The Relationship between Heme Oxygenase-1 Expression and Response to Cisplatin Containing Chemotherapy in Advanced Non-Small Cell Lung Cancer

2006 ◽  
Vol 60 (3) ◽  
pp. 314
Author(s):  
Doo Kyung Yang ◽  
Mee Sook Roh ◽  
Kyung Eun Lee ◽  
Ki Nam Kim ◽  
Ki Nam Lee ◽  
...  
2020 ◽  
Vol 47 (3) ◽  
pp. 1949-1964 ◽  
Author(s):  
Mariarita Spampinato ◽  
Giuseppe Sferrazzo ◽  
Valeria Pittalà ◽  
Michelino Di Rosa ◽  
Luca Vanella ◽  
...  

Lung Cancer ◽  
2012 ◽  
Vol 77 (1) ◽  
pp. 168-175 ◽  
Author(s):  
María S. Degese ◽  
Javier E. Mendizabal ◽  
Norberto A. Gandini ◽  
J. Silvio Gutkind ◽  
Alfredo Molinolo ◽  
...  

Biomolecules ◽  
2021 ◽  
Vol 11 (6) ◽  
pp. 917
Author(s):  
Valeria Sorrenti ◽  
Agata Grazia D’Amico ◽  
Ignazio Barbagallo ◽  
Valeria Consoli ◽  
Salvo Grosso ◽  
...  

In order to maintain redox homeostasis, non-small-cell lung cancer (NSCLC) increases the activation of many antioxidant systems, including the heme-oxygenase (HO) system. The overexpression of HO-1 has been often associated with chemoresistance and tumor aggressiveness. Our results clearly showed an overexpression of the HO-1 protein in A549 NSCLC cell lines compared to that in non-cancerous cells. Thus, we hypothesized that “off-label” use of tin mesoporphyrin, a well-known HO activity inhibitor clinically used for neonatal hyperbilirubinemia, has potential use as an anti-cancer agent. The pharmacological inhibition of HO activity caused a reduction in cell proliferation and migration of A549. SnMP treatment caused an increase in oxidative stress, as demonstrated by the upregulation of reactive oxygen species (ROS) and the depletion of glutathione (GSH) content. To support these data, Western blot analysis was performed to analyze glucose-6-phosphate dehydrogenase (G6PD), TP53-induced glycolysis and the apoptosis regulator (TIGAR), and the glutamate cysteine ligase catalytic (GCLC) subunit, as they represent the main regulators of the pentose phosphate pathway (PPP) and glutathione synthesis, respectively. NCI-H292, a subtype of the NSCLC cell line, did not respond to SnMP treatment, possibly due to low basal levels of HO-1, suggesting a cellular-dependent antitumorigenic effect. Altogether, our results suggest HO activity inhibition may represent a potential target for selective chemotherapy in lung cancer subtypes.


2018 ◽  
Vol 27 (12) ◽  
pp. 1518-1526 ◽  
Author(s):  
Patricia Erickson ◽  
Lisa D. Gardner ◽  
Christopher A. Loffredo ◽  
Diane Marie St. George ◽  
Elise D. Bowman ◽  
...  

2021 ◽  
Author(s):  
Longxia Dai ◽  
Quanwen Deng ◽  
Aibin Liu ◽  
Shuya He ◽  
Qiong Chen ◽  
...  

Abstract Background Lung cancer is a common malignant tumour and the leading cause of cancer death. Smoking is closely related to lung cancer, which can not only induce the occurrence of lung cancer but also affect its progress and prognosis. Objectives To investigated the relationship between smoking and 14-3-3σ protein expression in non-small-cell lung cancer (NSCLC), investigated the relationship between 14-3-3σ expression and cell migration in A549 cells induced by cigarette smoke extract (CSE) and explored whether DNA methylation plays a role in the decreased expression of 14-3-3σ induced by CSE. Methods 14-3-3σ protein expression was examined by immunohistochemistry in 152 NSCLC tissue samples. In vitro experiments were divided into three groups: The current smoking group (CS), the ex-smoking group (ES) and the normal control group (NC). Cell transfection was used for 14-3-3σ protein overexpression. The mRNA and protein expression levels of 14-3-3σ were detected by RT-PCR and Western blotting, respectively. Cell migration was detected by Transwell and wound-healing assays, and the methylation of 14-3-3σ was detected by methylation-specific PCR. Results 14-3-3σ protein expression was decreased in NSCLC patients with a history of smoking. The expression of 14-3-3σ was decreased in A549 cells treated with CSE. The migration capacity of A549 cells treated with CSE was enhanced. DNA methylation in the cigarette smoke-treated A549 cells was higher than that in the untreated cells. Conclusion Cigarette smoke induced reduction of 14-3-3σ expression can promote the progression of non-small cell lung cancer.


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