Testing the Addition of an Anti-cancer Drug, M6620, to the Usual Treatments (Carboplatin and Gemcitabine) and to Avelumab for Non-small Cell Lung Cancer

2020 ◽  
Author(s):  
Keyword(s):  
Lung Cancer ◽  
Small Cell Lung Cancer ◽  
Cell Lung Cancer ◽  
Small Cell ◽  
Cancer Drug ◽  
Small Cell Lung ◽  
Anti Cancer

scholarly journals CB13, a novel PPARγ ligand, overcomes radio-resistance via ROS generation and ER stress in human non-small cell lung cancer

2020 ◽  
Vol 11 (10) ◽  
Author(s):  
Tae Woo Kim ◽  
Da-Won Hong ◽  
Sung Hee Hong
Keyword(s):  
Lung Cancer ◽  
Cell Death ◽  
Er Stress ◽  
Small Cell Lung Cancer ◽  
Cell Lung Cancer ◽  
Small Cell ◽  
Cancer Drug ◽  
Small Cell Lung ◽  
Pparγ Agonist ◽  
Anti Cancer

Abstract Peroxisome proliferator-activated receptor gamma (PPARγ) is a well-known therapeutic target for type 2 diabetes as well as is a potential target for effective anti-cancer drug, since PPARγ ligands such as ciglitazone (Cig) frequently cause cell death in many types of cancer cells and suppress tumor growth. However, many cancer patients acquire chemo-resistance or radio-resistance after chemo or radiotherapy, and it is still unclear. In the difficulty of well-known anti-cancer drugs, we developed a novel PPARγ agonist CB13 (1-benzyl-5-(4-methylphenyl) pyrido [2,3-d]pyrimidine-2,4(1H,3H)-dione) and investigated the anti-cancer effect and cell death mechanism on human non-small cell lung cancer (NSCLC) cells. With anti-cancer effect of Cig, CB13 also causes inhibition of cell growth by decreasing cell viability, increasing the release of LDH, and increasing caspase-3, and caspase-9 activities. CB13 generates reactive oxygen species (ROS) and causes cell death via ER stress in NSCLC and radio-resistant NSCLC cells (A549R and H460R), and a combination of CB13 and radiation induces greater ER stress and cell death when compared to CB13 alone. Taken together, our results suggest that a combination of CB13 and radiation may overcome radio-resistance caused by radiotherapy.

scholarly journals Anti-Cancer Effects of REIC/Dkk-3-encoding Adenoviral Vector for the Treatment of Non-small Cell Lung Cancer

PLoS ONE ◽  
2014 ◽  
Vol 9 (2) ◽  
pp. e87900 ◽  
Author(s):  
Kazuhiko Shien ◽  
Norimitsu Tanaka ◽  
Masami Watanabe ◽  
Junichi Soh ◽  
Masakiyo Sakaguchi ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Small Cell Lung Cancer ◽  
Cell Lung Cancer ◽  
Adenoviral Vector ◽  
Small Cell ◽  
Small Cell Lung ◽  
Anti Cancer

scholarly journals Synergistic Anticancer Activity of Combined Use of Caffeic Acid with Paclitaxel Enhances Apoptosis of Non-Small-Cell Lung Cancer H1299 Cells in Vivo and in Vitro

2018 ◽  
Vol 48 (4) ◽  
pp. 1433-1442 ◽  
Author(s):  
Jie Min ◽  
Hua Shen ◽  
Wang Xi ◽  
Qing Wang ◽  
Liang Yin ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Small Cell Lung Cancer ◽  
Caffeic Acid ◽  
Cell Lung Cancer ◽  
Caspase 3 ◽  
Small Cell ◽  
Small Cell Lung ◽  
Caspase 9 ◽  
Anti Cancer

Background/Aims: Caffeic acid (CA) is known to possess multiple biological activities including anti-cancer activities. However, the molecular mechanisms underlying these activities in non-small-cell lung cancer (NSCLC) cells are not fully understood. We attempted to clarify whether CA could enhance paclitaxel (PTX)-induced cytotoxicity in H1299 cells. Methods: First, we tested the cytotoxic effects in both H1299 cells and normal human Bease-2b cells by cell proliferation experiments. Next, we use Annexin V/propidium iodide apoptosis analysis and flow cytometric analysis to investigate apoptosis and cell cycle arrest under the treatments mentioned above. To further pinpoint changes in apoptosis, we tested the caspase-associated apoptotic pathway, which involves the activities of caspase-3 and caspase-9. Moreover, apoptosis-related proteins and MAPK pathway proteins were examined by western blot. An H1299 xenograft nude mice model was used to further evaluate the tumor-suppressing effects of CA and PTX in vivo. Results: Combination treatment with low-dose CA and PTX decreased the proliferation of NSCLC H1299 cells but not normal Beas-2b cells. Flow cytometry showed that H1299 cells were arrested in the sub-G1 phase and apoptosis was significantly increased in H1299 cells after CA treatment. Caspase-3 and caspase-9 activities were both increased after CA treatment. Furthermore, CA increased the PTX-induced activation of Bax, Bid, and downstream cleaved PARP, and phosphorylation of extracellular signal regulated kinase1/2 and c-Jun NH2-terminal protein kinase1/2. An in vivo tumor-suppression assay demonstrated that CA and PTX combined treatment exerted a more effective suppressive effect on tumor growth in H1299 xenografts without causing significant adverse effects. Conclusions: Our results indicated that CA inhibited NSCLC H1299 cell growth by inducing apoptosis and CA and PTX combined produced a synergistic anti-cancer effect in H1299 cells.

Nicotinamide N-methyltransferase in Non-small Cell Lung Cancer: Promising Results for Targeted Anti-cancer Therapy

2013 ◽  
Vol 67 (3) ◽  
pp. 865-873 ◽  
Author(s):  
Davide Sartini ◽  
Stefano Morganti ◽  
Elena Guidi ◽  
Corrado Rubini ◽  
Antonio Zizzi ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Cancer Therapy ◽  
Small Cell Lung Cancer ◽  
Cell Lung Cancer ◽  
Small Cell ◽  
Small Cell Lung ◽  
Anti Cancer
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