PMID- 32521909
OWN - NLM
STAT- MEDLINE
DCOM- 20210208
LR  - 20210208
IS  - 2241-6293 (Electronic)
IS  - 1107-0625 (Linking)
VI  - 25
IP  - 2
DP  - 2020 Mar-Apr
TI  - Bleomycin inhibits proliferation and promotes apoptosis of brain glioma cells via 
      TGF-beta/Smad signaling pathway.
PG  - 1076-1083
AB  - PURPOSE: To investigate the influence of bleomycin (BLM) on the proliferation and 
      apoptosis of brain glioma cells through transforming growth factor-beta 
      (TGF-beta)/Smads signaling pathway. METHODS: The U87 brain glioma cells were 
      cultured in vitro and reacted with different concentrations of BLM (5 and 10 
      mU/mL), and the cell growth status of each group was observed under a microscope. 
      The cell proliferation activity was detected using Cell Counting Kit-8 (CCK-8) 
      assay, the percentage of 5-Ethynyl-2'-deoxyuridine (EdU)-positive cells in each 
      group was determined via EdU staining, and the apoptosis of U87 cells was tested 
      by means of terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling 
      (TUNEL) staining. In addition, reverse transcription-polymerase chain reaction 
      (RT-PCR) was performed to measure the messenger ribonucleic acid (mRNA) levels of 
      genes related to proliferation, apoptosis and the TGF-beta/Smads signaling pathway. 
      Finally, western blotting assay was performed to analyze the expression of the 
      TGF-beta/Smads signaling pathway. RESULTS: In the 5 mU/mL BLM group, the glioma 
      cells were in a poor growth status, with a low density, while the 10 mU/mL BLM 
      group exhibited the poorest growth status and the lowest density, and the 
      morphological structure trended toward normal. It was discovered via CCK-8 assay 
      and EdU staining that the number of cells and proliferation activity were 
      decreased markedly in the 10 mU/mL BLM group. According to TUNEL staining, 10 
      mU/mL BLM group had remarkably increased apoptotic cells, while negative control 
      (NC) group had fewer apoptotic cells. The gene assay results revealed that the 
      gene expressions of Bcl-2 and TGF-beta1 declined notably in the 10 mU/mL BLM group 
      but rose in the NC group, and the gene expression trends of Caspase-3 and Smad4 
      were the opposite. The protein assay results manifested that the expressions of 
      TGF-beta1 was obviously reduced, while that of Smad4 was evidently raised in the 10 
      mU/mL BLM group. CONCLUSION: BLM at an appropriate concentration can inhibit the 
      proliferation and promote apoptosis of brain glioma cells by repressing the 
      TGF-beta/Smads signaling pathway, thus ameliorating and treating brain glioma and 
      other related diseases.
FAU - Jin, Haiquan
AU  - Jin H
AD  - Department of Neurosurgery, the first People's Hospital of Huaihua City, Huaihua, 
      Hunan 418000, China.
FAU - Luo, Changjun
AU  - Luo C
LA  - eng
PT  - Journal Article
PL  - Cyprus
TA  - J BUON
JT  - Journal of B.U.ON. : official journal of the Balkan Union of Oncology
JID - 100883428
RN  - 0 (Antibiotics, Antineoplastic)
RN  - 0 (Transforming Growth Factor beta1)
RN  - 11056-06-7 (Bleomycin)
SB  - IM
MH  - Antibiotics, Antineoplastic/pharmacology/*therapeutic use
MH  - Apoptosis/*drug effects
MH  - Bleomycin/pharmacology/*therapeutic use
MH  - Cell Proliferation/*drug effects
MH  - Glioma/*drug therapy/genetics
MH  - Humans
MH  - Signal Transduction
MH  - Transforming Growth Factor beta1/*genetics
EDAT- 2020/06/12 06:00
MHDA- 2021/02/09 06:00
CRDT- 2020/06/12 06:00
PHST- 2020/06/12 06:00 [entrez]
PHST- 2020/06/12 06:00 [pubmed]
PHST- 2021/02/09 06:00 [medline]
PST - ppublish
SO  - J BUON. 2020 Mar-Apr;25(2):1076-1083.