Abstract
IQ motif containing GTPase-activating protein 3 (IQGAP3) is a member of the Rho family of guanosine-5′-triphosphatases (GTPases). IQGAP3 plays a crucial part in the development and progression of several types of cancer. However, the prognostic, upstream-regulatory, and immunological roles of IQGAP3 in human cancer types are not known. We found that IQGAP3 expression was increased in different types of human cancer. The high expression of IQGAP3 was correlated with tumor stage, lymph node metastasis, and a poor prognosis in diverse types of human cancer. The DNA methylation of IQGAP3 was highly and negatively correlated with IQGAP3 expression in diverse cancer types. High DNA methylation in IQGAP3 was correlated with better overall survival in human cancer types. High mRNA expression of IQGAP3 was associated with tumor mutational burden, microsatellite instability, immune cell infiltration, and immune modulators. Analyses of signaling pathway enrichment showed that IQGAP3 was involved in the cell cycle. IQGAP3 expression was associated with sensitivity to a wide array of drugs in cancer cells lines. We revealed that polypyrimidine tract–binding protein 1 (PTBP1) and an IQGAP3-associated lncRNA (IQGAP3AR)/let-7c-5p axis were potential regulations for IQGAP3 expression. We provided the first evidence to show that an IQGAP3AR/let-7c-5p/IQGAP3 axis has indispensable roles in the progression and immune response in different types of human cancer.
Highlights
Cancer is a major cause of death worldwide and results in considerable social and economic burdens
Our results indicated that IQ motifs containing GTPase-activating protein 3 (IQGAP3) expression was upregulated significantly in bladder urothelial carcinoma (BLCA), breast-invasive carcinoma (BRCA), cervical squamous cell carcinoma and endocervical adenocarcinoma (CESC), cholangiocarcinoma (CHOL), colon adenocarcinoma (COAD), esophageal carcinoma (ESCA), glioblastoma multiforme (GBM), head and neck squamous cell carcinoma (HNSC), kidney renal clear cell carcinoma (KIRC), kidney renal papillary cell carcinoma (KIRP), lung adenocarcinoma (LUAD), lung squamous cell carcinoma (LUSC), pancreatic adenocarcinoma (PAAD), pheochromocytoma and paraganglioma (PCPG), prostate adenocarcinoma (PRAD), rectal adenocarcinoma (READ), stomach adenocarcinoma (STAD), thyroid carcinoma (THCA), and uterine corpus endometrial carcinoma (UCEC)
We discovered that IQGAP3 had high expression in BLCA, BRCA, CESC, CHOL, COAD, ESCA, GBM, HNSC, KIRC, KIRP, LUAD, LUSC, PAAD, PCPG, PRAD, READ, STAD, THCA, and UCEC (Figure 1A)
Summary
Cancer is a major cause of death worldwide and results in considerable social and economic burdens. Function of IQGAP3 in Cancer (Swart-Mataraza et al, 2002), IQGAP1 has been shown to participate mainly in the regulation of cellular motility (Schmidt et al, 2008). Studies have indicated that IQGAP3 is located mainly in chromosome 1 at 1q21.3 and has been reported to act as an oncogene in different types of human cancer (Xu et al, 2016; Dongol et al, 2020; Zeng et al, 2020). IQGAP3 expression has been shown to be upregulated in high-grade serous ovarian cancer, and IQGAP3 depletion inhibits the proliferation, migration, and invasion of ovarian cancer cell lines markedly (Dongol et al, 2020). IQGAP3 silencing has been demonstrated to significantly reduce the proliferation, migration, and invasion ability, and induce apoptosis in pancreatic cancer cell lines (Xu et al, 2016). IQGAP3 appears to have important roles in cancer progression and could be a promising biomarker. The prognostic and immunological roles of IQGAP3 in human cancer are not known
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