gms | German Medical Science

Objective: Cold-inducible RNA binding protein (CIRBP) is a stress induced protein which plays a key role in RNA dynamics, translational efficiency and metabolism. Recent studies have implicated CIRBP in many human diseases including several types of cancer. In tumor CIRBP promotes tumor growth by coordinating the translation of selected transcripts associated with survival and proliferation. Its role in glioblastoma (GBM) has not yet been examined. Here, we examine its role in GBM by examining cell death and proliferation after downregulation of this protein in GBM cells.

Methods: Four Alexa 488 labeled siRNA’s were used for the downregulation of CIRBP in glioblastoma U87MG cell lines, using lipofectamine. Downregulation was confirmed by Western blot. Fluorescence-activated cell sorting (FACS) was used to determine apoptosis (Annexin-V), necrosis (propidium iodide) and proliferation (5-Ethynyl-2′-deoxyuridine) rate after downregulation of CIRBP.

Results: In order to increase the downregulation rate of CIRBP, four siRNA targeting different regions of CIRBP were transfected twice. The downregulation rate was ca. 80%, as shown by western blot. FACS based analysis showed the increase in apoptosis after the CIRBP downregulation, where the necrosis rate was unchanged. There was no change in proliferation efficacy under this condition.

Conclusion: The variations in CIRBP protein levels influence the apoptosis rate of glioblastoma cells. The role of CIRBP in protecting against apoptosis in GBM must be further examined and confirmed but could potentially define CIRBP as one of the GBM targets. Particularly its influence and possibility to sensitize GBM to standard of care therapy should be stressed, since the GBM represent a cancer type with a whole variety of genetic and epigenetic changes but no real valuable drug targets.