Abstract
The aim of the present study was to explore the effects of curcumin in combination with bevacizumab on the vascular endothelial growth factor (VEGF)/VEGF receptor (VEGFR)/K-ras pathway in hepatocellular carcinoma. A total of 30 Sprague Dawley (SD) rats were randomly divided into five groups: Control, model, curcumin, VEGF blocker, and curcumin + VEGF blocker groups. The mRNA levels of VEGF and VEGFR in all groups were subsequently measured by quantitative reverse transcriptase-polymerase chain reaction and the protein expression of K-ras was detected by western blot analysis. Compared with the control group, the mRNA levels of VEGF and VEGFR were revealed to be significantly increased in the model, curcumin and VEGF blocker groups. The VEGF mRNA levels in the curcumin, VEGF blocker and curcumin + VEGF blocker groups were all decreased when compared with the model group. In addition, the VEGF mRNA levels in the curcumin + VEGF blocker group were significantly lower compared with the curcumin group (P<0.05). The VEGF mRNA levels in the curcumin, VEGF blocker and curcumin + VEGF blocker groups were decreased when compared with the model group (P=0.0001). No significant differences in VEGF mRNA levels were identified between the VEGF blocker and curcumin groups (P=0.863), whereas the VEGF mRNA levels in the curcumin + VEGF blocker group were significantly lower than that of the curcumin group (P=0.025). Curcumin and the VEGF blocker are each capable of inhibiting hepatocellular carcinoma progression by regulating the VEGF/VEGFR/K-ras pathway. The combination of the two compounds has a synergistic effect on the inhibition of the effects of the VEGF signaling pathways in hepatocellular carcinoma progression.
Highlights
Curcumin is a polyphenolic compound that is extracted from ginger, turmeric and Curcuma rhizomes and exerts a wide range of antitumor effects, including the induction of tumor cell apoptosis, cell cycle arrest, and exhibits anti‐invasion and anti‐angiogenic properties [1]
The Vascular endothelial growth factor (VEGF) mRNA levels in the curcumin, VEGF blocker and curcumin + VEGF blocker groups were all lower compared with the model group (P
No significant difference was identified between the VEGF mRNA levels in the VEGF blocker group and those in the curcumin group (P>0.05), whereas those in the curcumin + VEGF blocker group were lower than those in the curcumin group (P
Summary
Curcumin is a polyphenolic compound that is extracted from ginger, turmeric and Curcuma rhizomes and exerts a wide range of antitumor effects, including the induction of tumor cell apoptosis, cell cycle arrest, and exhibits anti‐invasion and anti‐angiogenic properties [1]. Previous studies have revealed that the growth, invasion and metastasis of tumors all depend on angiogenesis [2,3,4]. Vascular endothelial growth factor (VEGF), comprising the superfamily of VEGFs, VEGF receptors (VEGFRs), downstream signaling proteins and certain nuclear transcription factors, can stimulate the proliferation of endothelial cells, which indicates an association between VEGF and the development, invasion and metastasis of tumors [5]. A rat HCC model is employed to determine the changes in mRNA levels of VEGF and VEGFR, and the expression of the K‐ras protein when curcumin is administered together with a biological target, in order to provide experimental evidence for design comprehensive therapy and improve clinical outcomes
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