PMID- 29589394
OWN - NLM
STAT- PubMed-not-MEDLINE
LR  - 20231112
IS  - 2093-596X (Print)
IS  - 2093-5978 (Electronic)
IS  - 2093-596X (Linking)
VI  - 33
IP  - 1
DP  - 2018 Mar
TI  - Combined Effects of Baicalein and Docetaxel on Apoptosis in 8505c Anaplastic 
      Thyroid Cancer Cells via Downregulation of the ERK and Akt/mTOR Pathways.
PG  - 121-132
LID - 10.3803/EnM.2018.33.1.121 [doi]
AB  - BACKGROUND: Anaplastic thyroid cancer (ATC) is one of the most lethal human 
      malignancies. Docetaxel, a microtubule stabilizer, is a common chemotherapeutic 
      agent used to treat various metastatic cancers. However, prolonged use results in 
      various side effects and drug resistance. Flavonoids, such as baicalein, are 
      accepted chemotherapeutic and dietary chemopreventive agents with many 
      advantages, such as greater accessibility, affordability, and lower toxicity, 
      compared with traditional chemotherapy agents. In this study, we evaluated 
      whether baicalein enhances the effects of docetaxel on apoptosis and metastasis 
      in 8505c ATC cells. METHODS: The 8505c cells were treated with baicalein or 
      docetaxel individually and in combination. Cell viability was measured by MTT 
      (thiazolyl blue tetrazolium bromide) assay, and apoptosis was detected by 
      fluorescence microscopy of Hoechst-stained cells. The expression of apoptotic 
      (Bax and caspase-3), anti-apoptotic (Bcl-2), angiogenic (vascular endothelial 
      growth factor [VEGF], transforming growth factor beta [TGF-beta], E-cadherin, and 
      N-cadherin), and signaling (extracellular signal-regulated kinase [ERK] mitogen 
      activated protein kinase [MAPK], Akt, and mammalian target of rapamycin [mTOR]) 
      proteins was determined by Western blot analysis. RESULTS: The combination of 
      baicalein (50 or 100 muM) and docetaxel (10 nM) significantly inhibited 
      proliferation and induced apoptosis compared with monotherapies. The combination 
      treatment significantly inhibited the expression of Bax, caspase-3, VEGF, TGF-beta1, 
      E-cadherin, N-cadherin, and mTOR, but decreased the expression of Bcl-2 and 
      significantly decreased the phosphorylation of ERK and Akt. CONCLUSION: The 
      combination of baicalein and docetaxel effectively induced apoptosis and 
      inhibited metastasis in 8505c cells through downregulation of apoptotic and 
      angiogenic protein expression and blocking of the ERK and Akt/mTOR pathways in 
      8505c cells. These results suggest that baicalein enhances the anticancer effects 
      of docetaxel in ATC.
CI  - Copyright (c) 2018 Korean Endocrine Society.
FAU - Park, Chan Ho
AU  - Park CH
AUID- ORCID: 0000-0003-2748-0625
AD  - Department of Internal Medicine, Ulsan University Hospital, University of Ulsan 
      College of Medicine, Ulsan, Korea.
FAU - Han, Se Eun
AU  - Han SE
AUID- ORCID: 0000-0002-8613-1671
AD  - Department of Internal Medicine, Ulsan University Hospital, University of Ulsan 
      College of Medicine, Ulsan, Korea.
FAU - Nam-Goong, Il Seong
AU  - Nam-Goong IS
AUID- ORCID: 0000-0002-0492-0467
AD  - Department of Internal Medicine, Ulsan University Hospital, University of Ulsan 
      College of Medicine, Ulsan, Korea.
FAU - Kim, Young Il
AU  - Kim YI
AUID- ORCID: 0000-0002-2960-1040
AD  - Department of Internal Medicine, Ulsan University Hospital, University of Ulsan 
      College of Medicine, Ulsan, Korea.
FAU - Kim, Eun Sook
AU  - Kim ES
AUID- ORCID: 0000-0002-9311-4642
AD  - Department of Internal Medicine, Ulsan University Hospital, University of Ulsan 
      College of Medicine, Ulsan, Korea. endo10@daum.net.
LA  - eng
PT  - Journal Article
PL  - Korea (South)
TA  - Endocrinol Metab (Seoul)
JT  - Endocrinology and metabolism (Seoul, Korea)
JID - 101554139
PMC - PMC5874188
OTO - NOTNLM
OT  - 8505c cells
OT  - Angiogenesis
OT  - Apoptosis
OT  - Baicalein
OT  - Combination therapy
OT  - Docetaxel
OT  - Thyroid carcinoma, anaplastic
COIS- No potential conflict of interest relevant to this article was reported.
EDAT- 2018/03/29 06:00
MHDA- 2018/03/29 06:01
PMCR- 2018/03/01
CRDT- 2018/03/29 06:00
PHST- 2017/11/07 00:00 [received]
PHST- 2018/01/24 00:00 [revised]
PHST- 2018/01/29 00:00 [accepted]
PHST- 2018/03/29 06:00 [entrez]
PHST- 2018/03/29 06:00 [pubmed]
PHST- 2018/03/29 06:01 [medline]
PHST- 2018/03/01 00:00 [pmc-release]
AID - 33.121 [pii]
AID - 10.3803/EnM.2018.33.1.121 [doi]
PST - ppublish
SO  - Endocrinol Metab (Seoul). 2018 Mar;33(1):121-132. doi: 10.3803/EnM.2018.33.1.121.