scholarly journals Hydrogen peroxide inhibits the growth of lung cancer cells via the induction of cell death and G1‑phase arrest

2018 ◽  
Author(s):  
Woo Park
Keyword(s):  
Lung Cancer ◽  
Hydrogen Peroxide ◽  
Cell Death ◽  
Cancer Cells ◽  
Lung Cancer Cells ◽  
G1 Phase ◽  
Phase Arrest ◽  
G1 Phase Arrest

Inhibitory Effect of Damulin B from Gynostemma pentaphyllum on Human Lung Cancer Cells

Planta Medica ◽  
2018 ◽  
Vol 85 (05) ◽  
pp. 394-405 ◽  
Author(s):  
Shao-Fang Xing ◽  
Lin-Hua Liu ◽  
Ma-Li Zu ◽  
Man Lin ◽  
Xin-Fang Zhai ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Cancer Cells ◽  
Human Lung ◽  
Inhibitory Effect ◽  
Lung Cancer Cells ◽  
Human Lung Cancer ◽  
G1 Phase ◽  
Phase Arrest ◽  
G1 Phase Arrest ◽  
Human Lung Cancer Cells

AbstractDamulin B, a dammarane-type saponin from steamed Gynostemma pentaphyllum, exhibits the strongest activity against human lung carcinoma A549 cells among the isolated active saponins. In this study, the structure-activity relationship of a series of saponin compounds was discussed. The inhibitory effect of damulin B on human lung cancer A549 and H1299 cells was investigated from apoptosis, cell cycle, and migration aspects. In vitro, human lung cancer cells were more susceptible to damulin B treatment than human normal fibroblasts. Damulin B exhibited a strong cytotoxic effect, as evidenced by the increase of apoptosis rate, reduction of mitochondrial membrane potential (MMP), generation of reactive oxygen species, and G0/G1 phase arrest. Furthermore, damulin B activated the following: both intrinsic and extrinsic apoptosis pathways along with early G1 phase arrest via the upregulation of the Bax, Bid, tBid, cleaved caspase-8, and p53 expression levels; downregulation of the procaspase-8/-9, CDK4, CDK6, and cyclin D1 expression levels; and more release of cytochrome c in the cytoplasm. In addition, antimigratory activities and suppressive effects on metastasis-related factors, such as MMP-2 and MMP-9, accompanied by the upregulation of IL-24 were revealed. Altogether, the results proved that damulin B could inhibit human lung cancer cells by inducing apoptosis, blocking the cell cycle at early G0/G1 phase and suppressing the migration. Hence, damulin B has potential therapeutic efficacy against lung cancer.

scholarly journals Lentivirus-mediated knockdown of TSP50 suppresses the growth of non-small cell lung cancer cells via G0/G1 phase arrest

2016 ◽  
Vol 35 (6) ◽  
pp. 3409-3418 ◽  
Author(s):  
WEN-LIANG QIAO ◽  
HAI-YANG HU ◽  
BO-WEN SHI ◽  
LI-JUAN ZANG ◽  
WEI JIN ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Small Cell Lung Cancer ◽  
Cancer Cells ◽  
Cell Lung Cancer ◽  
Small Cell ◽  
Lung Cancer Cells ◽  
G1 Phase ◽  
Small Cell Lung ◽  
Phase Arrest ◽  
G1 Phase Arrest

γ-Glutamylcyclotransferase Knockdown Inhibits Growth of Lung Cancer Cells Through G0/G1 Phase Arrest

2015 ◽  
Vol 30 (5) ◽  
pp. 211-216 ◽  
Author(s):  
Zhifeng Lin ◽  
Liwen Xiong ◽  
Jianhua Zhou ◽  
Jin Wang ◽  
Zhao Li ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Cancer Cells ◽  
Lung Cancer Cells ◽  
G1 Phase ◽  
Phase Arrest ◽  
G1 Phase Arrest

Reducing autophagy and inducing G1 phase arrest by aloperine enhances radio-sensitivity in lung cancer cells

2017 ◽  
Author(s):  
Zhijie Xu ◽  
Yuanliang Yan ◽  
Shuangshuang Zeng ◽  
Long Qian ◽  
Shuang Dai ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Cancer Cells ◽  
Lung Cancer Cells ◽  
G1 Phase ◽  
Phase Arrest ◽  
G1 Phase Arrest ◽  
Radio Sensitivity

scholarly journals Novel ferrocenyl derivatives exert anti-cancer effect in human lung cancer cells in vitro via inducing G1-phase arrest and senescence

2013 ◽  
Vol 34 (7) ◽  
pp. 960-968 ◽  
Author(s):  
Ying Li ◽  
Han-lin Ma ◽  
Lei Han ◽  
Wei-yong Liu ◽  
Bao-xiang Zhao ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Cancer Cells ◽  
Human Lung ◽  
Human Lung Cancer ◽  
G1 Phase ◽  
Phase Arrest ◽  
G1 Phase Arrest ◽  
Anti Cancer ◽  
Human Lung Cancer Cells

scholarly journals Combination of Arsenic Trioxide and Valproic Acid Efficiently Inhibits Growth of Lung Cancer Cells via G2/M-Phase Arrest and Apoptotic Cell Death

2020 ◽  
Vol 21 (7) ◽  
pp. 2649
Author(s):  
Hyun Kyung Park ◽  
Bo Ram Han ◽  
Woo Hyun Park
Keyword(s):  
Lung Cancer ◽  
Cell Death ◽  
Cancer Cells ◽  
Apoptotic Cell ◽  
Apoptotic Cell Death ◽  
Lung Cancer Cells ◽  
Phase Arrest ◽  
Anti Cancer ◽  
M Phase

Arsenic trioxide (ATO; As2O3) has anti-cancer effects in various solid tumors as well as hematological malignancy. Valproic acid (VPA), which is known to be a histone deacetylase inhibitor, has also anti-cancer properties in several cancer cells including lung cancer cells. Combined treatment of ATO and VPA (ATO/VPA) could synergistically enhance anti-cancer effects and reduce ATO toxicity ATO. In this study, the combined anti-cancer effects of ATO and VPA (ATO/VPA) was investigated in NCI-H460 and NCI-H1299 lung cancer cells in vitro and in vivo. A combination of 3 μM ATO and 3 mM VPA (ATO/VPA) strongly inhibited the growths of both lung cancer cell types. DNA flow cytometry indicated that ATO/VPA significantly induced G2/M-phase arrest in both cell lines. In addition, ATO/VPA strongly increased the percentages of sub-G1 cells and annexin V-FITC positive cells in both cells. However, lactate dehydrogenase (LDH) release from cells was not increased in ATO/VPA-treated cells. In addition, ATO/VPA increased apoptosis in both cell types, accompanied by loss of mitochondrial membrane potential (MMP, ∆Ψm), activation of caspases, and cleavage of anti-poly ADP ribose polymerase-1. Moreover, a pan-caspase inhibitor, Z-VAD, significantly reduced apoptotic cell death induced by ATO/VPA. In the xenograft model, ATO/VPA synergistically inhibited growth of NCI-H460-derived xenograft tumors. In conclusion, the combination of ATO/VPA effectively inhibited the growth of lung cancer cells through G2/M-phase arrest and apoptotic cell death, and had a synergistic antitumor effect in vivo.

scholarly journals Tubulin acetylation enhances lung cancer resistance to paclitaxel-induced cell death through Mcl-1 stabilization

2021 ◽  
Vol 7 (1) ◽  
Author(s):  
Onsurang Wattanathamsan ◽  
Rawikorn Thararattanobon ◽  
Ratchanee Rodsiri ◽  
Pithi Chanvorachote ◽  
Chanida Vinayanuwattikun ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Cell Death ◽  
Cancer Cells ◽  
Trichostatin A ◽  
Primary Lung Cancer ◽  
Lung Cancer Cells ◽  
Cancer Resistance ◽  
Apoptosis Resistance ◽  
Tubulin Acetylation ◽  
Cancer Aggressiveness

AbstractThe posttranslational modifications (PTMs) of microtubules have been reported to play an important role in cancer aggressiveness, including apoptosis resistance. In this study, we aimed to investigate the biological role of microtubule PTMs in the regulation of paclitaxel responsiveness. The acetylated tubulin (Ace-tub) level was strongly associated with paclitaxel sensitivity, as observed in patient-derived primary lung cancer cells and xenografted immunodeficient mice. We showed that paclitaxel-resistant H460 lung cancer cells, generated by a stepwise increase in paclitaxel, exhibited markedly increased tubulin acetylation and consequently acquired paclitaxel resistance. Upregulation of tubulin acetylation by overexpression of α-tubulin acetyltransferase 1 wild-type (αTAT1wt), an enzyme required for acetylation, or by treatment with trichostatin A (TSA), a histone deacetylase 6 (HDAC6) inhibitor, significantly attenuated paclitaxel-induced apoptosis. Investigation of the underlying mechanism revealed that the levels of antiapoptotic Mcl-1 appeared to increase in αTAT1wt-overexpressing and TSA-treated cells compared to control cells, whereas the levels of other antiapoptotic regulatory proteins were unchanged. On the other hand, decreased tubulin acetylation by αTAT1 RNA interference downregulated Mcl-1 expression in patient-derived primary lung cancer and paclitaxel-resistant lung cancer cells. A microtubule sedimentation assay demonstrated that Mcl-1 binds to microtubules preferentially at Ace-type, which prolongs the Mcl-1 half-life (T1/2). Furthermore, immunoprecipitation analysis revealed that polyubiquitination of Mcl-1 was extensively decreased in response to TSA treatment. These data indicate that tubulin acetylation enhances the resistance to paclitaxel-induced cell death by stabilizing Mcl-1 and protecting it from ubiquitin–proteasome-mediated degradation.

A synthetic 2,3-diarylindole induces cell death via apoptosis and autophagy in A549 lung cancer cells

2016 ◽  
Vol 26 (9) ◽  
pp. 2119-2123 ◽  
Author(s):  
Thanya Rukkijakan ◽  
Lukana Ngiwsara ◽  
Kriengsak Lirdprapamongkol ◽  
Jisnuson Svasti ◽  
Nared Phetrak ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Cell Death ◽  
Cancer Cells ◽  
Lung Cancer Cells ◽  
A549 Lung
Sign in / Sign up

Export Citation Format

Share Document