Bufalin Alters Gene Expressions Associated DNA Damage,  Cell Cycle, and Apoptosis in Human Lung Cancer NCI-H460 Cells in Vitro

Apigenin (4,5,7-trihydroxyflavone), a promising chemopreventive agent presented in fruits and vegetables, has been shown to induce cell cycle arrest and apoptosis in many types of human cancer cell lines. However, there is no available information to address the effects of apigenin on human lung cancer H460 cells. In the present studies, H460 cells were treated with apigenin for different time and then were analyzed for the morphological changes, induction of apoptosis, protein levels associated with apoptosis and results in dose-dependent induction of morphological changes, decrease in the percentage of viability, induced DNA damage and apoptosis; down-modulation of the protein expression of Bid, Bcl-2, procaspase-8; up-regulation of protein levels of Bax, caspase-3, AIF, cytochrome c, GRP78 and GADD153; decreased the levels of mitochondrial membrane potential and increased the productions of reactive oxygen species (ROS) and Ca2+ in H460 cells. Taken together, this is the first systematic in vitro study showing the involvement of apoptosis regulatory proteins as potential molecular targets of apigenin in human lung cancer H460 cells.

Download Full-text

Abstract 684: Trifluoperazine modulates DNA damage-induced cell death in human lung cancer cells through inhibition of DNA repair, cell cycle delays, and augmentation of pro-apoptotic signaling

10.1158/1538-7445.am10-684 ◽

2010 ◽

Author(s):

Dali Zong ◽

Petra Hååg ◽

Ihor Yakymovych ◽

Rolf Lewensohn ◽

Kristina Viktorsson

Keyword(s):

Lung Cancer ◽

Cell Cycle ◽

Dna Damage ◽

Cell Death ◽

Dna Repair ◽

Cancer Cells ◽

Human Lung ◽

Human Lung Cancer ◽

Apoptotic Signaling ◽

Human Lung Cancer Cells

Download Full-text

In vitro sequence-dependent interaction between paclitaxel and gefitinib in human lung cancer cell lines

Journal of Clinical Oncology ◽

10.1200/jco.2009.27.15_suppl.e22025 ◽

2009 ◽

Vol 27 (15_suppl) ◽

pp. e22025-e22025

Author(s):

H. Cheng ◽

Y. Wu ◽

S. An ◽

S. Dong ◽

H. Chen ◽

...

Keyword(s):

Lung Cancer ◽

Cell Cycle ◽

Cell Lines ◽

Human Lung ◽

Human Lung Cancer ◽

Lung Cancer Cell ◽

First Line ◽

Reverse Sequence ◽

Egfr Tki

e22025 Background: Cytotoxicity chemotherapy has been standard first line treatment for advanced NSCLC. Clinical trials comparing first line EGFR TKI therapy over cytotoxicity chemotherapy are under investigation in phase III trials. The aim of this study is to test the hypothesis that paclitaxel followed by gefitinib would be superior to the opposite order in EGFR TKI resistant cell lines because of cell signaling pathway and cell cycle interaction. Methods: we have used EGFR-TKI resistant human lung cancer cell lines A549, H1975 and H1650 as an in vitro model for defining the differential effects of opposite sequence of combination of cytotoxic drug and anti- EGFR agents on cell growth, signaling pathway, cell cycle distribution and induction of apoptosis. Results: Paclitaxel 24 hours followed by gefitinib 72 hours in A549, H1975 and H1650 cells produced synergistic effects, while the reverse sequence produced antagonistic effects. Exposure to paclitaxel resulted in an increased pEGFR and pAKT level, this increase of phosphorylation can be inhibited by the following gefitinib exposure, while the reverse sequence resulted in no change in EGFR and AKT phosphorylation. We confirmed that gefitinib arrested the cells in G1, paclitaxel arrested cells in S phase. The sequence of paclitaxel followed by gefitinib cause cells arrested in G1, while the reverse sequence cause cells arrested in S and G2 phase. Conclusions: These findings suggest that the sequence of paclitaxel followed by gefitinib may be superior to the reverse sequence in gefitinib resistant NSCLC, and support the investigation of these sequential treatment in the clinical setting. This work was supported by the grants from the National Natural Science Foundation of China (No. 30772531). No significant financial relationships to disclose.

Download Full-text

Anticancer Activity and Apoptotic Effects of Bulnesia sarmienti Against Human Lung Cancer H460 Cells

Oncology Research Featuring Preclinical and Clinical Cancer Therapeutics ◽

10.3727/096504009x12596189659321 ◽

2009 ◽

Vol 18 (5) ◽

pp. 259-267 ◽

Cited By ~ 5

Author(s):

Mohammad Lalmoddin Mollah ◽

Jae-Chan Song ◽

Chang-Ho Park ◽

Gee-Dong Lee ◽

Joo-Heon Hong ◽

...

Keyword(s):

Lung Cancer ◽

Anticancer Activity ◽

Human Lung ◽

Human Lung Cancer ◽

H460 Cells ◽

Apoptotic Effects

Download Full-text

Overexpression of cyclin L2 induces apoptosis and cell-cycle arrest in human lung cancer cells

Chinese Medical Journal ◽

10.1097/00029330-200705020-00010 ◽

2007 ◽

Vol 120 (10) ◽

pp. 905-909 ◽

Cited By ~ 14

Author(s):

Hong-li LI ◽

Tong-shan WANG ◽

Xiao-yu LI ◽

Nan LI ◽

Ding-zhi HUANG ◽

...

Keyword(s):

Lung Cancer ◽

Cell Cycle ◽

Cell Cycle Arrest ◽

Cancer Cells ◽

Human Lung ◽

Lung Cancer Cells ◽

Human Lung Cancer ◽

Cycle Arrest ◽

Human Lung Cancer Cells

Download Full-text

POU2F2 promotes the proliferation and motility of lung cancer cells by activating AGO1

BMC Pulmonary Medicine ◽

10.1186/s12890-021-01476-9 ◽

2021 ◽

Vol 21 (1) ◽

Author(s):

Ronggang Luo ◽

Yi Zhuo ◽

Quan Du ◽

Rendong Xiao

Keyword(s):

Lung Cancer ◽

Tumor Growth ◽

Cancer Cells ◽

Cancer Progression ◽

Human Lung ◽

Lung Cancer Cells ◽

Human Lung Cancer ◽

Cancer Tissues

Abstract Background To detect and investigate the expression of POU domain class 2 transcription factor 2 (POU2F2) in human lung cancer tissues, its role in lung cancer progression, and the potential mechanisms. Methods Immunohistochemical (IHC) assays were conducted to assess the expression of POU2F2 in human lung cancer tissues. Immunoblot assays were performed to assess the expression levels of POU2F2 in human lung cancer tissues and cell lines. CCK-8, colony formation, and transwell-migration/invasion assays were conducted to detect the effects of POU2F2 and AGO1 on the proliferaion and motility of A549 and H1299 cells in vitro. CHIP and luciferase assays were performed for the mechanism study. A tumor xenotransplantation model was used to detect the effects of POU2F2 on tumor growth in vivo. Results We found POU2F2 was highly expressed in human lung cancer tissues and cell lines, and associated with the lung cancer patients’ prognosis and clinical features. POU2F2 promoted the proliferation, and motility of lung cancer cells via targeting AGO1 in vitro. Additionally, POU2F2 promoted tumor growth of lung cancer cells via AGO1 in vivo. Conclusion We found POU2F2 was highly expressed in lung cancer cells and confirmed the involvement of POU2F2 in lung cancer progression, and thought POU2F2 could act as a potential therapeutic target for lung cancer.

Download Full-text

Cisplatin-induced hydroxyl radicals mediate pro-survival autophagy in human lung cancer H460 cells

Biological Research ◽

10.1186/s40659-021-00346-2 ◽

2021 ◽

Vol 54 (1) ◽

Author(s):

Somruethai Sumkhemthong ◽

Eakachai Prompetchara ◽

Pithi Chanvorachote ◽

Chatchai Chaotham

Keyword(s):

Lung Cancer ◽

Hydroxyl Radicals ◽

Human Lung ◽

Human Lung Cancer ◽

Radical Scavenger ◽

Apoptosis Resistance ◽

Lung Cancer Patients ◽

Human Lung Cancer Cells ◽

H460 Cells

Abstract Background Accumulated evidence demonstrates cisplatin, a recommended chemotherapy, modulating pro-survival autophagic response that contributes to treatment failure in lung cancer patients. However, distinct mechanisms involved in cisplatin-induced autophagy in human lung cancer cells are still unclear. Results Herein, role of autophagy in cisplatin resistance was indicated by a decreased cell viability and increased apoptosis in lung cancer H460 cells pre-incubated with wortmannin, an autophagy inhibitor, prior to treatment with 50 µM cisplatin for 24 h. The elevated level of hydroxyl radicals detected via flow-cytometry corresponded to autophagic response, as evidenced by the formation of autophagosomes and autolysosomes in cisplatin-treated cells. Interestingly, apoptosis resistance, autophagosome formation, and the alteration of the autophagic markers, LC3-II/LC3-I and p62, as well as autophagy-regulating proteins Atg7 and Atg3, induced by cisplatin was abrogated by pretreatment of H460 cells with deferoxamine, a specific hydroxyl radical scavenger. The modulations in autophagic response were also indicated in the cells treated with hydroxyl radicals generated via Fenton reaction, and likewise inhibited by pretreatment with deferoxamine. Conclusions In summary, the possible role of hydroxyl radicals as a key mediator in the autophagic response to cisplatin treatment, which was firstly revealed in this study would benefit for the further development of novel therapies for lung cancer.

Download Full-text