Nidogen-1 expression is associated with overall survival and temozolomide sensitivity in low-grade glioma patients

Abstract

We investigated the prognostic significance of nidogen-1 (NID1) in glioma. Oncomine, GEPIA, UALCAN, CCGA database analyses showed that NID1 transcript levels were significantly upregulated in multiple cancer types, including gliomas. Quantitative RT-PCR analyses confirmed that NID1 expression was significantly upregulated in glioma tissues compared to paired adjacent normal brain tissue samples (n=9). NID1 silencing enhanced in vitro apoptosis and the temozolomide sensitivity of U251 and U87-MG glioma cells. Protein-protein interaction network analysis using the STRING and GeneMANIA databases showed that NID1 interacts with several extracellular matrix proteins. TIMER database analysis showed that NID1 expression in low-grade gliomas was associated with tumor infiltration of B cells, CD4 + and CD8 + T cells, macrophages, neutrophils, and dendritic cells. Kaplan-Meier survival curve analysis showed that low-grade gliomas patients with high NID1 expression were associated with shorter overall survival. However, NID1 expression was not associated with overall survival in glioblastoma multiforme patients. These findings demonstrate that NID1 expression in glioma tissues is associated with overall survival of low-grade glioma patients and temozolomide sensitivity. NID1 is thus a potential prognostic biomarker and therapeutic target in low-grade glioma patients.

Single-cell epigenetic analysis reveals principles of chromatin states in H3.3-K27M gliomas

“…Among these genes that were both upregulated in H3-K27M-high cells and included in the published signature, were genes known to promote high proliferation and stemness, such as MET (Wallace et al, 2013), ID4 (Jeon et al, 2008), HEY-1 (Brun et al, 2018), VGF (Wang et al, 2018) and ITGA6 (Ying et al, 2014). The gene NID-1, whose expression levels correlated with shorter survival rates for patients (Zhang et al, 2021), was also elevated in H3-K27M-high cells. Finally, H3-K27M-low cells expressed higher levels of the tumor-suppressor gene CDKN2A (p16).…”

Single-cell epigenetic analysis reveals principles of chromatin states in H3.3-K27M gliomas

“…Among the genes upregulated in H3-K27Mhigh cells were genes promoting high proliferation and stemness, such as MET (Wallace et al, 2013), ID4 (Jeon et al, 2008), HEY-1 (Brun et al, 2018), VGF (Wang et al, 2018), and ITGA6 (Ying et al, 2014). The gene NID-1, whose expression levels correlated with patients' shorter survival rates (Zhang et al, 2021), was also elevated in H3-K27M-high cells. Finally, H3-K27M-low cells expressed higher levels of the tumor-suppressor gene CDKN2A (p16).…”

SOCS5 contributes to temozolomide resistance in glioblastoma by regulating Bcl-2-mediated autophagy

“…Subsequently, DNA mismatches cause DNA double-strand breaks and trigger cell death [ 10 , 11 ]. Although the use of TMZ improves the general survival rate of patients [ 12 ], the overall therapeutic effect and prognosis are unsatisfactory. The main factor limiting clinical efficiency is the development of resistance to TMZ in the majority of GBM patients [ 13 , 14 ], Overcoming this problem has become a key target for GBM research.…”