PMID- 35732438
OWN - NLM
STAT- MEDLINE
DCOM- 20220908
LR  - 20220908
IS  - 1347-5215 (Electronic)
IS  - 0918-6158 (Linking)
VI  - 45
IP  - 9
DP  - 2022 Sep 1
TI  - Bisdemethoxycurcumin Inhibits VEGF-Induced HUVECs Proliferation, Migration and 
      Invasion through AMPK/mTOR Pathway-Dependent Autophagy Activation and Cell Cycle 
      Arrest.
PG  - 1276-1282
LID - 10.1248/bpb.b22-00194 [doi]
AB  - Vascular endothelial growth factor (VEGF) is a key mediator of angiogenesis, 
      which plays a key role in the proliferation, migration and invasion of 
      endothelial cell. Bisdemethoxycurcumin (BDMC) is a natural demethoxy curcumin 
      derivative. In this study, we explored the mechanisms whereby BDMC is able to 
      influence the proliferative, migratory and invasive activity of human umbilical 
      vein endothelial cells (HUVECs) in response to VEGF treatment. These experiments 
      revealed that BDMC at 10 and 20 microM suppressed HUVECs proliferation in response to 
      VEGF (10 ng/mL) without impacting the proliferation in absence of VEGF. BDMC 
      treatment also signifantly suppressed VEGF-induced migratory and invasive 
      activity in HUVECs. However, the selective AMP-activated protein kinase (AMPK) 
      inhibitor compound C (3 microM) treatment signifantly reversed all of these effects. 
      Flow cytometric assay showed BDMC treatment was found to induce G0/G1 phase cell 
      cycle arrest. Western blotting further indicated that BDMC treatment increased 
      the ratios of p-AMPK/AMPK and LC3B/LC3A, up-regulated the expression of Beclin-1, 
      decreased the ratio of p-mammalian target of rapamycin (mTOR)/mTOR, 
      down-regulated the expression of cyclin D1 and CDK4. Overall, these data 
      suggested that BDMC may exert benefical effect on HUVECs activation by activating 
      autophagy and inducing cell cycle arrest through regulation of the AMPK/mTOR 
      pathway, which could provide a potential compound candidate for the treatment of 
      diseases related to VEGF overproduction.
FAU - Wang, Xianbin
AU  - Wang X
AD  - Department of Rheumatology and Immunology, The Affiliated Yantai Yuhuangding 
      Hospital of Qingdao University.
FAU - Qu, Tiantian
AU  - Qu T
AD  - Department of Rheumatology and Immunology, The Affiliated Yantai Yuhuangding 
      Hospital of Qingdao University.
FAU - Sun, Chuanfen
AU  - Sun C
AD  - Department of Rheumatology and Immunology, The Affiliated Yantai Yuhuangding 
      Hospital of Qingdao University.
FAU - Wang, Mingyu
AU  - Wang M
AD  - Department of Rheumatology and Immunology, The Affiliated Yantai Yuhuangding 
      Hospital of Qingdao University.
LA  - eng
PT  - Journal Article
DEP - 20220621
PL  - Japan
TA  - Biol Pharm Bull
JT  - Biological & pharmaceutical bulletin
JID - 9311984
RN  - 0 (Antineoplastic Agents)
RN  - 0 (Diarylheptanoids)
RN  - 0 (Vascular Endothelial Growth Factor A)
RN  - 2EFO1BP34R (bisdemethoxycurcumin)
RN  - EC 2.7.1.1 (MTOR protein, human)
RN  - EC 2.7.11.1 (TOR Serine-Threonine Kinases)
RN  - EC 2.7.11.31 (AMP-Activated Protein Kinases)
SB  - IM
MH  - AMP-Activated Protein Kinases/metabolism
MH  - *Antineoplastic Agents/pharmacology
MH  - Autophagy
MH  - Cell Cycle Checkpoints
MH  - Cell Proliferation
MH  - Diarylheptanoids
MH  - Human Umbilical Vein Endothelial Cells
MH  - Humans
MH  - Signal Transduction
MH  - TOR Serine-Threonine Kinases/metabolism
MH  - *Vascular Endothelial Growth Factor A
OTO - NOTNLM
OT  - autophagy
OT  - bisdemethoxycurcumin
OT  - cell cycle
OT  - human umbilical vein endothelial cell
EDAT- 2022/06/23 06:00
MHDA- 2022/09/09 06:00
CRDT- 2022/06/22 21:13
PHST- 2022/06/23 06:00 [pubmed]
PHST- 2022/09/09 06:00 [medline]
PHST- 2022/06/22 21:13 [entrez]
AID - 10.1248/bpb.b22-00194 [doi]
PST - ppublish
SO  - Biol Pharm Bull. 2022 Sep 1;45(9):1276-1282. doi: 10.1248/bpb.b22-00194. Epub 
      2022 Jun 21.