Abstract
Tumor-associated neutrophils (TANs) are important inflammatory infiltrating cells in the tumor microenvironment and are closely related to the development of human tumor. However, the underlying mechanism of TANs recruiting to glioma remains unknown. Herein, we identified that LINC01116 was significantly upregulated in glioma, and positively correlated with clinical malignancy and survival prognosis. LINC01116 regulated the progression of glioma in vitro and in vivo. RNA-seq analysis demonstrated that LINC01116 knockdown affected the expression of IL-1β, which promoted glioma proliferation and neutrophil recruitment. Furthermore, the co-culture of glioma cells and neutrophils showed that the accumulation of TANs promoted tumor proliferation via producing a host of cytokines. Mechanistically, LINC01116 activated IL-1β expression by recruiting the transcriptional regulator DDX5 to the IL-1β promoter. Our findings reveal that LINC01116 can promote glioma proliferation and neutrophil recruitment by regulating IL-1β, and may be served as a novel target for glioma therapy and prognosis.
Highlights
Glioma is currently the most common intracranial primary malignancy tumor with high heterogeneity[1,2]
The tumor microenvironment is composed of diverse cell types that are associated with tumor progression[6], including tumor-associated neutrophils (TANs), which is an important portion of the infiltrating immune cells[7]
The results showed that the expression level of LINC01116 was positively correlated with WHO pathological grade (P < 0.001), and histopathologic type (P < 0.001), indicating that the higher LINC01116 expression, the worse the prognosis of patients (Fig. 1d and Supplementary Table S2)
Summary
Glioma is currently the most common intracranial primary malignancy tumor with high heterogeneity[1,2]. The tumor microenvironment is composed of diverse cell types that are associated with tumor progression[6], including tumor-associated neutrophils (TANs), which is an important portion of the infiltrating immune cells[7]. Many patients with advanced tumor show high levels of neutrophils[8], and the neutrophil-to-lymphocyte ratio has been introduced as a significant prognostic factor for survival in many types of tumors[9,10,11,12,13]. Multiple evidence have shown that neutrophils can be recruited into the tumor microenvironment and transformed into the tumor-promoting phenotype under the effect of chemokines, cytokines, and growth factors secreted by both tumor and stromal cells[14,15,16,17]. TANs as feedback may participate in tumor progression by promoting cell proliferation, migration, and angiogenesis[18,19]
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