Article
Expression of potential tumour promoter LRIG2 is higher in secondary glioblastoma than in primary glioblastomas
Die Expression von LRIG2 ist höher in sekundären GBM als in primären Glioblastomen
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Published: | May 25, 2022 |
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Objective: The LRIG gene family consists of LRIG1-3 which encode integral membrane proteins. While LRIG1 and LRIG3 are believed to be tumor suppressors, LRIG2 seems to function as a tumor promoter. It has been reported that LRIG2 expression is upregulated in gliomas and increases with higher tumor grade. In this study, we aim to analyze and compare the expression of LRIG2 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 was performed, detecting LRIG2 with a primary antibody and a peroxidase-conjugated secondary antibody. Data was statistically analyzed using ANOVA, Kruskal-Wallis and Mann-Whitney-U tests. Immunofluorescence was performed on cryo slices of the same subgroups (n=3 per group) with a primary LRIG2 antibody and a Cy3-conjugated secondary antibody.
Results: In secondary glioblastomas, LRIG2 protein levels were significantly higher than in primary glioblastomas (pGBM 0.225 ± 0.2333 vs. sGBM 0.846 ± 0.2934; p=0.0039). LRIG2 showed a trend towards increased expression with heightened malignancy. Grade III gliomas tended to have a higher expression of LRIG2 than grade II gliomas (grade II 0.533 ± 0.339 vs. grade III 0.752 ± 0.294). Secondary glioblastomas had a tendency towards higher LRIG2 protein levels than grade III gliomas (grade III 0.752 ± 0.294 vs. sGBM 0.846 ± 0.295). High grade gliomas showed a trend towards expressing more LRIG2 than low grade gliomas (LGG 0.533 ± 0.229 vs. HGG 0.638 ± 0.387). A tendency towards a lower expression of LRIG2 in glioblastoma treated with chemotherapy compared to glioblastomas without chemotherapy treatment was seen (GBM - CTx 0.762 ± 0.409 vs. GBM + CTx 0.310 ± 0.367). Results could be confirmed with immunofluorescence.
Conclusion: We report that LRIG2 expression in secondary glioblastomas is significantly higher than in primary glioblastomas. This reinforces suggestions that LRIG2 might play an important role in the pathogenesis of glioblastomas and that it could be a potential marker for diagnosis or clinical decision making.