A study of the volatile organic compounds exhaled by lung cancer cells in vitro for breath diagnosis

Cancer ◽  
2007 ◽  
Vol 110 (4) ◽  
pp. 835-844 ◽  
Author(s):  
Xing Chen ◽  
Fengjuan Xu ◽  
Yue Wang ◽  
Yuefeng Pan ◽  
Deji Lu ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Volatile Organic Compounds ◽  
Cancer Cells ◽  
Organic Compounds ◽  
Lung Cancer Cells ◽  
Volatile Organic

A PRELIMINARY STUDY ON DETECTION OF LUNG CANCER CELLS BASED ON VOLATILE ORGANIC COMPOUNDS SENSING USING ELECTRONIC NOSE

2015 ◽  
Vol 77 (7) ◽  
Author(s):  
Reena Thriumani ◽  
Amanina Iymia Jeffreea ◽  
Ammar Zakaria ◽  
Yumi Zuhanis Has-Yun Hasyim ◽  
Khaled Mohamed Helmy ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Volatile Organic Compounds ◽  
Cancer Cells ◽  
Organic Compounds ◽  
Electronic Nose ◽  
Preliminary Investigation ◽  
Lung Cancer Cells ◽  
Polymer Sensors ◽  
Volatile Organic

 This paper proposes a preliminary investigation on the volatile production patterns generated from three sets of in-vitro cancerous cell samples of headspace that contains volatile organic compounds using the electronic nose system.  A commercialized electronic nose consisting of 32 conducting polymer sensors (Cyranose 320) is used to analyze the three classes of signals which are lung cancer cells grown in media, breast cancer cells grown in media and the blank media (without cells). Neural Network (PNN) based classification technique is applied to investigate the performance of an electronic nose (E-nose) system for cancerous lung cell classification.  

Analysis of volatile organic compounds (VOCs) in the headspace of NCI-H1666 lung cancer cells

2011 ◽  
Vol 7 (3) ◽  
pp. 153-161 ◽  
Author(s):  
Andreas Sponring ◽  
Wojciech Filipiak ◽  
Clemens Ager ◽  
Jochen Schubert ◽  
Wolfram Miekisch ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Volatile Organic Compounds ◽  
Cancer Cells ◽  
Organic Compounds ◽  
Lung Cancer Cells ◽  
Volatile Organic

scholarly journals Release of volatile organic compounds (VOCs) from the lung cancer cell line CALU-1 in vitro

2008 ◽  
Vol 8 (1) ◽  
pp. 17 ◽  
Author(s):  
Wojciech Filipiak ◽  
Andreas Sponring ◽  
Tomas Mikoviny ◽  
Clemens Ager ◽  
Jochen Schubert ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Volatile Organic Compounds ◽  
Cell Line ◽  
Organic Compounds ◽  
Cancer Cell ◽  
Cancer Cell Line ◽  
Lung Cancer Cell Line ◽  
Lung Cancer Cell ◽  
Volatile Organic

scholarly journals A study on volatile organic compounds emitted by in-vitro lung cancer cultured cells using gas sensor array and SPME-GCMS

BMC Cancer ◽  
2018 ◽  
Vol 18 (1) ◽  
Author(s):  
Reena Thriumani ◽  
Ammar Zakaria ◽  
Yumi Zuhanis Has-Yun Hashim ◽  
Amanina Iymia Jeffree ◽  
Khaled Mohamed Helmy ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Volatile Organic Compounds ◽  
Gas Sensor ◽  
Organic Compounds ◽  
Sensor Array ◽  
Cultured Cells ◽  
Gas Sensor Array ◽  
Volatile Organic

scholarly journals Circular RNA FLNA acts as a sponge of miR-486-3p in promoting lung cancer progression via regulating XRCC1 and CYP1A1

2021 ◽  
Author(s):  
Jiongwei Pan ◽  
Gang Huang ◽  
Zhangyong Yin ◽  
Xiaoping Cai ◽  
Enhui Gong ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Cancer Cells ◽  
Cancer Cell ◽  
Cancer Progression ◽  
Lung Cancer Cells ◽  
Luciferase Reporter ◽  
Migration And Invasion ◽  
Related Factors

AbstractSignificantly high-expressed circFLNA has been found in various cancer cell lines, but not in lung cancer. Therefore, this study aimed to explore the role of circFLNA in the progression of lung cancer. The target gene of circFLNA was determined by bioinformatics and luciferase reporter assay. Viability, proliferation, migration, and invasion of the transfected cells were detected by CCK-8, colony formation, wound-healing, and transwell assays, respectively. A mouse subcutaneous xenotransplanted tumor model was established, and the expressions of circFLNA, miR-486-3p, XRCC1, CYP1A1, and related genes in the cancer cells and tissues were detected by RT-qPCR, Western blot, or immunohistochemistry. The current study found that miR-486-3p was low-expressed in lung cancer. MiR-486-3p, which has been found to target XRCC1 and CYP1A1, was regulated by circFLNA. CircFLNA was located in the cytoplasm and had a high expression in lung cancer cells. Cancer cell viability, proliferation, migration, and invasion were promoted by overexpressed circFLNA, XRCC1, and CYP1A1 but inhibited by miR-486-3p mimic and circFLNA knockdown. The weight of the xenotransplanted tumor was increased by circFLNA overexpression yet reduced by miR-486-3p mimic. Furthermore, miR-486-3p mimic reversed the effect of circFLNA overexpression on promoting lung cancer cells and tumors and regulating the expressions of miR-486-3p, XRCC1, CYP1A1, and metastasis/apoptosis/proliferation-related factors. However, overexpressed XRCC1 and CYP1A1 reversed the inhibitory effect of miR-486-3p mimic on cancer cells and tumors. In conclusion, circFLNA acted as a sponge of miR-486-3p to promote the proliferation, migration, and invasion of lung cancer cells in vitro and in vivo by regulating XRCC1 and CYP1A1.

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

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.

Knockdown CYP2S1 inhibits lung cancer cells proliferation and migration

2021 ◽  
pp. 1-9
Author(s):  
Huan Guo ◽  
Baozhen Zeng ◽  
Liqiong Wang ◽  
Chunlei Ge ◽  
Xianglin Zuo ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Cell Proliferation ◽  
Cell Growth ◽  
Cancer Cells ◽  
Molecular Mechanisms ◽  
Lung Cancer Cells ◽  
Invasion And Migration ◽  
And Migration

BACKGROUND: The incidence of lung cancer in Yunnan area ranks firstly in the world and underlying molecular mechanisms of lung cancer in Yunnan region are still unclear. We screened a novel potential oncogene CYP2S1 used mRNA microassay and bioinformation database. The function of CYP2S1 in lung cancer has not been reported. OBJECTIVE: To investigate the functions of CYP2S1 in lung cancer. METHODS: Immunohistochemistry and Real-time PCR were used to verify the expression of CYP2S1. Colony formation and Transwell assays were used to determine cell proliferation, invasion and migration. Xenograft assays were used to detected cell growth in vivo. RESULTS: CYP2S1 is significantly up-regulated in lung cancer tissues and cells. Knockdown CYP2S1 in lung cancer cells resulted in decrease cell proliferation, invasion and migration in vitro. Animal experiments showed downregulation of CYP2S1 inhibited lung cancer cell growth in vivo. GSEA analysis suggested that CYP2S1 played functions by regulating E2F targets and G2M checkpoint pathway which involved in cell cycle. Kaplan-Meier analysis indicated that patients with high CYP2S1 had markedly shorter event overall survival (OS) time. CONCLUSIONS: Our data demonstrate that CYP2S1 exerts tumor suppressor function in lung cancer. The high expression of CYP2S1 is an unfavorable prognostic marker for patient survival.

scholarly journals Trichoderma asperellum T76-14 Released Volatile Organic Compounds against Postharvest Fruit Rot in Muskmelons (Cucumis melo) Caused by Fusarium incarnatum

2021 ◽  
Vol 7 (1) ◽  
pp. 46
Author(s):  
Warin Intana ◽  
Suchawadee Kheawleng ◽  
Anurag Sunpapao
Keyword(s):  
Volatile Organic Compounds ◽  
Organic Compounds ◽  
Cucumis Melo ◽  
Fungal Growth ◽  
Fruit Rot ◽  
Postharvest Disease ◽  
Dual Culture ◽  
Trichoderma Asperellum ◽  
Volatile Organic

Postharvest fruit rot caused by Fusarium incarnatum is a destructive postharvest disease of muskmelon (Cucumis melo). Biocontrol by antagonistic microorganisms is considered an alternative to synthetic fungicide application. The aim of this study was to investigate the mechanisms of action involved in the biocontrol of postharvest fruit rot in muskmelons by Trichoderma species. Seven Trichoderma spp. isolates were selected for in vitro testing against F. incarnatum in potato dextrose agar (PDA) by dual culture assay. In other relevant works, Trichoderma asperellum T76-14 showed a significantly higher percentage of inhibition (81%) than other isolates. Through the sealed plate method, volatile organic compounds (VOCs) emitted from T. asperellum T76-14 proved effective at inhibiting the fungal growth of F. incarnatum by 62.5%. Solid-phase microextraction GC/MS analysis revealed several VOCs emitted from T. asperellum T76-14, whereas the dominant compound was tentatively identified as phenylethyl alcohol (PEA). We have tested commercial volatile (PEA) against in vitro growth of F. incarnatum; the result showed PEA at a concentration of 1.5 mg mL−1 suppressed fungal growth with 56% inhibition. Both VOCs and PEA caused abnormal changes in the fungal mycelia. In vivo testing showed that the lesion size of muskmelons exposed to VOCs from T. asperellum T76-14 was significantly smaller than that of the control. Muskmelons exposed to VOCs from T. asperellum T76-14 showed no fruit rot after incubation at seven days compared to fruit rot in the control. This study demonstrated the ability of T. asperellum T76-14 to produce volatile antifungal compounds, showing that it can be a major mechanism involved in and responsible for the successful inhibition of F. incarnatum and control of postharvest fruit rot in muskmelons.

scholarly journals Antiproliferative Activity and Potential Mechanism of Marine-Sourced Streptoglutarimide H against Lung Cancer Cells

Marine Drugs ◽  
2021 ◽  
Vol 19 (2) ◽  
pp. 79
Author(s):  
Hengju Ge ◽  
Di Zhang ◽  
Muran Shi ◽  
Xiaoyuan Lian ◽  
Zhizhen Zhang
Keyword(s):  
Lung Cancer ◽  
Cell Cycle ◽  
Cancer Cells ◽  
Antiproliferative Activity ◽  
Lung Cancer Cells ◽  
Potential Mechanism ◽  
Nucleotide Synthesis ◽  
Factor C ◽  
Antiglioma Activity

In 2019, streptoglutarimide H (SGH) was characterized as a new glutarimide from the secondary metabolites produced by a marine-derived actinomycete Streptomyces sp. ZZ741 and shown to have in vitro antiglioma activity. However, the antiproliferative activity and potential mechanism of SGH against lung cancer cells have not yet been characterized. This study demonstrated that SGH significantly inhibited the proliferation of different lung cancer cells. In terms of mechanism of action, SGH downregulated cell cycle- and nucleotide synthesis-related proteins to block cell cycle at G0/G1 phase, reduced the expression levels of glycolytic metabolic enzymes to inhibit glycolysis, and downregulated the important cancer transcription factor c-Myc and the therapeutic target deubiquitinase USP28. Potent anticancer activity and multiple mechanisms indicated SGH to be a novel antitumor compound against lung cancer cells.

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