PMID- 30362980
OWN - NLM
STAT- MEDLINE
DCOM- 20200914
LR  - 20231213
IS  - 1473-5741 (Electronic)
IS  - 0959-4973 (Print)
IS  - 0959-4973 (Linking)
VI  - 30
IP  - 2
DP  - 2019 Feb
TI  - Baicalin induces apoptosis in SW480 cells through downregulation of the SP1 
      transcription factor.
PG  - 153-158
LID - 10.1097/CAD.0000000000000708 [doi]
AB  - Colorectal cancer occurs throughout the world but is most common in developed 
      countries. Cancer progression is believed to be driven by genetic mutations in 
      this complex condition. Risk factors for developing colorectal cancer include a 
      genetic family history, long-term ulcerative colitis, and colonic polyps. The use 
      of baicalin has been reported to be clinically efficacious against colon tumors 
      in Asian countries despite an unclear mechanism of action. Several cancers have 
      been found to be biologically dependent on the specificity protein 1 (sp1) 
      transcription factor family. We hypothesized that baicalin may exert its 
      chemotherapeutic effects by sp1 downregulation. Using the SW480 human colorectal 
      cancer cell line, we investigated the physiological properties of baicalin. Our 
      experiments were designed toward clarifying three goals: (a) to determine the 
      mRNA expression profile of transcription factors in colorectal cancer patients 
      using a microarray-based analysis; (b) to determine the effects of baicalin on 
      the sp1 transcription factor with western blotting and reporter cell assays; and 
      (c) to contrast the effects of mithramycin-A (an sp1 transcription factor 
      inhibitor) and baicalin using western blotting and reporter cell assays. Both 
      baicalin and mithramycin-A downregulated sp1 expression, attenuated SW480 cell 
      proliferation, and increased cell apoptosis. Baicalin inhibited sp1 expression 
      and led to SW480 apoptosis, thus clarifying the effect of this traditional 
      Chinese medicine compound in the treatment of colon cancer.
FAU - Ma, Wenkang
AU  - Ma W
AD  - GMU-GIBH Joint School of Life Sciences, Guangzhou Medical University.
FAU - Liu, Xueyuan
AU  - Liu X
AD  - Department of medicine, LiWan District Hospital of Chinese Medicine.
FAU - Du, Wei
AU  - Du W
AD  - Department of Pharmacy, The Second Affiliated Hospital of Guangzhou Medical 
      University, Guangzhou, People's Republic of China.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - England
TA  - Anticancer Drugs
JT  - Anti-cancer drugs
JID - 9100823
RN  - 0 (Anti-Inflammatory Agents, Non-Steroidal)
RN  - 0 (Biomarkers, Tumor)
RN  - 0 (Flavonoids)
RN  - 0 (Sp1 Transcription Factor)
RN  - 0 (SP1 protein, human)
RN  - 347Q89U4M5 (baicalin)
SB  - IM
MH  - Anti-Inflammatory Agents, Non-Steroidal/*pharmacology
MH  - *Apoptosis
MH  - Biomarkers, Tumor/genetics/*metabolism
MH  - Cell Proliferation
MH  - Colonic Neoplasms/drug therapy/genetics/metabolism/*pathology
MH  - Flavonoids/*pharmacology
MH  - Gene Expression Profiling
MH  - Gene Expression Regulation, Neoplastic/*drug effects
MH  - Humans
MH  - Sp1 Transcription Factor/*antagonists & inhibitors/genetics/metabolism
MH  - Tumor Cells, Cultured
PMC - PMC6365257
EDAT- 2018/10/27 06:00
MHDA- 2020/09/15 06:00
PMCR- 2019/02/06
CRDT- 2018/10/27 06:00
PHST- 2018/10/27 06:00 [pubmed]
PHST- 2020/09/15 06:00 [medline]
PHST- 2018/10/27 06:00 [entrez]
PHST- 2019/02/06 00:00 [pmc-release]
AID - 10.1097/CAD.0000000000000708 [doi]
PST - ppublish
SO  - Anticancer Drugs. 2019 Feb;30(2):153-158. doi: 10.1097/CAD.0000000000000708.