Turkish Neurosurgery
Diabetes Mellitus-Mediated MALAT1 Expression Induces Glioblastoma Aggressiveness
Aysen Akkurt Kocaeli1, Secil Ak Aksoy2, Melis Erçelik3, Gulcin Tezcan4, Cagla Tekin3, Hasan Kocaeli5, Ahmet Bekar5, Mevlut Ozgur Taskapilioglu5, Sahsine Tolunay6, Berrin Tunca3
1Bursa State Hospital, Department of Endocrinology, Bursa,
2Bursa Uludag University, Inegol Vocation School, Bursa,
3Bursa Uludag University, Department of Medical Biology, Faculty of Medicine, Bursa,
4Bursa Uludag University, Department of Fundamental Sciences, Faculty of Dentistry, Bursa,
5Bursa Uludag University, Department of Neurosurgery, Faculty of Medicine, Bursa,
6Bursa Uludag University, Department of Pathology, Faculty of Medicine, Bursa,
DOI: 10.5137/1019-5149.JTN.41845-22.2

Aim:Hyperglycemia and hyperinsulinemia increase the risk of glioblastoma (GB) by affecting the regulation of insulin-like growth factor (IGF). Metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) is involved in regulating IGF-1/PI3K/Akt signaling. This study was designed to describe the role of MALAT1 in GB progression in patients concurrently diagnosed with diabetes mellitus (DM).Material and Methods:Formalin-fixed paraffin-embedded (FFPE) tumor samples of 47 patients diagnosed with GB only and 13 patients diagnosed with GB and DM (GB-DM) were enrolled in this study. Data for P53 and Ki67 immunohistochemical staining of the tumors and blood HbA1c levels of patients with DM were retrospectively collected. MALAT1 expression was assessed using quantitative real-time polymerase chain reaction.Results:The coexistence of GB and DM induced the nuclear expression of P53 and Ki67 compared with GB only. MALAT1 expression was higher in GB-DM tumors than in GB only tumors. The expression of MALAT1 and HbA1c levels were positively correlated. Additionally, MALAT1 was positively correlated with tumoral P53 and Ki67. The disease-free survival of patients with GB-DM with high MALAT1 expression was shorter than that of those diagnosed with GB only and with a lower MALAT1 expression.Conclusion:Our findings suggest that one of the mechanisms of the facilitating effect of DM on GB tumor aggressiveness is via MALAT1 expression.

Corresponding author : Berrin Tunca