AI Article Synopsis
- The cytokine MIF promotes tumor cell growth and prevents apoptosis in malignant glioblastoma by influencing cell-cycle progression and angiogenesis.
- In vitro experiments demonstrated that reducing MIF levels in glioblastoma cells led to decreased growth rates, especially under conditions that typically prevent cell proliferation (contact inhibition).
- Findings also revealed that MIF plays a crucial role in maintaining uncontrolled cell growth by modulating proteins associated with contact inhibition, suggesting that targeting MIF could be a potential therapeutic strategy for treating glioblastomas.
Article Abstract
Background: Studies of the role of the cytokine macrophage-migration-inhibitory-factor (MIF) in malignant tumors have revealed its stimulating influence on cell-cycle progression, angiogenesis and anti-apoptosis.
Results: Here we show that in vitro targeting MIF in cultures of human malignant glioblastoma cells by either antisense plasmid introduction or anti-MIF antibody treatment reduced the growth rates of tumor cells. Of note is the marked decrease of proliferation under confluent and over-confluent conditions, implying a role of MIF in overcoming contact inhibition. Several proteins involved in contact inhibition including p27, p21, p53 and CEBPalpha are upregulated in the MIF antisense clones indicating a restoration of contact inhibition in the tumor cells. Correspondingly, we observed a marked increase in MIF mRNA and protein content under higher cell densities in LN18 cells. Furthermore, we showed the relevance of the enzymatic active site of MIF for the proliferation of glioblastoma cells by using the MIF-tautomerase inhibitor ISO-1.
Conclusion: Our study adds another puzzle stone to the role of MIF in tumor growth and progression by showing the importance of MIF for overcoming contact inhibition.
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Source |
|---|---|
| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2810303 | PMC |
| http://dx.doi.org/10.1186/1471-2407-9-464 | DOI Listing |
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