Abstract
In this study, expression of the SPC25 gene was characterized in breast cancer (BC), and its effects on BC development and progression, functions in BC cells, and potential underlying mechanisms were examined. Data from TCGAportal and FIREBROWSE indicated that SPC25 was upregulated in BC tissues compared to normal tissues, and CANCERTOOL indicated that higher SPC25 mRNA levels were associated with increased probability of recurrence and poorer survival in BC patients. BC patients with higher SPC25 expression displayed shorter distant metastasis-free survival, relapse-free survival, and overall survival. Colony formation and CCK-8 experiments confirmed that SPC25 promoted proliferation of BC cells. Single-cell analysis indicated that SPC25 is associated with cell cycle regulation, DNA damage and repair, and BC cell proliferation. SPC25 knockdown suppressed proliferation of BC cells. MiRNAs, circRNAs, RNA-binding proteins, transcription factors, and immune factors that might interact with SPC25 mRNA to promote BC were also identified. These findings suggest that SPC25 levels are higher in more malignant BC subtypes and are associated with poor prognosis in BC patients. In addition, DNA methyltransferase inhibitor and transcription factors inhibitor treatments targeting SPC25 might improve survival in BC patients.
Highlights
Breast cancer (BC) is one of the most common malignancies in women, and occurrences in young women are increasing [1,2]
Subgroup analysis based on race, age, molecular subtype, and immune subtype indicated that Spindle component 25 (SPC25) mRNA levels are significantly higher in breast cancer (BC) patients than in healthy individuals (Figure 1D–1H)
SPC25 expression was higher in basal breast cancer subtypes compared with other subtypes, suggesting that it might play a key role in basal stem cell-driven breast cancer [9]
Summary
Breast cancer (BC) is one of the most common malignancies in women, and occurrences in young women are increasing [1,2]. Despite significant advances in the diagnosis and treatment of tumors in recent years, survival times remain short for some BC patients. Tumorigenesis can arise from genetic instability in the cell cycle resulting from inaccurate chromosomal segregation, a process in which www.aging-us.com kinetochores play a crucial role [5]. A recent study reported that SPC25 is up-regulated in lung cancer and is associated with carcinogenesis, cancer cell growth, and metastasis [6]. SPC25 expression is elevated in prostate cancer (PrC) and affects proliferation and cell cycle progression in PrC cells [7,8]. Pathania and colleagues reported that SPC25 is significantly overexpressed in human breast tumor tissues and is associated with reduced overall survival in BC patients [9]. The detailed functions and molecular mechanisms of SPC25 in BC remain unknown
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