Apigenin induces apoptosis in human lung cancer H460 cells through caspase- and mitochondria-dependent pathways

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.

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

Molecules ◽

10.3390/molecules19056047 ◽

2014 ◽

Vol 19 (5) ◽

pp. 6047-6057 ◽

Cited By ~ 14

Author(s):

Shin-Hwar Wu ◽

Yung-Ting Hsiao ◽

Jaw-Chyum Chen ◽

Ju-Hwa Lin ◽

Shu-Chun Hsu ◽

...

Keyword(s):

Lung Cancer ◽

Cell Cycle ◽

Dna Damage ◽

Human Lung ◽

Human Lung Cancer ◽

Gene Expressions ◽

Damage Cell ◽

H460 Cells

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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

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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.

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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.

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