haustein M, Ramer R, Linnebacher M, Manda K, Hinz B Tags: Biochem Pharmacol Source Type: research

CANNABINOIDs INHIBIT angiogenic capacities of Endothelial cells via release of Tissue inhibitor of matrix metalloproteinases-1 from lung cancer cells.
Abstract Cannabinoids inhibit tumor neovascularisation as part of their tumorregressive action. However, the underlying mechanism is still under debate. In the present study the impact of cannabinoids on potential tumor-to-endothelial cell communication conferring anti-angiogenesis was studied. Cellular behaviour of human umbilical vein endothelial cells (HUVEC) associated with angiogenesis was evaluated by Boyden chamber, 2-dimensional tube formation and fibrin bead assay, with the latter assessing 3-dimensional sprout formation. Viability was quantified by the WST-1 test. Conditioned media (CM) from A549 lung ca...
Source: Biochemical Pharmacology - June 26, 2014 Category: Drugs & Pharmacology Authors: Ramer R, Fischer S, Haustein M, Manda K, Hinz B Tags: Biochem Pharmacol Source Type: research

Metformin-mediated downregulation of p38 mitogen-activated protein kinase-dependent excision repair cross-complementing 1 decreases DNA repair capacity and sensitizes human lung cancer cells to paclitaxel.
Abstract Metformin, an extensively used and well-tolerated drug for treating individuals with type 2 diabetes, has recently gained significant attention as an anticancer drug. On the other hand, paclitaxel (Taxol) is a new antineoplastic drug that has shown promise in the treatment of non-small cell lung cancer (NSCLC). High expression levels of excision repair cross-complementary 1 (ERCC1) in cancers have been positively associated with the DNA repair capacity and a poor prognosis in NSCLC patients treated with platinum-containing chemotherapy. In this current study, paclitaxel was found to increase phosphorylati...
Source: Biochemical Pharmacology - December 7, 2012 Category: Drugs & Pharmacology Authors: Tseng SC, Huang YC, Chen HJ, Chiu HC, Huang YJ, Wo TY, Weng SH, Lin YW Tags: Biochem Pharmacol Source Type: research