KIF2C is a Biomarker Correlated With Prognosis and Immunosuppressive Microenvironment in Human Tumors

Abstract

Kinesin superfamily member 2C (KIF2C) is an essential regulator of the cell cycle and its aberrant expression can promote tumor progression. However, the mechanism of KIF2C in pan-cancer is unclear.Data were obtained from public databases, including The Cancer Genome Atlas (TCGA), UALCAN, TIMER and CellMiner. The data came from public databases such as The Cancer Genome Atlas (TCGA), UALCAN, TIMER, and CellMiner. We analyzed the correlation of KIF2C with expression, prognosis, tumor mutation burden (TMB), microsatellite instability (MSI), mismatch repairs (MMR), immune infiltration and anticancer drug sensitivity by R language.KIF2C was highly expressed in several tumors and correlated with poor prognosis. KIF2C expression was significantly correlated with TMB, MSI, MMRs, and immune checkpoint genes, and with the level of immune cell infiltration such as tumor-associated macrophage (TAM), cancer-associated fibroblasts (CAFs), myeloid-derived suppressor cells (MDSCs) and Tregs. The GO and KEGG results suggest that KIF2C is involved in immune regulation in addition to cell cycle regulation.In addition, KIF2C is associated with DNA methylation, m6A modifications and m7G modifications. Our data suggest that KIF2C is a prognostic biomarker linked to immunosuppression, targeting KIF2C may improve the outcome of immunotherapy. Our findings indicate that KIF2C is a prognostic biomarker associated with immunosuppression, and that targeting KIF2C may improve the outcome of immunotherapy.

Identification of the relationship between single-cell N6-methyladenosine regulators and the infiltrating immune cells in esophageal carcinoma

“…Increasing research has revealed the significance of RNA m 6 A methylation in regulating and modulating immune cells [ [53] , [54] , [55] , [56] ]. A previous study showed that KIF2C expression was significantly tumor-associated macrophages (TAMs), which were involved in m 6 A modification [ 57 ]. Also， studies have demonstrated that C1q + TAMs are controlled by the m 6 A program and regulate tumor-infiltrating CD8 + T cells via the expression of numerous immunomodulatory ligands [ 55 ].…”

Identifying Biomarkers for Prognostic Treatment in Breast Cancer through Bioinformatics Analysis

“…19 Research suggests that the regulation of KIF2C in these tumor cells is disrupted, leading to enhanced mitotic defects and promoting tumor progression. 20 TTK protein kinase (TTK) is a dual-speci city protein kinase with the ability to phosphorylate tyrosine, serine, and threonine residues. It is associated with cell proliferation.…”

M7G-related tumor immunity: novel insights of RNA modification and potential therapeutic targets

“…Moreover, single cells RNA-seq analysis in HNSCC also revealed that METTL1 knockout could impair direct communication between stromal cells and epithelial cells via inhibition of IL-1b and its receptors 99 . Specific to each subtype, the infiltration of CAFs was demonstrated to be positively correlated with the m7G regulator KIF2C, and eIF4E could promote the oncogenic transformation of fibroblasts by facilitating nuclear export of cyclin D1 mRNAs 71 , 114 . Previous studies revealed that the endothelial cell line HUVEC could be shaped by METTL1.…”

“…The translation of TGF-β2 was upregulated by METTL1-dependent tRNA m7G modification, which could induce the differentiation of peripheral blood mononuclear cells (PBMCs) into PMN-MDSCs and increase their infiltration, thereby suppress the function of CD8 + T cells and promote HCC progression [76,113]. Moreover, clustering analysis in HCC demonstrated that the m7G modification level positively correlated with abundance of MDSCs in TIME, and some novel regulators such as NUDT16 and KIF2C were involved in MDSCs regulation [114,115]. On the contrary, comprehensive analysis based on m7G-related genes in skin cutaneous melanoma (SKM) suggested the higher overall survival regulated by EIF4E3 and IFIT5, which was associated with more immune infiltration including MDSCs [116].…”