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1.
Int J Mol Sci ; 21(5)2020 Mar 04.
Artigo em Inglês | MEDLINE | ID: mdl-32143309

RESUMO

Green tea (Camellia sinesis) is widely known for its anticancer and anti-inflammatory properties. Among the biologically active compounds contained in Camellia sinesis, the main antioxidant agents are catechins. Recent scientific research indicates that the number of hydroxyl groups and the presence of characteristic structural groups have a major impact on the antioxidant activity of catechins. The best source of these compounds is unfermented green tea. Depending on the type and origin of green tea leaves, their antioxidant properties may be uneven. Catechins exhibit the strong property of neutralizing reactive oxygen and nitrogen species. The group of green tea catechin derivatives includes: epicatechin, epigallocatechin, epicatechin gallate and epigallocatechin gallate. The last of these presents the most potent anti-inflammatory and anticancer potential. Notably, green tea catechins are widely described to be efficient in the prevention of lung cancer, breast cancer, esophageal cancer, stomach cancer, liver cancer and prostate cancer. The current review aims to summarize the potential anticancer effects and molecular signaling pathways of major green tea catechins. It needs to be clearly emphasized that green tea as well as green tea catechols cannot replace the standard chemotherapy. Nonetheless, their beneficial effects may support the standard anticancer approach.


Assuntos
Antioxidantes/farmacologia , Catequina/química , Chá/química , Animais , Anti-Inflamatórios/farmacologia , Anticarcinógenos/farmacologia , Catequina/análogos & derivados , Fermentação , Humanos , Células-Tronco Neoplásicas/efeitos dos fármacos , Polifenóis/química , Prognóstico
2.
Redox Biol ; 55: 102395, 2022 Sep.
Artigo em Inglês | MEDLINE | ID: mdl-35841627

RESUMO

Lung cancer is one of the most common cancers worldwide, causing nearly one million deaths each year. Herein, we present the effect of 2-methoxyestradiol (2-ME), the endogenous metabolite of 17ß-estradiol (E2), on non-small cell lung cancer (NSCLC) cells. We observed that 2-ME reduced the viability of lung adenocarcinoma in two-dimensional (2D) and three-dimensional (3D) spheroidal A549 cell culture models. Molecular modeling was carried out aiming to visualize amino acid residues within binding pockets of the acyl-protein thioesterases, namely 1 (APT1) and 2 (APT2), and thus to identify which ones were more likely involved in the interaction with 2-ME. Our findings suggest that 2-ME acts as an APT1 inhibitor enhancing protein palmitoylation and oxidative stress phenomena in the lung cancer cell. In order to support our data, metabolomics of blood serum from NSCLC patients was also performed. Moreover, computational analysis suggests that 2-ME as compared to other estrogen metabolism intermediates is relatively safe in terms of its possible non-receptor bioactivity within healthy human cells due to a very low electrophilic potential and hence no substantial risk of spontaneous covalent modification of biologically protective nucleophiles. We propose that 2-ME can be used as a selective tumor biomarker in the course of certain types of lung cancers and possibly as a therapeutic adjuvant or neoadjuvant.

3.
Stem Cell Res ; 52: 102239, 2021 04.
Artigo em Inglês | MEDLINE | ID: mdl-33601098

RESUMO

Currently, the world is facing the SARS-CoV-2 pandemic, coronavirus of acute respiratory distress syndrome 2, causes of COVID-19. Coronaviruses are RNA single-stranded viruses that have an envelope. In addition, coronaviruses are classified into four subfamilies: alpha, beta, gamma and delta coronaviruses. The first of them, cause mildly symptomatic or asymptomatic infections, while beta-coronaviruses are responsible for severe diseases. SARS-CoV-2 belongs to the group of beta-coronaviruses. Current available therapies use corticosteroids to reduce inflammation, non-specific antiviral drugs or antibiotics in the treatment of secondary bacterial infections. In addition, therapies based on the use of hydroxychloroquine, chloroquine, remdesvir, ribavirin, interferon or lopinavir-ritonavir were also initially used. Mesenchemical stem cells (MSCs) are widely used in cell therapies, which include both basic research and clinical trials. Their exceptional effectiveness and safety have been confirmed and documented in many clinical studies, which include a number of inflammatory diseases involving the immune system - one of them is systemic lupus erythematosus. Available data indicate the ability to differentiate MSCs and their immunomodulatory effects. In addition, through interactions with immune cells, which include, but are not limited to, macrophages and dendritic cells, or paracrine secretion, MSCs are able to secrete a number of types of cytokines. MSCs are also characterized by tissue regeneration and regulation of inflammation. Due to their properties, researchers turned to determine whether MSC transplantation is able to improve the outcome of patients with COVID-19 viral pneumonia. The presented review provides not only new knowledge in the field of molecular mechanisms of pro-regenerative action of stem cells, but also have the potential to open up new prospects of action to improve lung tissue regeneration in COVID-19 patients. In addition, in review mentioned about clinical trials using MSCs with a complete status, as well as the latest discoveries in molecular biology, a platform model of pluripotent stem cells in the SARS-CoV-2 study on 3D animal models and nanoconjugates based on stem cells.


Assuntos
COVID-19/terapia , Células-Tronco Mesenquimais/citologia , Transplante de Células-Tronco , Animais , Antivirais/uso terapêutico , Ensaios Clínicos como Assunto , Modelos Animais de Doenças , Humanos , Fatores Imunológicos , Inflamação , Pandemias , Medicina Regenerativa
4.
Antioxidants (Basel) ; 10(1)2021 Jan 16.
Artigo em Inglês | MEDLINE | ID: mdl-33467015

RESUMO

The role of autophagy is to degrade damaged or unnecessary cellular structures. Both in vivo and in vitro studies suggest a dual role of autophagy in cancer-it may promote the development of neoplasms, but it may also play a tumor protective function. The mechanism of autophagy depends on the genetic context, tumor stage and type, tumor microenvironment, or clinical therapy used. Autophagy also plays an important role in cell death as well as in the induction of chemoresistance of cancer cells. The following review describes the extensive autophagic cell death in relation to dietary polyphenols and cancer disease. The review documents increasing use of polyphenolic compounds in cancer prevention, or as agents supporting oncological treatment. Polyphenols are organic chemicals that exhibit antioxidant, anti-inflammatory, anti-angiogenic, and immunomodulating properties, and can also initiate the process of apoptosis. In addition, polyphenols reduce oxidative stress and protect against reactive oxygen species. This review presents in vitro and in vivo studies in animal models with the use of polyphenolic compounds such as epigallocatechin-3-gallate (EGCG), oleuropein, punicalgin, apigenin, resveratrol, pterostilbene, or curcumin and their importance in the modulation of autophagy-induced death of cancer cells.

5.
Artigo em Inglês | MEDLINE | ID: mdl-33466597

RESUMO

Malignant neoplasms are among the most common diseases and are responsible for the majority of deaths in the developed world. In contrast to men, available data show a clear upward trend in the incidence of lung cancer in women, making it almost as prevalent as breast cancer. Women might be more susceptible to the carcinogenic effect of tobacco smoke than men. Furthermore, available data indicate a much more frequent mutation of the tumor suppressor gene-p53 in non-small cell lung cancer (NSCLC) female patients compared to males. Another important factor, however, might lie in the female sex hormones, whose mitogenic or carcinogenic effect is well known. Epidemiologic data show a correlation between hormone replacement therapy (HRT) or oral contraceptives (OCs), and increased mortality rates due to the increased incidence of malignant tumors, including lung cancer. Interestingly, two types of estrogen receptors have been detected in lung cancer cells: ERα and ERß. The presence of ERα has been detected in tissues and non-small-cell lung carcinoma (NSCLC) cell lines. In contrast, overexpression of ERß is a prognostic marker in NSCLC. Herein, we summarize the current knowledge on the role of estrogens in the etiopathogenesis of lung cancer, as well as biological, hormonal and genetic sex-related differences in this neoplasm.


Assuntos
Carcinoma Pulmonar de Células não Pequenas , Neoplasias Pulmonares , Receptor alfa de Estrogênio/genética , Receptor beta de Estrogênio , Estrogênios , Feminino , Humanos , Neoplasias Pulmonares/induzido quimicamente , Neoplasias Pulmonares/epidemiologia , Masculino , Receptores de Estrogênio
6.
Antioxidants (Basel) ; 9(12)2020 Nov 30.
Artigo em Inglês | MEDLINE | ID: mdl-33266280

RESUMO

The catechins derived from green tea possess antioxidant activity and may have a potentially anticancer effect. PTP1B is tyrosine phosphatase that is oxidative stress regulated and is involved with prooncogenic pathways leading to the formation of a.o. breast cancer. Here, we present the effect of selected green tea catechins on enzymatic activity of PTP1B phosphatase and viability of MCF-7 breast cancer cells. We showed also the computational analysis of the most effective catechin binding with a PTP1B molecule. We observed that epigallocatechin, epigallocatechin gallate, epicatechin, and epicatechin gallate may decrease enzymatic activity of PTP1B phosphatase and viability of MCF-7 cells. Conclusions: From the tested compounds, epigallocatechin and epigallocatechin gallate were the most effective inhibitors of the MCF-7 cell viability. Moreover, epigallocatechin was also the strongest inhibitor of PTP1B activity. Computational analysis allows us also to conclude that epigallocatechin is able to interact and bind to PTP1B. Our results suggest also the most predicted binding site to epigallocatechin binding to PTP1B.

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