2017
DOI: 10.2152/jmi.64.262
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Regorafenib induces adaptive resistance of colorectal cancer cells via inhibition of vascular endothelial growth factor receptor

Abstract: : Recently, inhibition of tumor angiogenesis has become an important anti-cancer therapy. Tumor angiogenesis is regulated by multiple signaling pathways, including VEGF and VEGF receptor (VEGF-R), FGF and FGF receptor (FGF-R), and PDGF and PDGF receptor (PDGF-R) pathways. Thus, the antiangiogenic agents, such as regorafenib, simultaneously target those receptors on vascular endothelial cells. In addition to endothelial cells, cancer cells express the three receptors, suggesting that the antiangiogenic inhibito… Show more

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Cited by 16 publications
(7 citation statements)
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“…The growth of SR and ROS, res pectively, can cause lipids oxidation, 4-hydroxy-nonenal and malonic dialdehyde formation. The malonic dialdehyde can stimulate the activity of cyclooxygenase-2 (COX-2), which in turn catalyzes synthesis of prostaglandins and induces angiogenesis in RS tumors [7]. Fatty acids, the level of which increases in tumor during their own metabolism, produce electrons; their energy in mitochondrial ETC of tumor cells transform into ATP and SR due to fact that adipocytes mitochondria are dysfunctional ( Table 2).…”
Section: Resultsmentioning
confidence: 99%
“…The growth of SR and ROS, res pectively, can cause lipids oxidation, 4-hydroxy-nonenal and malonic dialdehyde formation. The malonic dialdehyde can stimulate the activity of cyclooxygenase-2 (COX-2), which in turn catalyzes synthesis of prostaglandins and induces angiogenesis in RS tumors [7]. Fatty acids, the level of which increases in tumor during their own metabolism, produce electrons; their energy in mitochondrial ETC of tumor cells transform into ATP and SR due to fact that adipocytes mitochondria are dysfunctional ( Table 2).…”
Section: Resultsmentioning
confidence: 99%
“…Зростання рівнів СР і, відповідно, ROS може викликати перекисне окиснення ліпідів та утворення 4-гідроксиноненалю та малонового діальдегіду. Останні здатні стимулювати активність циклооксигенази-2, що в свою чергу каталізує синтез простагландинів та індукує ангіогенез у пухлинах РПК [7]. Жирні кислоти, рівень яких зростає в ЖТ, у пухлині, метаболізуючи, продукують електрони, енергія яких в електронтранспортному ланцюзі (EТЛ) мітохондрій пухлинних клітин перетворюється в АТФ та СР, оскільки мітохондрії адипоцитів є дисфункціональними (див.…”
Section: об'єкт і методи дослідженняunclassified
“…Targeted agents against epidermal growth factor receptor (EGFR) and vascular endothelial growth factor receptor (VEGFR) and the multi-tyrosine kinase inhibitor regorafenib are also approved for the treatment of advanced CRC 2,3 . However, in addition to severe side effects of chemotherapy, drug resistance eventually induces relapse from persisting cancer cells also termed residual disease 4 , due to dynamic and adaptive activation of oncogenic signaling pathways that bypass treatment pressure [5][6][7] . It is widely accepted that the residual disease is formed by cancer stem-like cells (CSCs) originally existed in tumor and transformed from differentiated cancer cells through the epithelial-mesenchymal transition (EMT) during the period of treatment 4 .…”
Section: Introductionmentioning
confidence: 99%