scholarly journals CD105-Positive Cells in Pulmonary Arterial Blood of Adult Human Lung Cancer Patients Include Mesenchymal Progenitors

Stem Cells ◽  
2008 ◽  
Vol 26 (10) ◽  
pp. 2523-2530 ◽  
Author(s):  
Haruki Chiba ◽  
Genicihro Ishii ◽  
Ta-Kashi Ito ◽  
Kazuhiro Aoyagi ◽  
Hiroki Sasaki ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Cancer Patients ◽  
Human Lung ◽  
Human Lung Cancer ◽  
Mesenchymal Progenitors ◽  
Lung Cancer Patients ◽  
Adult Human ◽  
Arterial Blood ◽  
Pulmonary Arterial ◽  
Adult Human Lung

scholarly journals Role of caveolin-1 as a biomarker for radiation resistance and tumor aggression in lung cancer

PLoS ONE ◽  
2021 ◽  
Vol 16 (11) ◽  
pp. e0258951
Author(s):  
Dominic Leiser ◽  
Santanu Samanta ◽  
John Eley ◽  
Josh Strauss ◽  
Michael Creed ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Cancer Cells ◽  
Cancer Patients ◽  
Radiation Resistance ◽  
Human Lung ◽  
A549 Cells ◽  
Human Lung Cancer ◽  
Lung Cancer Patients ◽  
Caveolin 1 ◽  
Radiation Resistant

Radiation therapy plays a major role in the treatment of lung cancer patients. However, cancer cells develop resistance to radiation. Tumor radioresistance is a complex multifactorial mechanism which may be dependent on DNA damage and repair, hypoxic conditions inside tumor microenvironment, and the clonal selection of radioresistant cells from the heterogeneous tumor site, and it is a major cause of treatment failure in non–small cell lung cancer (NSCLC). In the present investigation caveolin-1 (CAV-1) has been observed to be highly expressed in radiation resistant A549 lung cancer cells. CRISPR-Cas9 knockout of CAV-1 reverted the cells to a radio sensitive phenotype. In addition, CAV-1 overexpression in parental A549 cells, led to radiation resistance. Further, gene expression analysis of A549 parental, radiation resistant, and caveolin-1 overexpressed cells, exhibited overexpression of DNA repair genes RAD51B, RAD18, SOX2 cancer stem cell marker, MMPs, mucins and cytoskeleton proteins in resistant and caveolin-1 over expressed A549 cells, as compared to parental A549 cells. Bioinformatic analysis shows upregulation of BRCA1, Nuclear Excision DNA repair, TGFB and JAK/STAT signaling pathways in radioresistant and caveolin-1 overexpressed cells, which may functionally mediate radiation resistance. Immunohistochemistry data demonstrated heterogeneous expression of CAV-1 gene in human lung cancer tissues, which was analogous to its enhanced expression in human lung cancer cell line model and mouse orthotopic xenograft lung cancer model. Also, TCGA PanCancer clinical studies have demonstrated amplification, deletions and missense mutation in CAV-1 gene in lung cancer patients, and that CAV-1 alteration has been linked to poor prognosis, and poor survival in lung cancer patients. Interestingly, we have also optimized ELISA assay to measure caveolin-1 protein in the blood of A549 radiation resistant human xenograft preclinical mouse model and discovered higher level of caveolin-1 (950 pg/ml) in tumor bearing animals treated with radiation, as compared to xenograft with radiosensitive lung cancer cells (450 pg/ml). Thus, we conclude that caveolin-1 is involved in radio-resistance and contributes to tumor aggression, and it has potential to be used as prognostic biomarker for radiation treatment response, and tumor progression for precision medicine in lung cancer patients.

scholarly journals Cisplatin-induced hydroxyl radicals mediate pro-survival autophagy in human lung cancer H460 cells

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.

scholarly journals Arterial blood gases predict long-term prognosis in stage I non-small cell lung cancer patients

BMC Surgery ◽  
2016 ◽  
Vol 16 (1) ◽  
Author(s):  
Shinjiro Mizuguchi ◽  
Takashi Iwata ◽  
Nobuhiro Izumi ◽  
Takuma Tsukioka ◽  
Shoji Hanada ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Cancer Patients ◽  
Blood Gases ◽  
Small Cell ◽  
Arterial Blood Gases ◽  
Small Cell Lung ◽  
Lung Cancer Patients ◽  
Arterial Blood ◽  
Long Term Prognosis
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