Article
Expression of potential tumour suppressor LRIG1 is higher in low grade gliomas and in secondary glioblastomas compared to high grade gliomas and primary glioblastomas
LRIG1 ist höher exprimiert in LGG und sekundären GBM als in HGG und primären GBM
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Published: | May 25, 2022 |
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Objective: The LRIG family of integral membrane proteins consists of LRIG1-3. While LRIG2 is believed to be a tumor promoter, LRIG1 and LRIG3 seem to function as tumor suppressors. In this study, we aim to analyze and compare the expression of LRIG1 in different types of gliomas.
Methods: Tumor tissue from seven subgroups (grade II, grade III, recurrent secondary glioblastoma with and without temozolomide treatment, primary glioblastoma without temozolomide treatment and recurrent primary glioblastoma with temozolomide treatment; n=5 per group) was obtained during neurosurgery. Quantitative western blot analysis with LRIG1 as primary antibody was performed. Data was statistically analyzed using ANOVA, Kruskal-Wallis and Mann-Whitney-U tests. Immunofluorescence was performed on cryo slices (n=3 per group) with LRIG1 as primary antibody.
Results: LRIG1 expression tended to negatively correlate with WHO grades. Low grade gliomas had significantly higher protein levels than high grade gliomas (LGG 0.215 ± 0.126 vs. HGG 0.079 ± 0.052; p=0.0118). Grade II gliomas showed the tendency towards a higher LRIG1 expression than grade III glioma, but the difference was not significant (grade II 0.215 ± 0.126 vs. grade III 0.153 ± 0.150). LRIG1 was significantly higher expressed in grade II glioma compared to secondary glioblastoma (grade II 0.215 ± 0.126 vs. sGBM 0.083 ± 0.038; p=0.0003). Grade III glioma also showed a trend towards a higher expression of LRIG1 than in secondary glioblastoma, although not significant (grade III 0.153 ± 0.150 vs. sGBM 0.083 ± 0.039). LRIG1 protein levels were significantly higher in secondary glioblastomas compared to primary glioblastomas (pGBM 0.052 ± 0.028 vs. sGBM 0.083 ± 0.038; p=0.014). Primary glioblastomas treated with chemotherapy showed a trend towards a lower expression of LRIG1 than those without treatment (pGBM - CTx 0.121 ± 0.136 vs. pGBM + CTx 0.059 ± 0.029). In secondary glioblastomas chemotherapy tended to correlate with a higher expression of LRIG1 (sGBM - CTx 0.084 ± 0.031 vs. sGBM + CTx 0.214 ± 0.230). Results could be confirmed with immunofluorescence.
Conclusion: LRIG1 expression in low grade gliomas is higher than in high grade gliomas. We report for the first time that secondary glioblastomas have higher LRIG1 protein levels than primary glioblastomas.