PMID- 17786368
OWN - NLM
STAT- MEDLINE
DCOM- 20071119
LR  - 20190606
IS  - 1021-335X (Print)
IS  - 1021-335X (Linking)
VI  - 18
IP  - 4
DP  - 2007 Oct
TI  - Inhibitory effects of retinoic acid and IIF on growth, migration and invasiveness 
      in the U87MG human glioblastoma cell line.
PG  - 1015-21
AB  - Glioblastomas, the most malignant and prevalent brain tumors which remain 
      incurable, are characterized by both extensive proliferation and invasive growth. 
      We previously reported a remarkable antitumoral effect of the retinoid 
      6-OH-11-O-hydroxyphenantrene (IIF) on neuroblastoma, leukemia and colon carcinoma 
      cells. In this study we examined the effect of IIF on proliferation, apoptosis 
      and cell invasion in the human glioblastoma cell line U87MG, in comparison with 
      all-trans-retinoic acid (RA). Our results showed that both retinoids induced cell 
      growth inhibition and apoptosis in a dose- and time-dependent manner. We also 
      demonstrated that the invasive ability of glioblastoma cells decreased after 
      treatment with IIF or RA. Since cell invasion involves a complex system of 
      tightly regulated proteases, matrix metalloproteinases (MMPs) and their specific 
      inhibitors, tissue inhibitors of MMPs (TIMPs), we analysed the effect of IIF on 
      MMP and TIMP expression in comparison with RA. Treatment with both retinoids 
      resulted in a marked decrease of MMP2 and MMP9 expression and of lytic activity 
      of MMP2. In addition, exposure to IIF led to enhanced expression of TIMP2. 
      Collectively, our results demonstrated the effectiveness of both IIF and RA in 
      inhibiting proliferation, cell migration, and the invasive potential of 
      glioblastoma U87MG cells. Notably, the anticancer activity of IIF, on the whole, 
      was more pronounced than that of RA. Therefore, these findings, besides providing 
      further evidence that IIF may be a powerful tool in the development of cancer 
      treatments, suggest that IIF may have therapeutic potential against the 
      invasiveness of brain tumors.
FAU - Papi, A
AU  - Papi A
AD  - Department of Experimental Evolutive Biology, University of Bologna, 40126 
      Bologna, Italy.
FAU - Bartolini, G
AU  - Bartolini G
FAU - Ammar, K
AU  - Ammar K
FAU - Guerra, F
AU  - Guerra F
FAU - Ferreri, A M
AU  - Ferreri AM
FAU - Rocchi, P
AU  - Rocchi P
FAU - Orlandi, M
AU  - Orlandi M
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - Greece
TA  - Oncol Rep
JT  - Oncology reports
JID - 9422756
RN  - 0 (Annexin A5)
RN  - 0 (Antineoplastic Agents)
RN  - 0 (IIF compound)
RN  - 0 (RNA, Messenger)
RN  - 0 (RNA, Neoplasm)
RN  - 127497-59-0 (Tissue Inhibitor of Metalloproteinase-2)
RN  - 5688UTC01R (Tretinoin)
RN  - EC 3.4.24.24 (Matrix Metalloproteinase 2)
RN  - EC 3.4.24.35 (Matrix Metalloproteinase 9)
SB  - IM
MH  - Annexin A5/metabolism
MH  - Antineoplastic Agents/*pharmacology
MH  - Blotting, Western
MH  - Brain Neoplasms/*drug therapy/pathology
MH  - Cell Movement/*drug effects
MH  - Cell Proliferation/*drug effects
MH  - Glioblastoma/*drug therapy/pathology
MH  - Humans
MH  - Matrix Metalloproteinase 2/genetics/metabolism
MH  - Matrix Metalloproteinase 9/genetics/metabolism
MH  - Neoplasm Invasiveness/pathology
MH  - RNA, Messenger/genetics/metabolism
MH  - RNA, Neoplasm/genetics/metabolism
MH  - Reverse Transcriptase Polymerase Chain Reaction
MH  - Tissue Inhibitor of Metalloproteinase-2/genetics/metabolism
MH  - Tretinoin/*analogs & derivatives/*pharmacology
MH  - Tumor Cells, Cultured/drug effects/pathology
EDAT- 2007/09/06 09:00
MHDA- 2007/12/06 09:00
CRDT- 2007/09/06 09:00
PHST- 2007/09/06 09:00 [pubmed]
PHST- 2007/12/06 09:00 [medline]
PHST- 2007/09/06 09:00 [entrez]
AID - 10.3892/or.18.4.1015 [doi]
PST - ppublish
SO  - Oncol Rep. 2007 Oct;18(4):1015-21. doi: 10.3892/or.18.4.1015.