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Myricetin Induces Apoptosis of Human Anaplastic Thyroid Cancer Cells via Mitochondria Dysfunction.

Abstract Thyroid cancer is the most common endocrine malignancy, with an increasing incidence worldwide. Most thyroid cancers are well differentiated and have a favorable outcome. However, undifferentiated thyroid cancers are one of the most lethal human malignancies. Anaplastic thyroid cancer (ATC) accounts for 2% of all thyroid cancers, and its median survival rate is low. ATC is responsible for more than one-third of thyroid cancer-related deaths. Myricetin is a flavonol compound found in walnuts, herbs, and various berries and is known to induce apoptotic death of various types of cancer cells. However, an anticancer effect of myricetin against human anaplastic thyroid cancer (HATCs) cells has not been demonstrated.
PMID
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Authors

Mayor MeshTerms
Keywords

Bax/BcL-2 ratio

Myricetin

cell cycle

human anaplastic thyroid cancer cells

Journal Title anticancer research
Publication Year Start




PMID- 28373432
OWN - NLM
STAT- MEDLINE
DA  - 20170404
DCOM- 20170413
LR  - 20170413
IS  - 1791-7530 (Electronic)
IS  - 0250-7005 (Linking)
VI  - 37
IP  - 4
DP  - 2017 Apr
TI  - Myricetin Induces Apoptosis of Human Anaplastic Thyroid Cancer Cells via
      Mitochondria Dysfunction.
PG  - 1705-1710
AB  - AIM: Thyroid cancer is the most common endocrine malignancy, with an increasing
      incidence worldwide. Most thyroid cancers are well differentiated and have a
      favorable outcome. However, undifferentiated thyroid cancers are one of the most 
      lethal human malignancies. Anaplastic thyroid cancer (ATC) accounts for 2% of all
      thyroid cancers, and its median survival rate is low. ATC is responsible for more
      than one-third of thyroid cancer-related deaths. Myricetin is a flavonol compound
      found in walnuts, herbs, and various berries and is known to induce apoptotic
      death of various types of cancer cells. However, an anticancer effect of
      myricetin against human anaplastic thyroid cancer (HATCs) cells has not been
      demonstrated. MATERIALS AND METHODS: In the present study, the anticancer effects
      and mechanism of action of myricetin were examined using SNU-80 HATC cells.
      SNU-80 HATC cells were treated with various concentrations of myricetin and
      compared with untreated controls. RESULTS: Myricetin significantly reduced HATC
      cell proliferation, by approximately 70%. A substantial proportion of dead cells 
      exhibited arrest in the sub-G1 phase. Myricetin also exhibited cytotoxicity and
      induced DNA condensation in SNU-80 HATC cells in a dose-dependent manner. The
      mechanism of myricetin-induced cell death involved an increase in the activation 
      of caspase cascades and the Bax:Bcl-2 ratio at a concentration of 100 muM.
      Myricetin also induced the release of apoptosis-inducing factor (AIF) from
      mitochondria into the cytosol and altered the mitochondrial membrane potential.
      CONCLUSION: Our results indicate that myricetin is a potent inducer of HATC cell 
      death and may thus prove useful in the development of therapeutic agents for
      HATC.
CI  - Copyright(c) 2017, International Institute of Anticancer Research (Dr. George J. 
      Delinasios), All rights reserved.
FAU - Jo, Sunhyo
AU  - Jo S
AD  - Department of Life Sciences, BK21-plus Research Team for Bioactive Control
      Technology, College of Natural Sciences, Chosun University, Gwangju, Republic of 
      Korea.
FAU - Ha, Tae Kwun
AU  - Ha TK
AD  - Department of Surgery, Inje University College of Medicine, Busan Paik Hospital, 
      Busan, Republic of Korea.
FAU - Han, Sang-Hun
AU  - Han SH
AD  - Department of Verterinary Internal Medicine, College of Verterinary Medicine,
      Seoul National University, Seoul, Republic of Korea.
FAU - Kim, Mi Eun
AU  - Kim ME
AD  - Department of Life Sciences, BK21-plus Research Team for Bioactive Control
      Technology, College of Natural Sciences, Chosun University, Gwangju, Republic of 
      Korea.
FAU - Jung, Inae
AU  - Jung I
AD  - Department of Life Sciences, BK21-plus Research Team for Bioactive Control
      Technology, College of Natural Sciences, Chosun University, Gwangju, Republic of 
      Korea.
FAU - Lee, Hee-Woo
AU  - Lee HW
AD  - Department of Verterinary Internal Medicine, College of Verterinary Medicine,
      Seoul National University, Seoul, Republic of Korea.
FAU - Bae, Sung Kwon
AU  - Bae SK
AD  - Department of Medical Management, Kosin University, Busan, Republic of Korea.
FAU - Lee, Jun Sik
AU  - Lee JS
AD  - Department of Life Sciences, BK21-plus Research Team for Bioactive Control
      Technology, College of Natural Sciences, Chosun University, Gwangju, Republic of 
      Korea [email protected]
LA  - eng
PT  - Journal Article
PL  - Greece
TA  - Anticancer Res
JT  - Anticancer research
JID - 8102988
RN  - 0 (Flavonoids)
RN  - 0 (Proto-Oncogene Proteins c-bcl-2)
RN  - 0 (Reactive Oxygen Species)
RN  - 0 (bcl-2-Associated X Protein)
RN  - 76XC01FTOJ (myricetin)
RN  - EC 3.4.22.- (Caspases)
SB  - IM
MH  - Apoptosis/*drug effects
MH  - Caspases/metabolism
MH  - Cell Cycle/drug effects
MH  - Cell Proliferation/drug effects
MH  - Flavonoids/*pharmacology
MH  - Humans
MH  - Membrane Potential, Mitochondrial/*drug effects
MH  - Mitochondria/drug effects/metabolism/*pathology
MH  - Proto-Oncogene Proteins c-bcl-2/metabolism
MH  - Reactive Oxygen Species/metabolism
MH  - Signal Transduction/drug effects
MH  - Thyroid Carcinoma, Anaplastic/drug therapy/metabolism/*pathology
MH  - Thyroid Neoplasms/drug therapy/metabolism/*pathology
MH  - Tumor Cells, Cultured
MH  - bcl-2-Associated X Protein/metabolism
OTO - NOTNLM
OT  - *Bax/BcL-2 ratio
OT  - *Myricetin
OT  - *cell cycle
OT  - *human anaplastic thyroid cancer cells
EDAT- 2017/04/05 06:00
MHDA- 2017/04/14 06:00
CRDT- 2017/04/05 06:00
PHST- 2017/01/21 [received]
PHST- 2017/03/07 [revised]
PHST- 2017/03/08 [accepted]
AID - 37/4/1705 [pii]
AID - 10.21873/anticanres.11502 [doi]
PST - ppublish
SO  - Anticancer Res. 2017 Apr;37(4):1705-1710.

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