scholarly journals A Novel Mono‐carbonyl Analogue of Curcumin Induces Apoptosis by Activating ER Stress in Non‐Small Lung Cancer Cells

2010 ◽  
Vol 24 (S1) ◽  
Author(s):  
Jian Xiao ◽  
Guang Liang ◽  
Yi Huang ◽  
Xiaokun Li ◽  
Elaine Studer ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Er Stress ◽  
Cancer Cells ◽  
Lung Cancer Cells

scholarly journals Targeted inhibition of GRP78 by HA15 promotes apoptosis of lung cancer cells accompanied by ER stress and autophagy

Biology Open ◽  
2020 ◽  
Vol 9 (11) ◽  
pp. bio053298
Author(s):  
Jingjing Wu ◽  
Youqile Wu ◽  
Xuemei Lian
Keyword(s):  
Lung Cancer ◽  
Protein Expression ◽  
Cell Viability ◽  
Er Stress ◽  
Cancer Cells ◽  
Lung Tumor ◽  
Lung Cancer Cells ◽  
Dependent Manner ◽  
Mice Model ◽  
Targeted Inhibition

ABSTRACTThis study investigated the pathophysiological role of GRP78 in the survival of lung cancer cells. Lung cancer patient data from public databases were used to analyze the expression of GRP78 and its influence on prognoses. In vivo, GRP78 protein expression was analyzed in an established urethane-induced lung tumor mouse model. In vitro, the effects of targeted inhibition of GRP78 by HA15 in lung cancer cells were assessed, with cell viability analyzed using a CCK-8 assay, cell proliferation using an EdU assay, apoptosis and cell cycle using flow cytometry, subcellular structure using electron microscopy, and relative mRNA and protein expression using RT-PCR, western blotting or immunofluorescence assays. The results showed that GRP78 was highly expressed in the lung tissue of lung cancer mice model or patients, and was associated with a poor prognosis. After inhibition of GRP78 in lung cancer cells by HA15, cell viability was decreased in a dose- and time-dependent manner, proliferation was suppressed and apoptosis promoted. Unfolded protein response signaling pathway proteins were activated, and the autophagy-related proteins and mRNAs were upregulated. Therefore, targeted inhibition of GRP78 by HA15 promotes apoptosis of lung cancer cells accompanied by ER stress and autophagy.

scholarly journals Furanodiene Induces Endoplasmic Reticulum Stress and Presents Antiproliferative Activities in Lung Cancer Cells

2012 ◽  
Vol 2012 ◽  
pp. 1-8 ◽  
Author(s):  
Wen-Shan Xu ◽  
Yuan-Ye Dang ◽  
Jia-Jie Guo ◽  
Guo-Sheng Wu ◽  
Jin-Jian Lu ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Endoplasmic Reticulum ◽  
Er Stress ◽  
Cancer Cells ◽  
Combined Treatment ◽  
Lung Cancer Cells ◽  
Chinese Medicinal Herb ◽  
Homologous Protein ◽  
D Cells

Furanodiene (FUR) is a natural terpenoid isolated fromCurcumae Rhizoma, a well-known Chinese medicinal herb that presents antiproliferation activities in several cancer cell lines. In this study, we demonstrated that FUR concentration dependently inhibits the cell proliferation of A549, NIH-H1299, and 95-D lung cancer cells.β-elemene, another terpenoid isolated fromCurcumae Rhizoma, exhibited weaker antiproliferative effects in A549 and NIH-H1299 cells and activities similar to FUR in 95-D cells. FUR significantly inhibited colony formation in A549 and 95-D cells and upregulated both the mRNA and protein expression levels of binding immunoglobulin protein (BIP) and C/EBP homologous protein (CHOP), indicating that endoplasmic reticulum (ER) stress is induced. FUR treatment led to the accumulation of CHOP in the nucleus, which further confirms induction of ER stress. Furthermore, combined treatment of FUR with paclitaxel showed significant synergetic activities in NIH-H1299 and 95-D cells, suggesting its potential roles in combination therapy. These findings provide a basis for the further study of the anticancer effectsin vivoand the internal mechanisms of FUR.

scholarly journals Novel CHOP activator LGH00168 induces necroptosis in A549 human lung cancer cells via ROS-mediated ER stress and NF-κB inhibition

2016 ◽  
Vol 37 (10) ◽  
pp. 1381-1390 ◽  
Author(s):  
Yi-ming Ma ◽  
Yan-min Peng ◽  
Qiong-hua Zhu ◽  
An-hui Gao ◽  
Bo Chao ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Er Stress ◽  
Cancer Cells ◽  
Human Lung ◽  
Lung Cancer Cells ◽  
Human Lung Cancer ◽  
Human Lung Cancer Cells

scholarly journals ER stress and autophagy are involved in the apoptosis induced by cisplatin in human lung cancer cells

2016 ◽  
Vol 35 (5) ◽  
pp. 2606-2614 ◽  
Author(s):  
SHAOMIN SHI ◽  
PING TAN ◽  
BINGDI YAN ◽  
RONG GAO ◽  
JIANJUN ZHAO ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Er Stress ◽  
Cancer Cells ◽  
Human Lung ◽  
Lung Cancer Cells ◽  
Human Lung Cancer ◽  
Human Lung Cancer Cells

The Superior Antitumor Effect of Self-Assembled Paclitaxel Nanofilaments for Lung Cancer Cells

2018 ◽  
Vol 16 (2) ◽  
pp. 171-178
Author(s):  
Mengyu He ◽  
Jiali Zhu ◽  
Na Yu ◽  
Hui Kong ◽  
Xiaoning Zeng ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Endoplasmic Reticulum ◽  
Er Stress ◽  
Cancer Cells ◽  
Antitumor Effect ◽  
Stress Proteins ◽  
A549 Cells ◽  
Lung Cancer Cells ◽  
Antitumor Effects ◽  
Self Assembled

Objectives: Paclitaxel (Ptx) has been regarded as one of the most effective chemotherapeutic drugs for lung cancers. Increasing studies focused on the nano-delivery system of Ptx due to its poor solubility and hypersensitivity. The aim of the recent study was to investigate the antitumor effects of self-assembled Ptx nano-filaments for lung cancer cells. </P><P> Methods: In the present study, we designed and synthesized novel Ptx-loaded nano-filaments through conjugation of Ptx and succinic acid (SA) (Ptx-SA, P-NFs). Non-small cell lung cancer (NSCLC) A549 and H460 cells were used for detecting the antitumor effects of P-NFs, including cytotoxicity, apoptosis, and migration. Western blotting was performed for analyzing mechanism. Results: P-NFs nano-filaments exerted superior antitumor effects against NSCLC cells compared with free Ptx using cytotoxicity tests. Furthermore, P-NFs nano-filaments were much more effective in inducing NSCLC cells apoptosis and inhibiting A549 cells migration than free Ptx. To elucidate the underlying mechanisms, the expression of apoptotic and endoplasmic reticulum (ER) stress proteins was detected. The results indicated that P-NFs nano-filaments enhanced the expression of bax/bcl-2, protein kinase RNA-like endoplasmic reticulum kinase (PERK), inositol-requiring enzyme 1&#945; (IRE1&#945;), phospho- c-Jun N-terminal kinase (p-JNK), and C/EPB homologous protein (CHOP), which suggested that the strong antitumor effect of P-NFs nano-filaments may be partially attributed to the activation ER stress. The current work demonstrated that P-NFs nano-filaments showed superior cytotoxicity of lung cancer cells, highlighting a novel profile of nano-filaments delivery systems as potential strategies for facilitating the therapeutic efficacy of Ptx in lung cancer treatment.

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