Curcumin: a potent agent to reverse epithelial-to-mesenchymal transition

ConclusionsIn this review, we summarize the mechanisms by which curcumin may affect EMT in cells under pathological conditions to understand its potential as a novel anti-tumor agent. Curcumin can exert chemo-preventive effects by inhibition and reversal of the EMT process through both TGF- β-dependent (e.g. in hepatoma and retinal pigment epithelial cancer) and -independent (e.g. in oral cancer, colorectal cancer, pancreatic cancer, hepatocellular carcinoma, breast cancer, melanoma, prostate cancer, bladder cancer, thyroid cancer and lung cancer) pathways. Curcumin can also mitigate chemoresistance through EMT suppression and promotion of the antiproliferative effects of conventional chemotherapeutics. Therefore, curcumin has the potential to be used as a novel adjunctive agent to prevent tumor metastasis, which may at least partly be attributed to its hampering of the EMT proc ess.
Source: Cellular Oncology - Category: Cancer & Oncology Source Type: research

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Publication date: Available online 21 November 2019Source: Journal of Cancer PolicyAuthor(s): Brandon Maser, Lisa M. Force, Paola Friedrich, Federico Antillon, Ramandeep S. Arora, Cristian A. Herrera, Carlos Rodriguez-Galindo, Rifat Atun, Avram DenburgAbstractTo help understand how health systems and sociopolitical contexts intersect with and impact the performance of childhood cancer care in low- and middle-income countries (LMICs), we have developed a systems-level framework for analyzing the performance of LMIC childhood cancer programs within their health system contexts: The Paediatric Oncology System Integration Tool...
Source: Journal of Cancer Policy - Category: Cancer & Oncology Source Type: research
Future Oncology, Ahead of Print.
Source: Future Oncology - Category: Cancer & Oncology Authors: Source Type: research
Cancer Biotherapy and Radiopharmaceuticals, Ahead of Print.
Source: Cancer Biotherapy and Radiopharmaceuticals - Category: Cancer & Oncology Authors: Source Type: research
Cancer Biotherapy and Radiopharmaceuticals, Ahead of Print.
Source: Cancer Biotherapy and Radiopharmaceuticals - Category: Cancer & Oncology Authors: Source Type: research
Date: Thursday, 12 19, 2019; Speaker: Cristine Delnevo, Ph.D., M.P.H., F.A.A.H.B., Director, Center for Tobacco Studies, Society and Policy Rutgers School of Public Health; Nir Eyal, D.Phil, Director, Center for Population-Level Bioethics (CPLB), Society and Policy Rutgers School of Public Health; https://epi.grants.cancer.gov/events/enrich-forum/
Source: NIH Calendar of Events - Category: American Health Source Type: events
Date: Tuesday, 12 03, 2019; Speaker: Erikka Loftfield, Ph.D., M.P.H., Research Fellow, Division of Cancer Epidemiology and Genetics (NCI); https://metabolomics-sig.nih.gov/events.html
Source: NIH Calendar of Events - Category: American Health Source Type: events
CONCLUSION: This mini-review will explain the present research status of Apigenin and will further throw some light on how Apigenin performs its anti-cancerous actions by interfering with the key cell-signaling pathways. PMID: 31746310 [PubMed - as supplied by publisher]
Source: Recent Patents on Anti-Cancer Drug Discovery - Category: Cancer & Oncology Tags: Recent Pat Anticancer Drug Discov Source Type: research
Nanomedicine, Ahead of Print.
Source: Nanomedicine - Category: Nanotechnology Authors: Source Type: research
CONCLUSIONS: Our observations indicate that treatment of Hep-2 laryngeal cancer cells with ELFEMF for 30 min at 25-50 mT and EP Au-NPs can cause cell damage inducing apoptosis and cell cycle arrest. PMID: 31746453 [PubMed - as supplied by publisher]
Source: Folia Histochemica et Cytobiologica - Category: Cytology Tags: Folia Histochem Cytobiol Source Type: research
In conclusion, osmotic burst of inflated complement-damaged cells may occur, but these bursts are most likely a consequence of metabolic collapse of the cell rather than the cause of cell death. The Complement Cell Death Mediator: A Concerted Action of Toxic Moieties Membrane pores caused by complement were first visualized by electron microscopy on red blood cell membranes as large ring structures (22). Similar lesions were viewed on E. coli cell walls (23). Over the years, ample information on the fine ultrastructure of the MAC that can activate cell death has been gathered (24) and has been recently further examined (...
Source: Frontiers in Immunology - Category: Allergy & Immunology Source Type: research
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