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1.
Eur J Pharmacol ; 769: 203-10, 2015 Dec 15.
Article in English | MEDLINE | ID: mdl-26593433

ABSTRACT

Exposure to arsenic is one of the major causes of lung cancer due to production of Reactive Oxygen Species (ROS). Herbal medicine is a new approach used for prevention or treatment of cancers. Among various herbal compounds, a lot of attention has been paid to curcumin, as antioxidant, anti-proliferative, anti-carcinogenic and anti-tumor and pro-apoptotic properties of curcumin have been well studied. In the present study, we investigated the effects of curcumin on lung cancer cell lines and arsenic-treated lung cancer cell lines, originated from different stages of lung cancer development. Here, we measured ROS generation and caspase 3/7 activity for both curcumin-treated cell lines and those co-treated with arsenic and curcumin. Then, we studied lipid peroxidation, intracellular ATP content, and cytochrome c release to further investigate how ROS generation and curcumin exert synergistic effects and direct cells toward apoptosis. According to our data, curcumin has a dual effect on ROS generation which is dependent on specific concentration as a threshold and seems to induce apoptosis by two different mechanisms. Moreover, for the first time we report that curcumin delays the drop in ATP levels in these cell lines and hence provides required energy for apoptosis process. Furthermore, western blot analysis reveals that release of cytochrome c is highest when ATP begins to drop in the presence of curcumin. To sum it up, it seems that curcumin is strong candidate for prevention or treatment of lung cancer, especially at stage 2.


Subject(s)
Adenosine Triphosphate/metabolism , Antineoplastic Agents/pharmacology , Apoptosis/drug effects , Curcumin/pharmacology , Lung Neoplasms/pathology , Mitochondria/drug effects , Reactive Oxygen Species/metabolism , Arsenic/pharmacology , Caspase 3/metabolism , Caspase 7/metabolism , Cell Survival/drug effects , Cytochromes c/metabolism , Dose-Response Relationship, Drug , Drug Interactions , Humans , Lipid Peroxidation/drug effects , Mitochondria/metabolism , Time Factors
2.
Hum Immunol ; 76(10): 770-4, 2015 Oct.
Article in English | MEDLINE | ID: mdl-26429330

ABSTRACT

Galectins constitute an evolutionary conserved family that binds to ß-galactosides. There is growing evidence that galectins are implicated in essential biological processes such as cellular communication, inflammation, differentiation and apoptosis. Galectin-3 is one of the best-known galectins, which is found in vertebrates. Galectin-3 has been shown to be expressed in some cell lines and plays important roles in several physiological and pathological processes, including cell adhesion, cell activation and chemoattraction, cell cycle, apoptosis, cell growth, and differentiation. Moreover, this galectin is of interest due to its involvement in regulation of cancer. Changes in galectin-3 expression are commonly seen in cancerous and pre-cancerous conditions and galectin-3 may be involved in the regulation of cancer cell activities that contribute to tumourigenesis, cancer progression and metastasis. Finally, galectin-3 seems to be involved in cell events in tumor microenvironment, and therefore it could be considered as a target in transitional cell carcinoma therapies. This review aims to describe recent progress in understanding the role of galectin-3 in cancer biology, with emphasis on bladder tumor progression and metastasis.


Subject(s)
Carcinogenesis/immunology , Carcinoma, Transitional Cell/immunology , Galectin 3/genetics , Gene Expression Regulation, Neoplastic , Neovascularization, Pathologic/immunology , Urinary Bladder Neoplasms/immunology , Animals , Antineoplastic Agents/therapeutic use , Blood Proteins , Carcinogenesis/drug effects , Carcinogenesis/genetics , Carcinogenesis/pathology , Carcinoma, Transitional Cell/drug therapy , Carcinoma, Transitional Cell/genetics , Carcinoma, Transitional Cell/pathology , Galectin 3/antagonists & inhibitors , Galectin 3/immunology , Galectins , Humans , Neoplasm Metastasis , Neovascularization, Pathologic/drug therapy , Neovascularization, Pathologic/genetics , Neovascularization, Pathologic/pathology , Signal Transduction , Tumor Microenvironment , Urinary Bladder/drug effects , Urinary Bladder/immunology , Urinary Bladder/pathology , Urinary Bladder Neoplasms/drug therapy , Urinary Bladder Neoplasms/genetics , Urinary Bladder Neoplasms/pathology
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