ASPM and TROAP gene expression as potential malignant tumor markers

Abstract

Background: Although increasing evidence supports a vital role for assembly factor for spindle microtubules (ASPM) and trophinin-associated protein (TROAP) in the tumorigenesis of some cancers, no systematic pancancer analyses of ASPM and TROAP have been performed. Thus, we aimed to investigate the potential functions of ASPM and TROAP across 31 cancer types.Methods: Based on datasets from The Cancer Genome Atlas (TCGA), Human Protein Atlas (HPA), Gene-Cloud of Biotechnology Information (GCBI) and Gene Expression Omnibus (GEO), we employed an array of bioinformatics methods to explore the potential oncogenic roles of ASPM and TROAP.Results: ASPM and TROAP, which were highly expressed in most cancers and presented a strict positive correlation, led to a decreased life expectancy among cancer patients. ASPM and TROAP both regulated cell replication in the S&G2 phase of the cell cycle. Through a protein-protein interaction network (PPI) analysis of ASPM and TROAP, we found that cell division cycle 20 (CDC20) was regulated by TROAP and functioned upstream of ASPM. Thus, TROAP can regulate the role of ASPM in cancers. Conclusions:The ASPM and TROAP have a significant positive correlation and similar expression profiles, and promote tumor malignancy and development in the S&G2 phase of the cell cycle. Since ASPM is one of the downstream targets of TROAP, TROAP and especially ASPM may be potential tumor makers and promising targets for therapeutic strategy.

TROAP Promotes the Proliferation, Migration, and Metastasis of Kidney Renal Clear Cell Carcinoma with the Help of STAT3

“…TROAP can affect tumor progression through various pathways; for example, it can promote disease progression through the Wnt3/survival protein signaling pathway in prostate cancer [16]. In addition, Han Liu et al found that TROAP regulated cell division cycle 20 (CDC20) and influenced spindle microtubules (ASPM) to promote malignant tumor development during the S and G2 phases of the cell cycle [17]. Lastly, TROAP can be used as the target of some microRNAs to inhibit the proliferative activity of cancer cells [13].…”

A Model-agnostic Computational Method for Discovering Gene–Phenotype Relationships and Inferring Gene Networks viain silicoGene Perturbation

“…Notable among the therapeutic target genes associated with breast cancer identified through this approach with the LOG model are TFPI2 [27][28][29], TROAP [30][31][32][33], and TONSL [34][35][36]. In the MLP model, critical genes such as TNNT1 [37,38] and AQP7 [39][40][41] were also identified as potential therapeutic targets.…”

The neurological and non-neurological roles of the primary microcephaly-associated protein ASPM

“…For example, the microcephaly gene DONSON encodes a replication fork protein that maintains genome stability by stabilizing stalled forks and activating replication checkpoints (Reynolds et al, 2017). Several bioinformatic methods have indicated that ASPM, along with its upstream regulator trophinin-associated protein (TROAP) and downstream factor cell division cycle 20 (CDC20), may regulate cell replication during the S and G2 cell cycle phases; however, details of the mechanism involved remain unknown (Liu et al, 2022). Recently, a study carried out by our group in HeLa cells uncovered the function of ASPM in maintaining genome stability in response to replication stress .…”