A synthesized butyrolactone derivative in combination with chloroquine can inhibit cancer cell growth and lysosome vacuolation induced by chloroquine in A549 lung cancer cells

RSC Advances ◽  
2016 ◽  
Vol 6 (59) ◽  
pp. 54099-54101
Author(s):  
Xin-Peng Chen ◽  
Chuan-Dong Fan ◽  
Le Su ◽  
Bao-Xiang Zhao ◽  
Jun-Ying Miao
Keyword(s):  
Lung Cancer ◽  
Cell Growth ◽  
Atpase Activity ◽  
Cancer Cells ◽  
Cancer Cell ◽  
Lung Cancer Cells ◽  
Cancer Cell Growth ◽  
Non Coding Rna ◽  
A549 Lung

3BDO in combination with chloroquine could elevate the Na+,K+-ATPase activity and decrease the expression of competing endogenous non-coding RNA TGFB2-OT1. Therefore, ​ the combination inhibited the cells growth and lysosomal vacuolation induced by CQ.

scholarly journals Novel 2-step synthetic indole compound 1,1,3-tri(3-indolyl)cyclohexane inhibits cancer cell growth in lung cancer cells and xenograft models

Cancer ◽  
2008 ◽  
Vol 113 (4) ◽  
pp. 815-825 ◽  
Author(s):  
Ching-Hsiao Lee ◽  
Ching-Fa Yao ◽  
Sin-Ming Huang ◽  
Shengkai Ko ◽  
Yi-Hung Tan ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Cell Growth ◽  
Cancer Cells ◽  
Cancer Cell ◽  
Lung Cancer Cells ◽  
Cancer Cell Growth ◽  
Indole Compound ◽  
Xenograft Models

scholarly journals Beclin1-induced Autophagy Abrogates Radioresistance of Lung Cancer Cells by Suppressing Osteopontin

2012 ◽  
Vol 53 (3) ◽  
pp. 422-432 ◽  
Author(s):  
Seung-Hee Chang ◽  
Arash Minai-Tehrani ◽  
Ji-Young Shin ◽  
Sungjin Park ◽  
Ji-Eun Kim ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Cell Growth ◽  
Cancer Cells ◽  
Cancer Cell ◽  
Human Lung ◽  
Lung Cancer Cells ◽  
Human Lung Cancer ◽  
Lung Cancer Cell ◽  
Cancer Cell Growth ◽  
Human Lung Cancer Cells

Abstract Osteopontin (OPN) serves as an indicator of resistance to radiotherapy. However, the role of OPN in the development of acquired radioresistance in human lung cancer cells has not yet been fully elucidated. Therefore, the potential importance of OPN as a marker of lung cancer with a potential significant role in the development of radioresistance against repeated radiotherapy has prompted us to define the pathways by which OPN regulates lung cancer cell growth. In addition, autophagy has been reported to play a key role in the radiosensitization of cancer cells. Here, we report that increased OPN expression through induction of nuclear p53 following irradiation was inhibited by exogenous beclin-1 (BECN1). Our results clearly show that BECN1 gene expression led to induction of autophagy and inhibition of cancer cell growth and angiogenesis. Our results suggest that the induction of autophagy abrogated the radioresistance of the cancer cells. Interestingly, we showed that knockdown of OPN by lentivirus-mediated shRNA induced the autophagy of human lung cancer cell. Taken together, these results suggest that OPN and BECN1 can be molecular targets for overcoming radioresistance by controlling autophagy.

scholarly journals Glutamate-ammonia ligase promotes lung cancer cell growth through an enzyme-independent upregulation of CaMK2G under a glutamine-sufficient condition

2019 ◽  
Author(s):  
Jiangsha Zhao ◽  
Xiankun Zeng ◽  
Steven X. Hou
Keyword(s):  
Lung Cancer ◽  
Cell Growth ◽  
Cancer Cells ◽  
Cancer Cell ◽  
Lung Cancer Cells ◽  
Sufficient Condition ◽  
Lung Cancer Cell ◽  
Cancer Cell Growth ◽  
Calcium Calmodulin Dependent ◽  
Survival And Growth

SUMMARYGlutamate-ammonia ligase (GLUL) is highly expressed in many cancer cells. Synthesizing glutamine by its enzyme function has been found to be important for supporting cancer cell survival and growth under glutamine restriction. However, GLUL’s functions under a glutamine-sufficient condition still have not been uncovered. Here we find that GLUL is highly expressed in lung cancer cells and provides survival and growth advantages under both glutamine restriction and adequacy conditions. Knocking down GLUL can block lung cancer cell growth in an enzyme-independent way when glutamine is sufficient. Mechanistically, GLUL regulates Calcium/Calmodulin Dependent Protein Kinase II Gamma (CaMK2G) expression at the transcription level, and CaMK2G is a major mediator in controlling cell growth under GLUL. The transcriptional regulation of CaMK2G is partially mediated by SMAD4. Our data unveil a new enzyme-independent function of GLUL in lung cancer cells under a glutamine-sufficient condition.

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.

Chloroquine inhibits cell growth and induces cell death in A549 lung cancer cells

2006 ◽  
Vol 14 (9) ◽  
pp. 3218-3222 ◽  
Author(s):  
Chuandong Fan ◽  
Weiwei Wang ◽  
Baoxiang Zhao ◽  
Shangli Zhang ◽  
Junying Miao
Keyword(s):  
Lung Cancer ◽  
Cell Death ◽  
Cell Growth ◽  
Cancer Cells ◽  
Lung Cancer Cells ◽  
A549 Lung

scholarly journals TIMP-2 modulates cancer cell transcriptional profile and enhances E-cadherin/beta-catenin complex expression in A549 lung cancer cells

Oncotarget ◽  
2013 ◽  
Vol 4 (1) ◽  
pp. 163-173 ◽  
Author(s):  
Dimitra Bourboulia ◽  
HuiYing Han ◽  
Sandra Jensen-Taubman ◽  
Noah Gavil ◽  
Biju Isaac ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Cancer Cells ◽  
Cancer Cell ◽  
Transcriptional Profile ◽  
Lung Cancer Cells ◽  
Beta Catenin ◽  
A549 Lung ◽  
Complex Expression ◽  
E Cadherin

Fluorinated thiazolidinols cause cell death in A549 lung cancer cells via PI3K/AKT/mTOR and MAPK/ERK signalling pathways

MedChemComm ◽  
2016 ◽  
Vol 7 (6) ◽  
pp. 1197-1203 ◽  
Author(s):  
Ravindra M. Kumbhare ◽  
Tulshiram L. Dadmal ◽  
Dinesh Kumar ◽  
M. Janaki Ramaiah ◽  
Anudeep Kota ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Cell Death ◽  
Cancer Cells ◽  
Cancer Cell ◽  
Lung Cancer Cells ◽  
Signalling Pathways ◽  
Lung Cancer Cell ◽  
Cancer Cell Death ◽  
A549 Lung Cancer Cell ◽  
A549 Lung

Fluorinated thiazolidinols cause A549 lung cancer cell death by acting via PI3K/Akt/mTOR and MEK/ERK pathways.

Synthesis of 6-cinnamoyl-2H-benzo[b][1,4]oxazin-3(4H)-ones and their effects on A549 lung cancer cell growth

2014 ◽  
Vol 79 ◽  
pp. 95-101 ◽  
Author(s):  
Xue-Wen Zhou ◽  
Han-Lin Ma ◽  
Xuan Zhang ◽  
Shi-Yao Jing ◽  
Jun-Ying Miao ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Cell Growth ◽  
Cancer Cell ◽  
Lung Cancer Cell ◽  
Cancer Cell Growth ◽  
A549 Lung Cancer Cell ◽  
A549 Lung
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