TY - JOUR
T1 - Angiogenesis and oxidative stress in metastatic tumor progression
T2 - Pathogenesis and novel therapeutic approach of colon cancer
AU - AU YEUNG, Kathy K W
AU - KO, Joshua
N1 - Funding Information:
Our research has been supported by the Hong Kong Baptist University Faculty Research Fund FRG/11-12/II-89, FRG/09-10/II-40 and FRG/08-09/II-51.
PY - 2017/8/1
Y1 - 2017/8/1
N2 - Background: When tumor cells are under hypoxic condition or other forms of oxidative stress, one of the survival mechanisms is to undergo angiogenesis, involving dissemination of existing vessels or neovascularization to antagonize the apoptotic drive and to facilitate migration to secondary sites. Methods: This paper reveals the pathogenesis of tumor angiogenesis, particularly during hypoxia and other forms of oxidative stress in cancer cells. Results: Following successive invasion of the extracellular matrix (ECM), new blood vessels penetrate and supply nutrients to tumor tissues for growth and metastasis. The metastatic power of cancers is determined by a series of angiogenic and metastatic factors. These factors could allow neoplastic tissues to survive and withstand the stress induced by hypoxia and/or disruption of the ECM, including vascular endothelial growth factor and matrix metalloproteinases that were found to be highly elevated in tumor tissues of colon cancer patients. These aggressive factors could be regulated by cancer signaling pathways such as the phosphatidylinositol 3-kinase/Akt/ mTOR cascade. In fact, mTOR (the mammalian target of rapamycin) acts as a central regulator of many cellular activities involving growth and differentiation through regulation of cell cycle progression, cell size, cell migration and survival, including those in tumor cells. Several novel therapeutic approaches that target the angiogenic drive of cancers have been introduced, including compounds derived from natural products and synthetic chemicals. Conclusion: This article highlights the importance of angiogenesis and oxidative stress on the development of advanced and metastatic colon cancers, and provides new insights on alternative and effective treatment options.
AB - Background: When tumor cells are under hypoxic condition or other forms of oxidative stress, one of the survival mechanisms is to undergo angiogenesis, involving dissemination of existing vessels or neovascularization to antagonize the apoptotic drive and to facilitate migration to secondary sites. Methods: This paper reveals the pathogenesis of tumor angiogenesis, particularly during hypoxia and other forms of oxidative stress in cancer cells. Results: Following successive invasion of the extracellular matrix (ECM), new blood vessels penetrate and supply nutrients to tumor tissues for growth and metastasis. The metastatic power of cancers is determined by a series of angiogenic and metastatic factors. These factors could allow neoplastic tissues to survive and withstand the stress induced by hypoxia and/or disruption of the ECM, including vascular endothelial growth factor and matrix metalloproteinases that were found to be highly elevated in tumor tissues of colon cancer patients. These aggressive factors could be regulated by cancer signaling pathways such as the phosphatidylinositol 3-kinase/Akt/ mTOR cascade. In fact, mTOR (the mammalian target of rapamycin) acts as a central regulator of many cellular activities involving growth and differentiation through regulation of cell cycle progression, cell size, cell migration and survival, including those in tumor cells. Several novel therapeutic approaches that target the angiogenic drive of cancers have been introduced, including compounds derived from natural products and synthetic chemicals. Conclusion: This article highlights the importance of angiogenesis and oxidative stress on the development of advanced and metastatic colon cancers, and provides new insights on alternative and effective treatment options.
KW - Angiogenesis
KW - Chemotherapy
KW - Colon cancer
KW - Metastasis
KW - MTOR
KW - Oxidative stress
UR - http://www.scopus.com/inward/record.url?scp=85027554931&partnerID=8YFLogxK
U2 - 10.2174/1381612823666170228124105
DO - 10.2174/1381612823666170228124105
M3 - Review article
C2 - 28245762
AN - SCOPUS:85027554931
VL - 23
SP - 3952
EP - 3961
JO - Current Pharmaceutical Design
JF - Current Pharmaceutical Design
SN - 1381-6128
IS - 27
ER -