MIR17HG: MIR17HG, a long non-coding RNA, has been extensively studied in various cancers, including colon cancer [PMC9247659]. It has been found to be closely associated with tumor immunity [PMC9247659]. In primary human CD34+ progenitor cells, the binding of TAL1 and E47 to MIR17HG was examined [PMC7722897]. MIR17HG was found to be expressed in both endothelial cells (ECs) and glioma-conditioned ECs (GECs) [PMC6180493]. The promoter activity of MIR17HG was increased by β-catenin and Δ45-β-catenin, but not by the LEF1 binding site-mutated reporter [PMC6549003]. In glioma tissues and cells, the expression of FXR1 and MIR17HG was elevated [PMC6348679]. Several single nucleotide polymorphisms (SNPs) in MIR17HG were genotyped to determine their effect on glioma risk or prognosis [PMC7547478]. The association of the MIR17HG rs17735387 polymorphism with stage III/IV HNSCC risk remained noteworthy [PMC7707933]. In the Chinese Han population, certain SNPs in MIR17HG were associated with increased or decreased colorectal cancer risk [PMC7457078]. MYC appears to regulate the expression of MIR17HG along with mir-17 and mir-20a [PMC9780260]. It has been observed that MIR17HG performs oncogenic functions in both NK-cells and T-cells [PMC5620138], while its expression is dysregulated in T-cell lymphoma and early T-cell progenitor ALL [PMC5944955]. Humans with heterozygous microdeletions in the MIR17HG locus had severe skeletal abnormalities [PMC9710060]. The downregulation of miRNAs encoded by MIR17HG has been observed in MB231RN-LM cells, a cellular subline of MDA-MB-231, isolated from spontaneous lung cells [PMC9954167]. MIR17HG has been found to promote colorectal cancer tumorigenesis and metastasis by sponging miR-375 to increase NF-κB/RELA expression and upregulate PD-L1 [PMC8424797].