scholarly journals Pharmacological Modulation of Cytotoxicity and Cellular Uptake of Anti-cancer Drugs by PDE5 Inhibitors in Lung Cancer Cells

2013 ◽  
Vol 31 (1) ◽  
pp. 86-96 ◽  
Author(s):  
Qing Li ◽  
Yan Shu
Keyword(s):  
Lung Cancer ◽  
Cancer Cells ◽  
Cellular Uptake ◽  
Lung Cancer Cells ◽  
Cancer Drugs ◽  
Pde5 Inhibitors ◽  
Pharmacological Modulation ◽  
Anti Cancer

scholarly journals Ursolic acid exerts anti-cancer activity by suppressing vaccinia-related kinase 1-mediated damage repair in lung cancer cells

2015 ◽  
Vol 5 (1) ◽  
Author(s):  
Seong-Hoon Kim ◽  
Hye Guk Ryu ◽  
Juhyun Lee ◽  
Joon Shin ◽  
Amaravadhi Harikishore ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Cancer Cells ◽  
Ursolic Acid ◽  
Catalytic Domain ◽  
Lung Cancer Cells ◽  
Cancer Drugs ◽  
Lung Cancer Patients ◽  
Mitotic Kinases ◽  
Anti Cancer ◽  
Cancer Agent

Abstract Many mitotic kinases have been targeted for the development of anti-cancer drugs and inhibitors of these kinases have been expected to perform well for cancer therapy. Efforts focused on selecting good targets and finding specific drugs to target are especially needed, largely due to the increased frequency of anti-cancer drugs used in the treatment of lung cancer. Vaccinia-related kinase 1 (VRK1) is a master regulator in lung adenocarcinoma and is considered a key molecule in the adaptive pathway, which mainly controls cell survival. We found that ursolic acid (UA) inhibits the catalytic activity of VRK1 via direct binding to the catalytic domain of VRK1. UA weakens surveillance mechanisms by blocking 53BP1 foci formation induced by VRK1 in lung cancer cells and possesses synergistic anti-cancer effects with DNA damaging drugs. Taken together, UA can be a good anti-cancer agent for targeted therapy or combination therapy with DNA damaging drugs for lung cancer patients.

scholarly journals An Anti-Cancer Peptide LVTX-8 Inhibits the Proliferation and Migration of Lung Tumor Cells by Regulating Causal Genes’ Expression in p53-Related Pathways

Toxins ◽  
2020 ◽  
Vol 12 (6) ◽  
pp. 367
Author(s):  
Peng Zhang ◽  
Yujie Yan ◽  
Junting Wang ◽  
Xiaoping Dong ◽  
Gaihua Zhang ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Cell Growth ◽  
Cancer Cells ◽  
Cancer Cell ◽  
High Efficiency ◽  
Lung Tumor ◽  
Lung Cancer Cells ◽  
Helical Conformation ◽  
Anti Cancer ◽  
And Migration

Spider venom has been found to show its anticancer activity in a variety of human malignancies, including lung cancer. In this study, we investigated the anti-cancer peptide toxin LVTX-8, with linear amphipathic alpha-helical conformation, designed and synthesized from the cDNA library of spider Lycosa vittata. Multiple cellular methods, such as CCK-8 assay, flow cytometry, colony formation assay, Transwell invasion and migration assay, were performed to detect peptide-induced cell growth inhibition and anti-metastasis in lung cancer cells. Our results demonstrated that LVTX-8 displayed strong cytotoxicity and anti-metastasis towards lung cancer in vitro. Furthermore, LVTX-8 could suppress the growth and metastasis of lung cancer cells (A549 and H460) in nude mouse models. Transcriptomics, integrated with multiple bioinformatics analysis, suggested that the molecular basis of the LVTX-8-mediated inhibition of cancer cell growth and metastasis manifested in two aspects: Firstly, it could restrain the activity of cancer cell division and migration through the functional pathways, including “p53 hypoxia pathway” and “integrin signaling”. Secondly, it could regulate the expression level of apoptotic-related proteins, which may account for programmed apoptosis of cancer cells. Taken together, as an anticancer peptide with high efficiency and acceptable specificity, LVTX-8 may become a potential precursor of a therapeutic agent for lung cancer in the future.

scholarly journals Erratum: Corrigendum: Ursolic acid exerts anti-cancer activity by suppressing vaccinia-related kinase 1-mediated damage repair in lung cancer cells

2015 ◽  
Vol 5 (1) ◽  
Author(s):  
Seong-Hoon Kim ◽  
Hye Guk Ryu ◽  
Juhyun Lee ◽  
Joon Shin ◽  
Amaravadhi Harikishore ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Cancer Cells ◽  
Ursolic Acid ◽  
Lung Cancer Cells ◽  
Damage Repair ◽  
Anti Cancer ◽  
Cancer Activity

ErbB4 increases the proliferation potential of human lung cancer cells and its blockage can be used as a target for anti-cancer therapy

2006 ◽  
Vol 119 (2) ◽  
pp. 269-274 ◽  
Author(s):  
Alex Starr ◽  
Joel Greif ◽  
Akiva Vexler ◽  
Maia Ashkenazy-Voghera ◽  
Valery Gladesh ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Cancer Therapy ◽  
Cancer Cells ◽  
Human Lung ◽  
Lung Cancer Cells ◽  
Human Lung Cancer ◽  
Anti Cancer ◽  
Human Lung Cancer Cells ◽  
Proliferation Potential

scholarly journals Comparative Proteomic Analysis of Anti-Cancer Mechanism by Periplocin Treatment in Lung Cancer Cells

2014 ◽  
Vol 33 (3) ◽  
pp. 859-868 ◽  
Author(s):  
Zejun Lu ◽  
Qi Song ◽  
Jinliang Yang ◽  
Xiangfei Zhao ◽  
Xinhong Zhang ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Cancer Cells ◽  
Proteomic Analysis ◽  
Lung Cancer Cells ◽  
Comparative Proteomic Analysis ◽  
Anti Cancer

scholarly journals Albanol B from Mulberries Exerts Anti-Cancer Effect through Mitochondria ROS Production in Lung Cancer Cells and Suppresses In Vivo Tumor Growth

2020 ◽  
Vol 21 (24) ◽  
pp. 9502
Author(s):  
Thanh Nam Phan ◽  
Okwha Kim ◽  
Manh Tuan Ha ◽  
Cheol Hwangbo ◽  
Byung-Sun Min ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Cell Cycle ◽  
Cell Cycle Arrest ◽  
Cancer Cells ◽  
Cyclin B1 ◽  
Lung Cancer Cells ◽  
Ros Production ◽  
Cycle Arrest ◽  
Mitochondrial Ros ◽  
Anti Cancer

Albanol B (ABN-B), an arylbenzofuran derivative isolated from mulberries, has been shown to have anti-Alzheimer’s disease, anti-bacterial and antioxidant activities. The aim of this study was to investigate the anti-cancer effect of this compound against lung cancer cells. The results show that ABN-B inhibited the proliferation of four human lung cancer cell lines (A549, BZR, H1975, and H226) and induced apoptosis, based on the cleavage of caspase-7 and PARP (poly (ADP-ribose) polymerase), as well as the downregulation of Bcl-2. ABN-B also induced cell cycle arrest at G2/M by down-regulating the expression of CKD1 (cyclin-dependent kinase 1) and cyclin B1, but up-regulating p21 (cyclin-dependent kinase inhibitor 1) expression. Notably, ABN-B increased the production of mitochondrial reactive oxygen species (ROS); however, treatment with mito-TEMPO (a specific mitochondrial antioxidant) blocked ABN-B-induced cell cycle arrest at G2/M and apoptosis, as well as the up-regulation of p21 and down-regulation of CDK1 and cyclin B1 induced by ABN-B. At the molecular level, ABN-B-induced mitochondrial ROS production increased the phosphorylation levels of AKT (protein kinase B) and ERK1/2 (extracellular signal-regulated kinase 1/2), while the inhibition of these kinases blocked the ABN-B-induced up-regulation of p21 and down-regulation of CDK1 and cyclin B1. Moreover, ABN-B significantly suppressed tumor growth in Ex-3LL (Lewis lung carcinoma) tumor-bearing mice. Taken together, these results suggest that ABN-B can exert an anti-cancer effect by inducing apoptosis and cell cycle arrest at G2/M through mitochondrial ROS production in lung cancer cells.

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