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Antiangiogenic activity of vitexicarpine in experimentally induced hepatocellular carcinoma: Impact on vascular endothelial growth factor pathway.

Abstract Angiogenesis plays important roles in progression of hepatocellular carcinoma. The antiangiogenic mechanisms of vitexicarpine are not fully defined. Therefore, we conducted the following study to evaluate the antiangiogenic mechanism and antitumor activity of vitexicarpine in vivo model of hepatocellular carcinoma through modulation of vascular endothelial growth factor signaling pathway. Hepatocellular carcinoma was induced in Sprague Dawley rats by thioacetamide. Hepatocellular carcinoma was assessed by measuring serum alpha-fetoprotein and investigating liver sections stained with hematoxylin/eosin. Hepatocellular carcinoma rats were injected with vitexicarpine (150 mg/kg) for 2 weeks. Hepatic vascular endothelial growth factor was measured by enzyme-linked immunosorbent assay. Protein and expression of hepatic phospho-Ser473-AKT (p-AKT) and phospho-Tyr419-Src (p-Src) were determined. The apoptotic pathway was evaluated by assessment of protein expression of caspase-3. Vitexicarpine increased rats' survival time and decreased serum alpha-fetoprotein as well as it ameliorated fibrosis and massive hepatic tissue breakdown. It attenuated hepatocellular carcinoma-induced protein and gene expression of vascular endothelial growth factor, p-AKT, p-Src, and caspase-3. In conclusion, this study suggests that vitexicarpine possesses both antiangiogenic and antitumor activities through inhibition of vascular endothelial growth factor, p-AKT/AKT, and p-Src with subsequent inhibition of apoptotic pathway.
PMID
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Authors

Mayor MeshTerms
Keywords

Hepatocellular carcinoma

angiogenesis

caspase-3

p-AKT

p-Src

vascular endothelial growth factor

Journal Title tumour biology : the journal of the international society for oncodevelopmental biology and medicine
Publication Year Start




PMID- 28651490
OWN - NLM
STAT- MEDLINE
DA  - 20170627
DCOM- 20170710
LR  - 20170713
IS  - 1423-0380 (Electronic)
IS  - 1010-4283 (Linking)
VI  - 39
IP  - 6
DP  - 2017 Jun
TI  - Antiangiogenic activity of vitexicarpine in experimentally induced hepatocellular
      carcinoma: Impact on vascular endothelial growth factor pathway.
PG  - 1010428317707376
LID - 10.1177/1010428317707376 [doi]
AB  - Angiogenesis plays important roles in progression of hepatocellular carcinoma.
      The antiangiogenic mechanisms of vitexicarpine are not fully defined. Therefore, 
      we conducted the following study to evaluate the antiangiogenic mechanism and
      antitumor activity of vitexicarpine in vivo model of hepatocellular carcinoma
      through modulation of vascular endothelial growth factor signaling pathway.
      Hepatocellular carcinoma was induced in Sprague Dawley rats by thioacetamide.
      Hepatocellular carcinoma was assessed by measuring serum alpha-fetoprotein and
      investigating liver sections stained with hematoxylin/eosin. Hepatocellular
      carcinoma rats were injected with vitexicarpine (150 mg/kg) for 2 weeks. Hepatic 
      vascular endothelial growth factor was measured by enzyme-linked immunosorbent
      assay. Protein and expression of hepatic phospho-Ser473-AKT (p-AKT) and
      phospho-Tyr419-Src (p-Src) were determined. The apoptotic pathway was evaluated
      by assessment of protein expression of caspase-3. Vitexicarpine increased rats'
      survival time and decreased serum alpha-fetoprotein as well as it ameliorated
      fibrosis and massive hepatic tissue breakdown. It attenuated hepatocellular
      carcinoma-induced protein and gene expression of vascular endothelial growth
      factor, p-AKT, p-Src, and caspase-3. In conclusion, this study suggests that
      vitexicarpine possesses both antiangiogenic and antitumor activities through
      inhibition of vascular endothelial growth factor, p-AKT/AKT, and p-Src with
      subsequent inhibition of apoptotic pathway.
FAU - Hassoun, Shimaa M
AU  - Hassoun SM
AD  - 1 Department of Biochemistry, Faculty of Pharmacy, Mansoura University, Mansoura,
      Egypt.
FAU - Abdel-Rahman, Noha
AU  - Abdel-Rahman N
AD  - 1 Department of Biochemistry, Faculty of Pharmacy, Mansoura University, Mansoura,
      Egypt.
FAU - Eladl, Entsar I
AU  - Eladl EI
AD  - 2 Department of Pathology, Oncology Center, Faculty of Medicine, Mansoura
      University, Mansoura, Egypt.
FAU - El-Shishtawy, Mamdouh M
AU  - El-Shishtawy MM
AD  - 1 Department of Biochemistry, Faculty of Pharmacy, Mansoura University, Mansoura,
      Egypt.
LA  - eng
PT  - Journal Article
PL  - United States
TA  - Tumour Biol
JT  - Tumour biology : the journal of the International Society for Oncodevelopmental
      Biology and Medicine
JID - 8409922
RN  - 0 (Angiogenesis Inhibitors)
RN  - 0 (Neoplasm Proteins)
RN  - 0 (Vascular Endothelial Growth Factor A)
RN  - 0 (alpha-Fetoproteins)
RN  - 075T165X8M (Thioacetamide)
RN  - 7V515PI7F6 (Apigenin)
RN  - 9VP70K75OK (vitexin)
SB  - IM
MH  - Angiogenesis Inhibitors/administration & dosage
MH  - Animals
MH  - Apigenin/*administration & dosage
MH  - Apoptosis/drug effects
MH  - Carcinoma, Hepatocellular/chemically induced/*drug therapy/genetics/pathology
MH  - Cell Line, Tumor
MH  - Cell Proliferation/drug effects
MH  - Gene Expression Regulation, Neoplastic/drug effects
MH  - Humans
MH  - Liver Neoplasms/chemically induced/*drug therapy/genetics/pathology
MH  - Neoplasm Proteins/biosynthesis/genetics
MH  - Neovascularization, Pathologic/chemically induced/*drug
      therapy/genetics/pathology
MH  - Rats
MH  - Signal Transduction/drug effects
MH  - Thioacetamide/toxicity
MH  - Vascular Endothelial Growth Factor A/*genetics
MH  - Xenograft Model Antitumor Assays
MH  - alpha-Fetoproteins/metabolism
OTO - NOTNLM
OT  - Hepatocellular carcinoma
OT  - angiogenesis
OT  - caspase-3
OT  - p-AKT
OT  - p-Src
OT  - vascular endothelial growth factor
EDAT- 2017/06/28 06:00
MHDA- 2017/07/14 06:00
CRDT- 2017/06/28 06:00
AID - 10.1177/1010428317707376 [doi]
PST - ppublish
SO  - Tumour Biol. 2017 Jun;39(6):1010428317707376. doi: 10.1177/1010428317707376.