PMID- 25674233
OWN - NLM
STAT- MEDLINE
DCOM- 20151028
LR  - 20220408
IS  - 1936-2625 (Electronic)
IS  - 1936-2625 (Linking)
VI  - 7
IP  - 12
DP  - 2014
TI  - Dihydroartemisinin inhibits cell proliferation via AKT/GSK3beta/cyclinD1 pathway and 
      induces apoptosis in A549 lung cancer cells.
PG  - 8684-91
AB  - Lung cancer is the most common cause of cancer-related death in the world. The 
      main types of lung cancer are small cell lung carcinoma (SCLC) and non-small-cell 
      lung carcinoma (NSCLC); non small cell lung carcinoma (NSCLC) includes squamous 
      cell carcinoma (SCC), adenocarcinoma and large cell carcinoma, Non small cell 
      lung carcinoma accounts for about 80% of the total lung cancer cases. 
      Dihydroartemisinin (DHA) inhibits cell proliferation and induces apoptosis in 
      several cancer cell lines. The effects of DHA on cell growth and proliferation in 
      lung cancer cells remain to be elucidated. Here, we demonstrate that DHA 
      inhibited cell proliferation in the A549 lung cancer cell line through 
      suppression of the AKT/Gsk-3beta/cyclin D1 signaling pathway. DHA significantly 
      inhibited cell proliferation of A549 cells in a concentration and time dependent 
      manner as determined by MTS assay. Flow cytometry analysis demonstrated that DHA 
      treatment of A549 cells resulted in cell cycle arrest at the G1 phase, which 
      correlated with apparent downregulation of both mRNA and protein levels of both 
      PCNA and cyclin D1. These results suggest that DHA is a potential natural product 
      for the treatment of lung cancer.
FAU - Liao, Kui
AU  - Liao K
AD  - Department of Oncology, The First Affiliated Hospital of Chongqing Medical 
      University Chongqing 400016, China.
FAU - Li, Juan
AU  - Li J
AD  - Department of Pharmacy, The Fifth People's Hospital of Chongqing Chongqing 
      400016, China.
FAU - Wang, Zhiling
AU  - Wang Z
AD  - Department of Oncology, The First Affiliated Hospital of Chongqing Medical 
      University Chongqing 400016, China.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20141201
PL  - United States
TA  - Int J Clin Exp Pathol
JT  - International journal of clinical and experimental pathology
JID - 101480565
RN  - 0 (Antineoplastic Agents)
RN  - 0 (Artemisinins)
RN  - 136601-57-5 (Cyclin D1)
RN  - 6A9O50735X (artenimol)
RN  - EC 2.7.11.1 (GSK3B protein, human)
RN  - EC 2.7.11.1 (Glycogen Synthase Kinase 3 beta)
RN  - EC 2.7.11.1 (Proto-Oncogene Proteins c-akt)
RN  - EC 2.7.11.26 (Glycogen Synthase Kinase 3)
SB  - IM
MH  - Antineoplastic Agents/*pharmacology
MH  - Apoptosis/*drug effects
MH  - Artemisinins/*pharmacology
MH  - Cell Line, Tumor
MH  - Cell Proliferation/drug effects
MH  - Cyclin D1/metabolism
MH  - Flow Cytometry
MH  - Glycogen Synthase Kinase 3/metabolism
MH  - Glycogen Synthase Kinase 3 beta
MH  - Humans
MH  - Immunohistochemistry
MH  - Lung Neoplasms/metabolism/*pathology
MH  - Proto-Oncogene Proteins c-akt/metabolism
MH  - Real-Time Polymerase Chain Reaction
MH  - Signal Transduction/*drug effects
PMC - PMC4314032
OTO - NOTNLM
OT  - Dihydroartemisinin
OT  - cell cycle
OT  - cell proliferation
OT  - cyclinD1
EDAT- 2015/02/13 06:00
MHDA- 2015/10/29 06:00
PMCR- 2014/12/01
CRDT- 2015/02/13 06:00
PHST- 2014/10/07 00:00 [received]
PHST- 2014/12/01 00:00 [accepted]
PHST- 2015/02/13 06:00 [entrez]
PHST- 2015/02/13 06:00 [pubmed]
PHST- 2015/10/29 06:00 [medline]
PHST- 2014/12/01 00:00 [pmc-release]
PST - epublish
SO  - Int J Clin Exp Pathol. 2014 Dec 1;7(12):8684-91. eCollection 2014.