MicroRNA-224 is implicated in lung cancer pathogenesis through targeting caspase-3 and caspase-7

Abstract Background Considering the advantages of using medicinal herbs as supplementary treatments to sensitize conventional anti-cancer drugs, studying functional mechanisms and regulatory effects of Echinacea purpurea (as a non-cannabinoid plant) and Cannabis sativa (as a cannabinoid plant) are timely and required. The potential effects of such herbs on lung cancer cell growth, apoptosis, cell cycle distribution, cellular reactive oxygen species (ROS) level, caspase activity and their cannabinomimetic properties on the CB2 receptor are addressed in the current study. Methods The cytotoxic effect of both herb extracts on the growth of lung cancer cells (A549) was assessed using the MTT assay. The annexin-V-FITC staining and propidium iodide (PI) staining methods were applied for the detection of apoptosis and cell cycle distribution using flow cytometry. The cellular level of ROS was measured using 7′-dichlorofluorescin diacetate (DCFH-DA) as a fluorescent probe in flow cytometry. The caspase 3 activity was assessed using a colorimetric assay Kit. Results Echinacea purpurea (EP) root extract induced a considerable decrease in A549 viable cells, showing a time and dose-dependent response. The cell toxicity of EP was accompanied by induction of early apoptosis and cell accumulation at the sub G1 phase of the cell cycle. The elevation of cellular ROS level and caspase 3 activity indicate ROS-induced caspase-dependent apoptosis following the treatment of A549 cells by EP extract. The observed effects of EP extract on A549 growth and death were abrogated following blockage of CB2 using AM630, a specific antagonist of the CB2 receptor. Increasing concentrations of Cannabis sativa (CS) induced A549 cell death in a time-dependent manner, followed by induction of early apoptosis, cell cycle arrest at sub G1 phase, elevation of ROS level, and activation of caspase 3. The CB2 blockage caused attenuation of CS effects on A549 cell death which revealed consistency with the effects of EP extract on A549 cells. Conclusions The pro-apoptotic effects of EP and CS extracts on A549 cells and their possible regulatory role of CB2 activity might be attributed to metabolites of both herbs. These effects deserve receiving more attention as alternative anti-cancer agents. Graphical abstract

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Role of lung and gut microbiota on lung cancer pathogenesis

Journal of Cancer Research and Clinical Oncology ◽

10.1007/s00432-021-03644-0 ◽

2021 ◽

Author(s):

Yue Zhao ◽

Yuxia Liu ◽

Shuang Li ◽

Zhaoyun Peng ◽

Xiantao Liu ◽

...

Keyword(s):

Lung Cancer ◽

Gut Microbiota ◽

Cancer Progression ◽

Gut Microbiome ◽

Intestinal Flora ◽

Inflammatory Factors ◽

Cancer Pathogenesis ◽

Research Findings ◽

Relationship Of

Abstract Background Lung cancer is the leading cause of cancer-related deaths worldwide (Ferlay et al., Int J Cancer 136:E359–386, 2015). In addition, lung cancer is associated with the highest mortality among all cancer types (Wu et al., Exp Ther Med 16:3004–3010, 2018). Previous studies report that microbiota play an important role in lung cancer. Notably, changes in lung and gut microbiota, are associated with progression of lung cancer. Several studies report that lung and gut microbiome promote lung cancer initiation and development by modulating metabolic pathways, inhibiting the function of immune cells, and producing pro-inflammatory factors. In addition, some factors such as microbiota dysbiosis, affect production of bacteriotoxins, genotoxicity and virulence effect, therefore, they play a key role in cancer progression. These findings imply that lung and gut microbiome are potential markers and targets for lung cancer. However, the role of microbiota in development and progression of lung cancer has not been fully explored. Purpose The aim of this study was to systemically review recent research findings on relationship of lung and gut microbiota with lung cancer. In addition, we explored gut–lung axis and potential mechanisms of lung and gut microbiota in modulating lung cancer progression. Conclusion Pulmonary and intestinal flora influence the occurrence, development, treatment and prognosis of lung cancer, and will provide novel strategies for prevention, diagnosis, and treatment of lung cancer.

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Radix Tetrastigma Inhibits the Non-Small Cell Lung Cancer via Bax/Bcl-2/Caspase-9/Caspase-3 Pathway

Nutrition and Cancer ◽

10.1080/01635581.2021.1881569 ◽

2021 ◽

pp. 1-13

Author(s):

Yonglu Li ◽

Yaxuan Wang ◽

Xin Yu ◽

Ting Yu ◽

Xiaodong Zheng ◽

...

Keyword(s):

Lung Cancer ◽

Small Cell Lung Cancer ◽

Cell Lung Cancer ◽

Caspase 3 ◽

Small Cell ◽

Small Cell Lung ◽

Caspase 9

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Antiapoptotic function of Bcl-2 in mast cells is dependent on its association with heat shock protein 90β

Blood ◽

10.1182/blood-2005-07-2648 ◽

2006 ◽

Vol 107 (4) ◽

pp. 1413-1420 ◽

Cited By ~ 34

Author(s):

Cellina Cohen-Saidon ◽

Irit Carmi ◽

Avishai Keren ◽

Ehud Razin

Keyword(s):

Mast Cell ◽

Rna Interference ◽

Mast Cells ◽

Heat Shock ◽

Heat Shock Protein ◽

Caspase 3 ◽

Caspase 7 ◽

Antiapoptotic Activity ◽

Novel Strategy ◽

First Time

In the present study, we demonstrated that the antiapoptotic function of Bcl-2 in mast cells is significantly dependent on its association with the heat shock protein 90β (Hsp90β). Dissociation of these 2 proteins inhibits the antiapoptotic activity of Bcl-2 by initiating the release of cytochrome c from mitochondria into cytosol and increasing the activity of caspase 3 and caspase 7, resulting in mast-cell apoptosis. The antiapoptotic activity of Bcl-2 was greatly affected by knocking-out specifically Hsp90β using the RNA interference approach. Thus, for the first time, it has been shown that Hsp90β might modulate the antiapoptotic activity of Bcl-2 at least in mast cells. These findings could have implications for a novel strategy of regulating apoptosis in patients with mastocytosis and other mast cell–associated diseases.

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A topical antioxidant solution containing vitamin C, vitamin E, and ferulic acid prevents ultraviolet radiation-induced caspase-3 and caspase-7 induction in skin

Journal of the American Academy of Dermatology ◽

10.1016/j.jaad.2004.10.642 ◽

2005 ◽

Vol 52 (3) ◽

pp. P158 ◽

Cited By ~ 1

Keyword(s):

Vitamin E ◽

Vitamin C ◽

Ultraviolet Radiation ◽

Ferulic Acid ◽

Caspase 3 ◽

Caspase 7 ◽

Radiation Induced

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Apoptosis Induction of Agave lechuguilla Torrey Extract on Human Lung Adenocarcinoma Cells (SK-LU-1)

International Journal of Molecular Sciences ◽

10.3390/ijms19123765 ◽

2018 ◽

Vol 19 (12) ◽

pp. 3765 ◽

Cited By ~ 4

Author(s):

Luis Anguiano-Sevilla ◽

Eugenia Lugo-Cervantes ◽

Cynthia Ordaz-Pichardo ◽

Jorge Rosas-Trigueros ◽

María Jaramillo-Flores

Keyword(s):

Cell Death ◽

Caspase 3 ◽

Ethanol Extract ◽

Fragmentation Pattern ◽

Intrinsic Pathway ◽

Adenocarcinoma Cells ◽

Human Lung Adenocarcinoma Cells ◽

Caspase 7 ◽

Mcf 7 ◽

Apoptotic Signal

In this study, an ethanol extract of Agave lechuguilla was evaluated against six carcinogenic cell lines (HCT-15, MCF-7, PC-3, U-251, SK-LU-1 and K-562) with an inhibition of 75.7 ± 2.3% against the SK-LU-1 line. Based on the previous result, the extract was hydrolyzed and fractionated, to which the IC50 was determined; the cell line was more sensitive to the fractionated extract with an IC50 6.96 ± 0.15 µg/mL. Characterization by mass spectrometry showed the presence of kaempferol, quercetin and a flavonoid dimer formed by afzelechin-4β-8-quercetin, according to the generated fragmentation pattern. The fractionated extract presented cell death by apoptosis with 39.8% at 24 h. Molecular docking was performed with the molecules found to try to describe cell death by apoptosis through death receptors such as FasCD95, TNF-R1, DR4/5 and blocking signaling on the EGFR and K-Ras MAPK/ERK pathway, as well as through the intrinsic pathway activating tBID, which promotes the amplification of the apoptotic signal due to the activation of caspase-3, and consequently caspase-7. In addition to the activation of the IIb complex associated with cell death due to necroptosis.

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The Specific Role of Periodontal Disease in Lung Cancer Pathogenesis

Modern Approaches in Dentistry and Oral Health Care ◽

10.32474/madohc.2018.01.000108 ◽

2018 ◽

Vol 1 (2) ◽

Author(s):

Nikolaos Andreas Chrysanthakopoulos

Keyword(s):

Lung Cancer ◽

Periodontal Disease ◽

Specific Role ◽

Cancer Pathogenesis

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Dual Nature of Relationship between Mycobacteria and Cancer

International Journal of Molecular Sciences ◽

10.3390/ijms22158332 ◽

2021 ◽

Vol 22 (15) ◽

pp. 8332

Author(s):

Marek Fol ◽

Piotr Koziński ◽

Jakub Kulesza ◽

Piotr Białecki ◽

Magdalena Druszczyńska

Keyword(s):

Lung Cancer ◽

Antitumor Agents ◽

Experimental Studies ◽

Tumor Development ◽

Mycobacterium Ulcerans ◽

Epidemiological Evidence ◽

Dual Nature ◽

Mycobacterial Infections ◽

Cancer Pathogenesis ◽

The Relationship

Although the therapeutic effect of mycobacteria as antitumor agents has been known for decades, recent epidemiological and experimental studies have revealed that mycobacterium-related chronic inflammation may be a possible mechanism of cancer pathogenesis. Mycobacterium tuberculosis and non-tuberculous Mycobacterium avium complex infections have been implicated as potentially contributing to the etiology of lung cancer, whereas Mycobacterium ulcerans has been correlated with skin carcinogenesis. The risk of tumor development with chronic mycobacterial infections is thought to be a result of many host effector mechanisms acting at different stages of oncogenesis. In this paper, we focus on the nature of the relationship between mycobacteria and cancer, describing the clinical significance of mycobacteria-based cancer therapy as well as epidemiological evidence on the contribution of chronic mycobacterial infections to the increased lung cancer risk.

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Expression levels of caspase-3 and gasdermin E and their involvement in the occurrence and prognosis of lung cancer

10.21203/rs.3.rs-189686/v1 ◽

2021 ◽

Author(s):

yuanli huang ◽

GuangHui Zhang ◽

Qing Zhu ◽

Xia Wu ◽

LIGao Wu

Keyword(s):

Lung Cancer ◽

Caspase 3 ◽

Clinical Stage ◽

The Body ◽

Caspase 8 ◽

Survival Prognosis ◽

Expression Levels ◽

Protein Levels ◽

Normal Tissues ◽

Related Proteins

Abstract Background Pyroptosis plays a dual role in the development of cancer and malignancy, and as such, may potentially be a new target for cancer treatment. However, the inflammatory response to pyroptosis may have adverse effects on the body. The roles of gasdermin E (GSDME), caspases, and related proteins associated with pyroptosis in cancer remain controversial. This study aimed to explore whether the expression levels of caspase-3 and GSDME affect the clinical stage, pathological grade, and survival prognosis of patients with lung cancer. Methods We examined the protein levels of GSDME, caspase-3, caspase-8, and caspase-9 in lung tissues from 100 patients with lung cancer by using immunohistochemistry. Results We found that GSDME, caspase-3, and caspase-8 were more highly expressed in the tumor tissues than in the adjacent normal tissues. Moreover, we found that GSDME could serve as a prognostic factor because there was a positive correlation between its expression level and the postoperative survival rate of patients with lung cancer. Conclusions GSDME may be an independent factor affecting the prognosis of patients with lung cancer. However, the role of GSDME and its related proteins in cancer requires further research.

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