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1.
Histol Histopathol ; 31(8): 933-42, 2016 Aug.
Article in English | MEDLINE | ID: mdl-26853489

ABSTRACT

Endometriosis is a benign gynecological disease affecting approximately 10-15% of women of reproductive age and 25-50% of all infertile women. It is characterized by the presence of glands and/or endometrial stroma outside the uterine cavity. Angiogenesis is a crucial process for the development and maintenance of endometriotic lesions. The Wnt/ß-catenin pathway is a major promoter of angiogenesis in both physiological and pathological conditions. In the present study, we evaluated the expression of molecules related to the Wnt/ß-catenin pathway in a rat model of peritoneal endometriosis. mRNA analyses showed significantly increased expression of Wnt4 and Wnt7b and decreased expression of Gsk3beta and E-cadherin in endometriotic lesions. However, there were no differences in ß-catenin and Fzd2 mRNA expression. In addition, we observed a significant increase of nuclear ß-catenin in endometriotic lesions, a hallmark of Wnt/ ß-catenin pathway activation. Stromal ß-catenin staining was found in 45.4% of endometrial tissues and 77.8% of endometriotic lesions. ß-catenin nuclear localization was found in 18.2% of the endometrial tissues and 33.3% of endometriotic lesions. Finally, the expression of galectin-3, a regulator of this pathway, was increased in endometriosis. In summary, this pattern of Wnt/ß-catenin components expression suggests an increased activity of this pathway in endometriosis.


Subject(s)
Endometriosis/metabolism , Wnt Signaling Pathway/physiology , Animals , Blotting, Western , Disease Models, Animal , Endometriosis/physiopathology , Female , Fluorescent Antibody Technique , Rats , Rats, Sprague-Dawley , Real-Time Polymerase Chain Reaction , Transcriptome , beta Catenin/metabolism
3.
J Pharm Pharmacol ; 67(12): 1744-55, 2015 Dec.
Article in English | MEDLINE | ID: mdl-26407531

ABSTRACT

OBJECTIVES: The hormonal treatment for endometriosis frequently fails to completely eradicate endometriotic implants. A new therapeutic treatment is needed. This study investigates the in-vitro effect of Copaifera langsdorffii oil-resin on human eutopic and ectopic endometrium stromal cell cultures (EuESCs and EctESCs). METHODS: A nanocomposite system containing the copaiba oil-resin (NanoCOR) was developed and acute toxicity test was performed. Endometrial stromal cells (ESCs) from non-endometriotics controls (CESCs), EuESCs and EctESCs were isolated and treated with different concentrations of NanoCOR, at different time intervals to evaluate its effect on cell morphology, proliferation, viability, necrosis and apoptosis induction. KEY FINDINGS: When treated with 50 µg/ml of NanoCOR, the morphology of EctESCs changed, as the actin microfilaments were disorganized, disassembled or disrupted. Moreover, at 24 h of treatment with NanoCOR, the EctESCs viability was inhibited, and a significant number of these cells underwent apoptosis. In EuESCs, these effects were observed only at 48 h. Finally, the treatment of EctESCs with NanoCOR increased the lactate dehydrogenase release into the extracellular medium more than in EuESCs. CONCLUSIONS: Our data indicate that NanoCOR has a greater impact on the behaviour of human endometriotic stromal cells than on the eutopic endometrium stromal cells, supporting the idea that NanoCOR should be further investigated as a novel and valuable alternative to treat endometriosis.


Subject(s)
Cell Shape/drug effects , Endometriosis/drug therapy , Endometrium/drug effects , Fabaceae/chemistry , Plant Oils/pharmacology , Resins, Plant/pharmacology , Stromal Cells/drug effects , Trees , Actin Cytoskeleton/drug effects , Actin Cytoskeleton/pathology , Animals , Apoptosis/drug effects , Case-Control Studies , Cell Proliferation/drug effects , Cell Survival/drug effects , Cells, Cultured , Dose-Response Relationship, Drug , Endometriosis/pathology , Endometrium/pathology , Female , Humans , Male , Mice , Nanoparticles , Necrosis , Phytotherapy , Plant Oils/isolation & purification , Plant Oils/toxicity , Plants, Medicinal , Rainforest , Resins, Plant/isolation & purification , Resins, Plant/toxicity , Stromal Cells/pathology , Time Factors , Tropical Climate
4.
Clin Exp Metastasis ; 31(4): 461-74, 2014 Apr.
Article in English | MEDLINE | ID: mdl-24488147

ABSTRACT

Tumor establishment, growth, and survival are supported by interactions with microenvironment components. Here, we investigated whether the interactions between prostate cancer cells and cortical astrocytes are associated to a potential role for astrocytes in tumor establishment. We demonstrate that astrocytes interact in vitro with prostatic cancers cells derived from different metastatic sites. Astrocytes and their secreted extracellular matrix, stimulate DU145 cell (a brain-derived prostate tumor cell line) proliferation while inhibiting cell death and modulating the expression of several genes related to prostate cancer progression, suggesting the activation of EMT process in these cells. In contrast, DU145 cells and their conditioned medium inhibited cell proliferation and induced cell death of astrocytes. On the other hand, the astrocytes were unable to significantly induce an increment of LNCaP cell (a lymph node-derived prostate tumor cell line) proliferative activity. In addition, LNCaP cells were also unable to induce cell death of astrocytes. Thus, we believe that DU145 cells, but not LNCaP cells, present an even more aggressive behavior when interacting with astrocytes. These results provide an important contribution to the elucidation of the cellular mechanisms involved in the brain microenvironment colonization.


Subject(s)
Astrocytes/pathology , Brain Neoplasms/secondary , Cell Communication , Cell Movement , Prostatic Neoplasms/pathology , Apoptosis , Astrocytes/metabolism , Brain Neoplasms/genetics , Cell Proliferation , Gene Expression Profiling , Humans , Male , Prostatic Neoplasms/genetics , RNA, Messenger/genetics , Real-Time Polymerase Chain Reaction , Reverse Transcriptase Polymerase Chain Reaction , Tumor Cells, Cultured , Tumor Microenvironment
5.
PLoS One ; 8(5): e62773, 2013.
Article in English | MEDLINE | ID: mdl-23667519

ABSTRACT

Pituitary adenomas comprise approximately 10-15% of intracranial tumors and result in morbidity associated with altered hormonal patterns, therapy and compression of adjacent sella turcica structures. The use of functional foods containing carotenoids contributes to reduce the risk of chronic diseases such as cancer and vascular disorders. In this study, we evaluated the influence of different concentrations of beta-carotene and lycopene on cell viability, colony formation, cell cycle, apoptosis, hormone secretion, intercellular communication and expression of connexin 43, Skp2 and p27(kip1) in ACTH-secreting pituitary adenoma cells, the AtT20 cells, incubated for 48 and 96 h with these carotenoids. We observed a decrease in cell viability caused by the lycopene and beta-carotene treatments; in these conditions, the clonogenic ability of the cells was also significantly decreased. Cell cycle analysis revealed that beta-carotene induced an increase of the cells in S and G2/M phases; furthermore, lycopene increased the proportion of these cells in G0/G1 while decreasing the S and G2/M phases. Also, carotenoids induced apoptosis after 96 h. Lycopene and beta-carotene decreased the secretion of ACTH in AtT20 cells in a dose-dependent manner. Carotenoids blocked the gap junction intercellular communication. In addition, the treatments increased the expression of phosphorylated connexin43. Finally, we also demonstrate decreased expression of S-phase kinase-associated protein 2 (Skp2) and increased expression of p27(kip1) in carotenoid-treated cells. These results show that lycopene and beta-carotene were able to negatively modulate events related to the malignant phenotype of AtT-20 cells, through a mechanism that could involve changes in the expression of connexin 43, Skp2 and p27(kip1); and suggest that these compounds might provide a novel pharmacological approach to the treatment of Cushing's disease.


Subject(s)
Adenoma/pathology , Adrenocorticotropic Hormone/metabolism , Apoptosis/drug effects , Carotenoids/pharmacology , Pituitary Neoplasms/pathology , beta Carotene/pharmacology , Animals , Cell Cycle/drug effects , Cell Line, Tumor , Cell Proliferation/drug effects , Cell Survival/drug effects , Connexin 43/metabolism , Cyclin-Dependent Kinase Inhibitor p27/metabolism , Gap Junctions/drug effects , Gap Junctions/metabolism , Lycopene , Mice , Phosphorylation/drug effects , S-Phase Kinase-Associated Proteins/metabolism
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