scholarly journals 12-Deoxyphorbol Esters Induce Growth Arrest and Apoptosis in Human Lung Cancer A549 Cells Via Activation of PKC-δ/PKD/ERK Signaling Pathway

2020 ◽  
Vol 21 (20) ◽  
pp. 7579
Author(s):  
Ju-Ying Tsai ◽  
Dóra Rédei ◽  
Judit Hohmann ◽  
Chin-Chung Wu
Keyword(s):  
Lung Cancer ◽  
Anticancer Agents ◽  
Cell Cycle Progression ◽  
Nuclear Translocation ◽  
Growth Arrest ◽  
A549 Cells ◽  
Cell Types ◽  
Human Lung Cancer ◽  
M Phase ◽  
Induced Apoptosis

Prostratin, a non-tumor promoting 12-deoxyphorbol ester, has been reported as a protein kinase C (PKC) activator and is shown to have anti-proliferative activity in certain cancer cell types. Here we show that GRC-2, a prostratin analogue isolated from Euphorbia grandicornis, is ten-fold more potent than prostratin for inhibiting the growth of human non-small cell lung cancer (NSCLC) A549 cells. Flow cytometry assay revealed that GRC-2 and prostratin inhibited cell cycle progression at the G2/M phase and induced apoptosis. The cytotoxic effect of GRC-2 and prostratin was accompanied by activation and nuclear translocation of PKC-δ and PKD as well as hyperactivation of extracellular signal-related kinase (ERK). Knockdown of either PKC-δ, PKD or ERK significantly protected A549 cancer cells from GRC-2- and prostratin-induced growth arrest as well as apoptosis. Taken together, our results have shown that prostratin and a more potent analogue GRC-2 reduce cell viability in NSCLC A549 cells, at least in part, through activation of the PKC-δ/PKD/ERK pathway, suggesting the potential of prostratin and GRC-2 as anticancer agents.

scholarly journals Tetrazolium Violet Induced Apoptosis and Cell Cycle Arrest in Human Lung Cancer A549 Cells

2012 ◽  
Vol 20 (2) ◽  
pp. 177-182 ◽  
Author(s):  
Xiao-Hong Zhang ◽  
Nan Zhang ◽  
Jian-Mei Lu ◽  
Qing-Zhong Kong ◽  
Yun-Feng Zhao
Keyword(s):  
Lung Cancer ◽  
Cell Cycle ◽  
Cell Cycle Arrest ◽  
Human Lung ◽  
A549 Cells ◽  
Human Lung Cancer ◽  
Cycle Arrest ◽  
Tetrazolium Violet ◽  
Induced Apoptosis

Synthesis of 5-Alkynyltetrandrine Derivatives and Evaluation of their Anticancer Activity on A549 Cell Lines

2019 ◽  
Vol 19 (12) ◽  
pp. 1454-1462 ◽  
Author(s):  
Nana Niu ◽  
Tingli Qu ◽  
Jinfang Xu ◽  
Xiaolin Lu ◽  
Graham J. Bodwell ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Caspase 3 ◽  
Human Lung ◽  
A549 Cells ◽  
Human Lung Cancer ◽  
Coupling Reactions ◽  
Apoptotic Pathway ◽  
Future Design ◽  
Cyt C ◽  
Induced Apoptosis

Background: Lung cancer is one of the most prevalent malignancies and thus the development of novel therapeutic agents for managing lung cancer is imperative. Tetrandrine, a bis-benzyltetrahydroisoquinoline alkaloid isolated from Stephania tetrandra S. Moore, has been found to exert cytotoxic effects on cancerous cells. Methods: A series of 5-alkynyltetrandrine derivatives was synthesized via the Sonogashira cross-coupling reactions and evaluated as potential anti-tumor agents. The anti-tumor activities of 12 compounds on lung cancer cells (A549) were evaluated using the MTT method. The population of apoptotic cells was measured using a TUNEL assay. Real-time PCR quantified the gene expression levels of Bcl-2, Bax, survivin and caspase-3. The content of Cyt-C was detected using a Human Cyt-C ELISA kit. Results: Most of these compounds exhibited better activities than tetrandrine itself on A549 cells. Among them, compound 7 showed the highest cytotoxicity among the tested compounds against human lung adenocarcinoma A549 cells with an IC50 of 2.94 µM. Preliminary mechanistic studies indicated that compound 7 induced apoptosis of human lung cancer A549 cells and increased the level of the proapoptotic gene Bax, release of Cyt-C from mitochondria and activation of caspase-3 genes. Conclusion: The results suggest that compound 7 exerts its antitumor activity against A549 cells through the induction of the intrinsic (mitochondrial) apoptotic pathway. These findings will contribute to the future design of more effective anti-tumor agents in lung cancer therapy.

Naringenin up-regulates the expression of death receptor 5 and enhances TRAIL-induced apoptosis in human lung cancer A549 cells

2011 ◽  
Vol 55 (2) ◽  
pp. 300-309 ◽  
Author(s):  
Cheng-Yun Jin ◽  
Cheol Park ◽  
Hye Jin Hwang ◽  
Gi-Young Kim ◽  
Byung Tae Choi ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Human Lung ◽  
Death Receptor ◽  
A549 Cells ◽  
Human Lung Cancer ◽  
Death Receptor 5 ◽  
Induced Apoptosis

scholarly journals Resistin increases cisplatin-induced cytotoxicity in lung adenocarcinoma A549 cells via a mitochondria-mediated pathway

2021 ◽  
Author(s):  
Wei-Jing Gong ◽  
Tao Zhou ◽  
Jia-Qiang Xu ◽  
Yi-Fei Huang ◽  
Li-Ping Xiang ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Caspase 3 ◽  
Reactive Oxygen Species Generation ◽  
A549 Cells ◽  
Chemotherapeutic Agents ◽  
Lung Cancer Patients ◽  
M Phase ◽  
Advanced Stages ◽  
Lung Adenocarcinoma A549 ◽  
Induced Apoptosis

Abstract Lung cancer is the most commonly diagnosed cancer with a high mortality rate. Cisplatin is one of the most important chemotherapeutic agents for the treatment of lung cancer patients, especially in advanced stages. Recent studies showed that cisplatin may interact with mitochondria which may partly account for its cytotoxicity. In the study, we explored the effect of resistin on cisplatin-induced cytotoxicity in A549 cells and assessed whether mitochondria-dependent apoptosis was involved. Our results found that 25 ng/ml resistin could significantly increase cisplatin-induced apoptosis and G2/M phase arrest, enhance reactive oxygen species generation, exacerbate the collapse of mitochondrial membrane potential, promote the distribution of cytochrome C in the cytoplasm from mitochondria, and activate caspase 3. Therefore, the results suggested that resistin might increase cisplatin-induced cytotoxicity via a mitochondria-mediated pathway in A549 cells. However, the precise mechanism has yet to be explored in the future.

Brazilian green propolis induced apoptosis in human lung cancer A549 cells through mitochondrial-mediated pathway

2015 ◽  
Vol 67 (10) ◽  
pp. 1448-1456 ◽  
Author(s):  
Yahima Frión-Herrera ◽  
Alexis Díaz-García ◽  
Jenny Ruiz-Fuentes ◽  
Hermis Rodríguez-Sánchez ◽  
José Maurício Sforcin
Keyword(s):  
Lung Cancer ◽  
Human Lung ◽  
A549 Cells ◽  
Human Lung Cancer ◽  
Induced Apoptosis ◽  
Brazilian Green Propolis

scholarly journals DNA Damage Induced Cellular Senescence and It’s PTEN Armed Exosomes - The Warriors Against Prostate Carcinoma Cells

2021 ◽  
Author(s):  
Parimal Karmakar ◽  
Sougata Ghosh Chowdhury ◽  
Rachayeeta Ray ◽  
Debalina Bhattacharya
Keyword(s):  
Lung Cancer ◽  
Cancer Cells ◽  
Western Blotting ◽  
Prostate Carcinoma ◽  
Human Lung ◽  
Growth Arrest ◽  
A549 Cells ◽  
Lung Cancer Cells ◽  
Human Lung Cancer ◽  
Pc3 Cells

Abstract Exosomes are one type of small extracellular vesicles having a size range of 30–150 nm and secreted by the endosomal compartment of most eukaryotic cells. It has been found that exosomes can serve as a communicating vehicle to transfer information among cells and thus can be associated with numerous physiological and pathological functions. In this study, we have isolated exosomes from two different human cancer cell lines. Isolated exosomes were characterized by scanning electron microscopy, DLS and by western blotting. It was observed that exosomes isolated from mock treated human lung epithelial carcinoma (A549) cells or Hela cells exerted growth arrest to the human prostate carcinoma (PC3) cells, but no growth arrest was observed in case of normal human lung fibroblast cell line (WI38). Additionally, exosomes isolated from PC3 cells have no effect on PC3 cells. This is also true for exosomes isolated from H2O2 induced senescent human lung cancer cells (A549). Analysis of exosome content by western blotting reveals the presence of PTEN in the exosome of lung cancer cells. Functional analysis of PTEN pathways in PC3 cells indicates the inactivation of Akt in exosome treated cells. Therefore, from our study we have concluded that exosomes secreted from A549 cells which contain functional PTEN, may be used for delivery of PTEN to cancer cells without functional PTEN.

scholarly journals Crocus sativusL. (Saffron) Stigma Aqueous Extract Induces Apoptosis in Alveolar Human Lung Cancer Cells through Caspase-Dependent Pathways Activation

2013 ◽  
Vol 2013 ◽  
pp. 1-12 ◽  
Author(s):  
Saeed Samarghandian ◽  
Abasalt Borji ◽  
Seyed Kazem Farahmand ◽  
Reza Afshari ◽  
Saeideh Davoodi
Keyword(s):  
Lung Cancer ◽  
Cancer Cells ◽  
Aqueous Extract ◽  
Morphological Changes ◽  
Flow Cytometric Analysis ◽  
A549 Cells ◽  
Lung Cancer Cells ◽  
Human Lung Cancer ◽  
Dependent Manner ◽  
Induced Apoptosis

Worldwide, lung cancer is the most common form of cancer. Saffron has been used in folk medicine for centuries. We investigated the potential of saffron to induce cytotoxic and apoptotic effects in lung cancer cells (A549). We also examined the caspase-dependent pathways activation of saffron-induced apoptosis against the A549 cells. A549 cells were incubated with different concentrations of saffron extract; then cell morphological changes, cell viability, and apoptosis were determined by the normal invertmicroscope, MTT assay, Annexin V and propidium iodide, and flow cytometric analysis, respectively. Activated caspases were detected by treatment of saffron in lung cancer cells using fluorescein-labeled inhibitors of polycaspases. The proliferation of the A549 cells were decreased after treatment with saffron in a dose- and time-dependent manner. The percentage of apoptotic cells increased with saffron concentrations. Saffron induced morphological changes, decreased percentage of viable cells, and induced apoptosis. Saffron could induce apoptosis in the A549 cells and activate caspase pathways. The levels of caspases involved in saffron-induced apoptosis in the A549 cells indicating caspase-dependent pathway were induced by saffron. The anticancer activity of the aqueous extract of saffron could be attributed partly to its inhibition of the cell proliferation and induction of apoptosis in cancer cells through caspase-dependent pathways activation.

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