scholarly journals Effect of autophagy inhibition on chemotherapy-induced apoptosis in A549 lung cancer cells

2013 ◽  
Vol 5 (4) ◽  
pp. 1261-1265 ◽  
Author(s):  
FEIFEI LIU ◽  
DONGLEI LIU ◽  
YANG YANG ◽  
SONG ZHAO
Keyword(s):  
Lung Cancer ◽  
Cancer Cells ◽  
Lung Cancer Cells ◽  
Induced Apoptosis ◽  
Autophagy Inhibition ◽  
A549 Lung

Smad7 sensitizes A549 lung cancer cells to cisplatin-induced apoptosis through heme oxygenase-1 inhibition

2012 ◽  
Vol 420 (2) ◽  
pp. 288-292 ◽  
Author(s):  
Woo-Kwang Jeon ◽  
Hey-Young Hong ◽  
Won-Chan Seo ◽  
Kyu-Hyoung Lim ◽  
Hui-Young Lee ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Cancer Cells ◽  
Heme Oxygenase ◽  
Lung Cancer Cells ◽  
Heme Oxygenase 1 ◽  
Induced Apoptosis ◽  
A549 Lung

scholarly journals Antidepressant Drug Enhanced Trail Receptor-2 Expression and Sensitized Lung Cancer Cells to Trail-Induced Apoptosis via Inhibition of Autophagic Flux

2020 ◽  
Author(s):  
K.M.A. Zinnah ◽  
Jae-Won Seol ◽  
Sang-Youel Park
Keyword(s):  
Lung Cancer ◽  
Cell Death ◽  
Cancer Cells ◽  
Antidepressant Drug ◽  
Lung Cancer Cells ◽  
Autophagic Flux ◽  
Trail Receptor ◽  
Treatment Needs ◽  
Induced Apoptosis ◽  
Autophagy Inhibition

Autophagy, an alternative cell death mechanism, is also termed programmed cell death type II. Autophagy in cancer treatment needs to be regulated. In our study, autophagy inhibition by desipramine or the autophagy inhibitor chloroquine (CQ) enhanced tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) receptor-2 [death receptor (DR5)] expression and subsequently TRAIL-induced apoptosis in TRAIL-resistant A549 lung cancer cells. Genetic inhibition of DR5 substantially reduced desipramine-enhanced TRAIL-mediated apoptosis, proving that DR5 was required to increase TRAIL sensitivity in TRAIL-resistant cancer cells. Desipramine treatment upregulated p62 expression and promoted conversion of light chain 3 (LC3)-I to its lipid-conjugated form, LC3-II, indicating that autophagy inhibition occurred at the final stages of autophagic flux. Transmission electron microscopy analysis showed the presence of condensed autophagosomes, which resulted from the late stages of autophagy inhibition by desipramine. TRAIL, in combination with desipramine or CQ, augmented the expression of apoptosis-related proteins cleaved caspase-8 and cleaved caspase-3. Our results contributed to the understanding of the mechanism underlying the synergistic anti-cancer effect of desipramine and TRAIL and presented a novel mechanism of DR5 upregulation. These findings demonstrated that autophagic flux inhibition by desipramine potentiated TRAIL-induced apoptosis, suggesting that appropriate regulation of autophagy is required for sensitizing TRAIL-resistant cancer cells to TRAIL-mediated apoptosis.

Glossogin, a novel phenylpropanoid from Glossogyne tenuifolia, induced apoptosis in A549 lung cancer cells

2008 ◽  
Vol 46 (12) ◽  
pp. 3785-3791 ◽  
Author(s):  
Hsia-Fen Hsu ◽  
Jer-Yiing Houng ◽  
Chih-Feng Kuo ◽  
Nina Tsao ◽  
Yang-Chang Wu
Keyword(s):  
Lung Cancer ◽  
Cancer Cells ◽  
Lung Cancer Cells ◽  
Induced Apoptosis ◽  
Glossogyne Tenuifolia ◽  
A549 Lung

scholarly journals Shikonin Induces Apoptosis, Necrosis, and Premature Senescence of Human A549 Lung Cancer Cells through Upregulation of p53 Expression

2015 ◽  
Vol 2015 ◽  
pp. 1-13 ◽  
Author(s):  
Yueh-Chiao Yeh ◽  
Tsun-Jui Liu ◽  
Hui-Chin Lai
Keyword(s):  
Lung Cancer ◽  
Cancer Cells ◽  
Cell Fate ◽  
Specific Inhibitor ◽  
Lung Cancer Cells ◽  
Premature Senescence ◽  
Dependent Manner ◽  
P53 Expression ◽  
Induced Apoptosis ◽  
A549 Lung

Shikonin, a natural naphthoquinone pigment isolated fromLithospermum erythrorhizon, has been reported to suppress growth of various cancer cells. This study was aimed to investigate whether this chemical could also inhibit cell growth of lung cancer cells and, if so, works via what molecular mechanism. To fulfill this, A549 lung cancer cells were treated with shikonin and then subjected to microscopic, biochemical, flow cytometric, and molecular analyses. Compared with the controls, shikonin significantly induced cell apoptosis and reduced proliferation in a dose-dependent manner. Specially, lower concentrations of shikonin (1–2.5 μg/mL) cause viability reduction; apoptosis and cellular senescence induction is associated with upregulated expressions of cell cycle- and apoptotic signaling-regulatory proteins, while higher concentrations (5–10 μg/mL) precipitate both apoptosis and necrosis. Treatment of cells with pifithrin-α, a specific inhibitor of p53, suppressed shikonin-induced apoptosis and premature senescence, suggesting the role of p53 in mediating the actions of shikonin on regulation of lung cancer cell proliferation. These results indicate the potential and dose-related cytotoxic actions of shikonin on A549 lung cancer cells via p53-mediated cell fate pathways and raise shikonin a promising adjuvant chemotherapeutic agent for treatment of lung cancer in clinical practice.

Pharbitis Nil (PN) induces apoptosis and autophagy in lung cancer cells and autophagy inhibition enhances PN-induced apoptosis

2017 ◽  
Vol 208 ◽  
pp. 253-263 ◽  
Author(s):  
Hyun Jin Jung ◽  
Ju-Hee Kang ◽  
Seungho Choi ◽  
Youn Kyoung Son ◽  
Kang Ro Lee ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Cancer Cells ◽  
Lung Cancer Cells ◽  
Pharbitis Nil ◽  
Induced Apoptosis ◽  
Autophagy Inhibition

Effects of Banxia Xiexin Decoction (半夏泻心汤) on Cisplatin-Induced Apoptosis of Human A549 Lung Cancer Cells

2018 ◽  
Vol 24 (6) ◽  
pp. 436-441 ◽  
Author(s):  
Ha-Rim Kim ◽  
Guem-San Lee ◽  
Mi-Seong Kim ◽  
Do-Gon Ryu ◽  
Hong-Seob So ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Cancer Cells ◽  
Lung Cancer Cells ◽  
Banxia Xiexin Decoction ◽  
Induced Apoptosis ◽  
Human A549 ◽  
A549 Lung

Novel morpholin-3-one derivatives induced apoptosis and elevated the level of P53 and Fas in A549 lung cancer cells

2007 ◽  
Vol 15 (11) ◽  
pp. 3889-3895 ◽  
Author(s):  
Qiuxia He ◽  
Xingshang Zhu ◽  
Mei Shi ◽  
Baoxiang Zhao ◽  
Jing Zhao ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Cancer Cells ◽  
Lung Cancer Cells ◽  
Induced Apoptosis ◽  
A549 Lung
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