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Glioblastoma multiforme (GBM) is a poor prognosis type of tumour due to its resistance to chemo and radiotherapy.  SOCS1  and  SOCS3  have been associated with tumour progression and response to treatments in different kinds of cancers, including GBM. In this study, cell lines of  IDH -wildtype GBM from primary cultures were obtained, and the role of  SOCS1  and  SOCS3  in the radiotherapy response was analysed. Fifty-two brain aspirates from GBM patients were processed, and six new cell lines of  IDH -wildtype GBM were established. These new cell lines were characterized according to the WHO classification of CNS tumours.  SOCS1  and  SOCS3  expression levels were determined, at mRNA level by Q-PCR, at protein level by immunocytochemistry, and Western blot analysis. The results showed that  SOCS1  and  SOCS3  are overexpressed in GBM, as compared to a non-tumoral brain RNA pool.  SOCS1  and  SOCS3  expression were reduced by siRNA, and it was found that  SOCS3  inhibition increases radioresistance in GBM cell lines, suggesting a key role of  SOCS3  in radioresistant acquisition. In addition, radioresistant clonal populations obtained by selective pressure on these cell cultures also showed a significant decrease in  SOCS3  expression, while  SOCS1  remained unchanged. Furthermore, the induction of  SOCS3  expression, under a heterologous promoter, in a radiotherapy resistant GBM cell line increased its radiosensitivity, supporting an important implication of  SOCS3  in radiotherapy resistance acquisition. Finally, the treatment with TSA in the most radioresistant established cell line produced an increase in the effect of radiotherapy, that correlated with an increase in the expression of  SOCS3 . These effects of TSA disappeared if the increase in the expression of  SOCS3  prevented with an siRNA against  SOCS3 . Thus,  SOCS3  signal transduction pathway (JAK/STAT) could be useful to unmask new putative targets to improve radiotherapy response in GBM.

Radiotherapy resistance acquisition in Glioblastoma. Role of SOCS1 and SOCS3