scholarly journals IL-26 Involed in the Pathogenesis of Malignant Pleural Effusion Through Affecting the Differentiation of Th22 and the Biological Behavior of Lung Cancer Cells

2020 ◽  
Author(s):  
Y. Niu ◽  
Q. Zhou
Keyword(s):  
Lung Cancer ◽  
Pleural Effusion ◽  
Cancer Cells ◽  
Malignant Pleural Effusion ◽  
Lung Cancer Cells ◽  
Biological Behavior

scholarly journals Soluble Fas in malignant pleural effusion and its expression in lung cancer cells

2003 ◽  
Vol 94 (3) ◽  
pp. 302-307 ◽  
Author(s):  
Kayo Mitani ◽  
Yasuhiko Nishioka ◽  
Kazue Yamabe ◽  
Hirohisa Ogawa ◽  
Toyokazu Miki ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Pleural Effusion ◽  
Cancer Cells ◽  
Malignant Pleural Effusion ◽  
Lung Cancer Cells ◽  
Soluble Fas

scholarly journals Plasma-activated medium as adjuvant therapy for lung cancer with malignant pleural effusion

2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Yi-Jing Cheng ◽  
Ching-Kai Lin ◽  
Chao-Yu Chen ◽  
Po-Chien Chien ◽  
Ho-Hsien Chuan ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Pleural Effusion ◽  
Adjuvant Therapy ◽  
Cancer Cells ◽  
Malignant Pleural Effusion ◽  
A549 Cells ◽  
Atmospheric Pressure Plasma ◽  
Cost Effective ◽  
Thermal Therapy ◽  
Systemic Side Effects

Abstract This study compared effects of plasma-activated medium (PAM) with effects of conventional clinical thermal therapy on both lung cancer cells and benign cells for management of malignant pleural effusion (MPE). For MPE treatment, chemotherapy, photodynamic therapy, and thermal therapy are used but caused systemic side effects, patient photosensitivity, and edema, respectively. Recent studies show that plasma induces apoptosis in cancer cells with minor effects on normal cells and is cost-effective. However, the effects of plasma on MPE have not been investigated previously. This study applied a nonthermal atmospheric-pressure plasma jet to treat RPMI medium to produce PAM, carefully controlled the long-life reactive oxygen and nitrogen species concentration in PAM, and treated the cells. The influence of PAM treatment on the microenvironment of cells was also checked. The results indicated that PAM selectively inhibited CL1–5 and A549 cells, exerting minor effects on benign mesothelial and fibroblast cells. In contrast to selective lethal effects of PAM, thermal therapy inhibited both CL1–5 and benign mesothelial cells. This study also found that fibroblast growth factor 1 is not the factor explaining why PAM can selectively inhibit CL1–5 cells. These results indicate that PAM is potentially a less-harmful and cost-effective adjuvant therapy for MPE.

Rapid purification of lung cancer cells in pleural effusion through spiral microfluidic channels for diagnosis improvement

Lab on a Chip ◽  
2020 ◽  
Vol 20 (21) ◽  
pp. 4007-4015
Author(s):  
Ping-Hsien Tsou ◽  
Pei-Huan Chiang ◽  
Zi-Ting Lin ◽  
Hui-Chen Yang ◽  
Hsiang-Lin Song ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Pleural Effusion ◽  
Cancer Cells ◽  
Causes Of Death ◽  
Lung Cancer Cells ◽  
Microfluidic Channels ◽  
Rapid Purification

Lung cancer is one of the leading causes of death worldwide.

scholarly journals Morphine promotes the malignant biological behavior of non-small cell lung cancer cells through the MOR/Src/mTOR pathway

2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Xingyun Liu ◽  
Jia Yang ◽  
Chengwei Yang ◽  
Xiang Huang ◽  
Mingming Han ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Small Cell Lung Cancer ◽  
Cancer Cells ◽  
Cell Lung Cancer ◽  
Small Cell ◽  
Lung Cancer Cells ◽  
Biological Behavior ◽  
Migration And Invasion ◽  
Small Cell Lung ◽  
H460 Cells

Abstract Background Morphine, a µ-opioid receptor (MOR) agonist, has been shown to be related to the activity of cancer cells, and a higher morphine dosage reduces the survival time of patients with lung cancer. However, the effect of morphine on the malignant behavior of lung cancer cells remains unclear. The aim of this study was to investigate the specific molecular mechanism by which morphine regulates the malignant biological behavior of non-small cell lung cancer. Methods Immunofluorescence staining and Western blot analyses were performed to detect MOR expression. H460 non-small cell lung cancer cells were used in this study, and cell proliferation, the cell cycle and apoptosis were evaluated using Cell Counting Kit-8 (CCK-8) and flow cytometry assays, respectively. Cell migration and invasion were detected using wound healing and Transwell assays. The effect of morphine on lung cancer development in vivo was examined by performing a xenograft tumor assay following morphine treatment. Results Morphine promoted the growth of H460 cells both in vivo and in vitro. Morphine enhanced cell migration and invasion, modified cell cycle progression through the S/G2 transition and exerted an antiapoptotic effect on H460 cells. Additionally, morphine increased Rous sarcoma oncogene cellular homolog (Src) phosphorylation and activated the phosphoinositide 3 kinase (PI3K)/protein kinase B (AKT)/mammalian target of rapamycin (mTOR) pathway. Treatment with the MOR antagonist methylnaltrexone (MNTX) and the Src inhibitor protein phosphatase 1 (PP1) reduced the phosphorylation induced by morphine. Furthermore, MNTX, PP1, and the PI3K/AKT inhibitor deguelin reversed the antiapoptotic effect of morphine on lung cancer cells. Conclusion Morphine promotes the malignant biological behavior of H460 cells by activating the MOR and Src/mTOR signaling pathways.

Cross-talking between bone marrow-derived cells and lung cancer cells

2009 ◽  
Vol 27 (15_suppl) ◽  
pp. e19068-e19068
Author(s):  
J. Zhang ◽  
M. Liao ◽  
X. Niu ◽  
J. Xiang ◽  
Y. Zhao ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Bone Marrow ◽  
Bone Metastasis ◽  
Cancer Cells ◽  
Stromal Cells ◽  
A549 Cells ◽  
Lung Cancer Cells ◽  
Biological Behavior ◽  
High Bone ◽  
Bone Marrow Derived Cells

e19068 Background: Disseminated cancer cells may initially require local nutrients and growth factors to thrive and survive in bone marrow. However, data on the influence of bone marrow derived cells(BMDC, also called bone stromal cells in some publication) on lung cancer cells is largely unexplored. This study is to explore the effect from bone marrow derived cells on biological behavior of lung cancer cells. Methods: The difference among lung cancer cell lines in their abilities to bone metastasis was tested using SCID animal model. Supernatant of bone marrow aspiration(BM) and condition medium from human bone stromal cells(BSC) were used to study the activity of bone stromal factors. Affymetrix gene chip U133A 2.0 was used to study the gene expression profile of H460 cells, after exposure to secreted proteins from bone stromal cells. Results: In accordance with other literature repors, H460 was found with high bone metastasis potential, while SPC-A1 and A549 cells were low bone metastasis lung cancer cells. We found bone stromal factors significantly increased the proliferation, invasion, adhesion and expression of angiogenosis-related factors, and inhibited the apoptosis for high bone metastasis H460 lung cancer cells. These biologic effects were not seen in SPC-A1 or A549 cells, which are low bone metastasis lung cancer cells. Adhesion of H460 cells to bone stromal cells consistently up-regulated 31 genes. Ontoexpress software showed main function of 31 genes were associated with signal transduction pathways(5 genes), and adhesion molecule(5 genes), including integrin b3 and ADAMTS-1, two potential targets related with bone metastasis. Conclusions: We concluded bone marrow derived cells had a profound effect on biological behavior of lung cancers, therefore favoring the growth of lung cancer cells in bone. No significant financial relationships to disclose.

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