PMID- 23244151
OWN - NLM
STAT- MEDLINE
DCOM- 20130604
LR  - 20211203
IS  - 2476-762X (Electronic)
IS  - 1513-7368 (Linking)
VI  - 13
IP  - 10
DP  - 2012
TI  - Beta-asarone induces LoVo colon cancer cell apoptosis by up-regulation of 
      caspases through a mitochondrial pathway in vitro and in vivo.
PG  - 5291-8
AB  - Beta-asarone is one of the main bioactive constituents in traditional Chinese 
      medicine Acorus calamu. Previous studies have shown that it has antifungal and 
      anthelmintic activities. However, little is known about its anticancer effects. 
      This study aimed to determine inhibitory effects on LoVo colon cancer cell 
      proliferation and to clarify the underlying mechanisms in vitro and in vivo. 
      Dose-response and time-course anti-proliferation effects were examined by MTT 
      assay. Our results demonstrated that LoVo cell viability showed dose- and 
      time-dependence on beta-asarone. We further assessed anti-proliferation effects as 
      beta-asarone-induced apoptosis by annexin V-fluorescein isothiocyanate/propidium 
      iodide assay using a flow cytometer and observed characteristic nuclear 
      fragmentation and chromatin condensation of apoptosis by microscopy. Moreover, we 
      found the apoptosis to be induced through the mitochondrial/caspase pathway by 
      decreasing mitochondrial membrane potential (MMP) and reducing the Bcl-2-to-Bax 
      ratio, in addition to activating the caspase-9 and caspase-3 cascades. 
      Additionally, the apoptosis could be inhibited by a pan-caspase inhibitor, 
      carbobenzoxy-valyl-alanyl-aspartyl-[O-methyl]-fluoromethylketone (Z-VAD-FMK). 
      When nude mice bearing LoVo tumor xenografts were treated with beta-asarone, tumor 
      volumes were reduced and terminal deoxynucleotide transferase-mediated dUTP nick 
      end labeling (TUNEL) assays of excised tissue also demonstrated apoptotic 
      changes. Taken together, these findings for the first time provide evidence that 
      beta-asarone can suppress the growth of colon cancer and the induced apoptosis is 
      possibly mediated through mitochondria/caspase pathways.
FAU - Zou, Xi
AU  - Zou X
AD  - Department of Oncology, The Affiliated Hospital of Nanjing University of Chinese 
      Medicine, Jiangsu Province, Nanjing, China.
FAU - Liu, Shen-Lin
AU  - Liu SL
FAU - Zhou, Jin-Yong
AU  - Zhou JY
FAU - Wu, Jian
AU  - Wu J
FAU - Ling, Bo-Fan
AU  - Ling BF
FAU - Wang, Rui-Ping
AU  - Wang RP
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - Thailand
TA  - Asian Pac J Cancer Prev
JT  - Asian Pacific journal of cancer prevention : APJCP
JID - 101130625
RN  - 0 (Allylbenzene Derivatives)
RN  - 0 (Anisoles)
RN  - 0 (Fibrinolytic Agents)
RN  - 0 (RNA, Messenger)
RN  - 0 (asarone)
RN  - EC 3.4.22.- (Caspases)
SB  - IM
MH  - Allylbenzene Derivatives
MH  - Animals
MH  - Anisoles/*pharmacology
MH  - Apoptosis/*drug effects
MH  - Blotting, Western
MH  - Caspases/*metabolism
MH  - Cell Proliferation/*drug effects
MH  - Colonic Neoplasms/drug therapy/metabolism/*pathology
MH  - Fibrinolytic Agents/*pharmacology
MH  - Humans
MH  - Membrane Potential, Mitochondrial/*drug effects
MH  - Mice
MH  - Mice, Nude
MH  - RNA, Messenger/genetics
MH  - Real-Time Polymerase Chain Reaction
MH  - Reverse Transcriptase Polymerase Chain Reaction
MH  - Tumor Cells, Cultured
EDAT- 2012/12/19 06:00
MHDA- 2013/06/05 06:00
CRDT- 2012/12/19 06:00
PHST- 2012/12/19 06:00 [entrez]
PHST- 2012/12/19 06:00 [pubmed]
PHST- 2013/06/05 06:00 [medline]
AID - 10.7314/apjcp.2012.13.10.5291 [doi]
PST - ppublish
SO  - Asian Pac J Cancer Prev. 2012;13(10):5291-8. doi: 10.7314/apjcp.2012.13.10.5291.