Severity: Warning
Message: file_get_contents(https://...@gmail.com&api_key=61f08fa0b96a73de8c900d749fcb997acc09&a=1): Failed to open stream: HTTP request failed! HTTP/1.1 429 Too Many Requests
Filename: helpers/my_audit_helper.php
Line Number: 197
Backtrace:
File: /var/www/html/application/helpers/my_audit_helper.php
Line: 197
Function: file_get_contents
File: /var/www/html/application/helpers/my_audit_helper.php
Line: 271
Function: simplexml_load_file_from_url
File: /var/www/html/application/helpers/my_audit_helper.php
Line: 3165
Function: getPubMedXML
File: /var/www/html/application/controllers/Detail.php
Line: 597
Function: pubMedSearch_Global
File: /var/www/html/application/controllers/Detail.php
Line: 511
Function: pubMedGetRelatedKeyword
File: /var/www/html/index.php
Line: 317
Function: require_once
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The inhibitory activities of tea catechins against carcinogenesis and cancer cell growth have been demonstrated in a large number of laboratory studies. Many mechanisms for modulating cancer signaling and metabolic pathways have been proposed based on numerous studies in cell lines with (-)-epigallocatechin-3-gallate, the most abundant and active tea catechin. Nevertheless, the molecular basis for the proposed mechanisms and whether these mechanisms indeed contribute to the anticancer activities in vivo are not clearly known. This chapter reviews the basic redox properties of tea catechins, their binding to key enzymes and signal transduction proteins, and other mechanisms that lead to suppression of cell proliferation, increased apoptosis, and inhibition of angiogenesis. More weight is put on studies in vivo over experiments in vitro. It also discusses key issues involved in extrapolating results from cell line studies to mechanistic insights in vivo.
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Source |
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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5659712 | PMC |
http://dx.doi.org/10.1016/B978-0-12-802215-3.00010-0 | DOI Listing |