Abstract
Pancreatic adenocarcinoma (PAAD) is a malignant tumor with high morbidity and mortality worldwide. Members from the structural maintenance of chromosomes (SMC) gene family function as oncogenes in various tumor types, but their roles in PAAD have not been elucidated. In this study, we aimed to explore the role of the SMC family in tumor progression and cancer immune infiltration in PAAD using integrative bioinformatic analyses. The results showed that the SMC 1A, 2, 3, 4, and 6 were overexpressed in PAAD tissues; of these, SMC 1A, 4, 5, and 6 could be potential prognostic biomarkers for PAAD. The expression of SMC genes was found to be strongly associated with immune cell infiltration. According to the infiltrative status of various immune cells, the mRNA expression of SMC genes in PAAD was associated with the overall and recurrence-free survival of patients. In conclusion, the SMC gene family is associated with PAAD and may be involved in tumorigenesis and cancer-immune interactions; thus, members from this gene family may serve as promising prognostic and therapeutic biomarkers of PAAD.
Highlights
Pancreatic adenocarcinoma (PAAD) is one of the most prevalent types of cancers worldwide, showing high mortality and transfer rates [1]
We found that the mRNA expression of the structural maintenance of chromosomes (SMC) gene family was increased in most human cancers (Figure 1A)
The results showed an abundant expression of SMC1A, SMC4, and SMC6 in PAAD tissues; SMC2 was expressed weakly, compared to that in the normal tissues (Figure 2)
Summary
Pancreatic adenocarcinoma (PAAD) is one of the most prevalent types of cancers worldwide, showing high mortality and transfer rates [1]. The incidence of PAAD has recently increased, with 5-year survival rates of 2–9% [2]. Because the clinical symptoms of PAAD are insidious and atypical, the diagnosis and treatment for this condition pose a critical challenge [3]. Cancer cells usually disseminate by the time >80% of PAAD patients are initially diagnosed, making surgical removal ineffective [4]. Diagnosis and treatment are key to improving the prognosis of PAAD patients [5, 6]. New molecular markers and therapeutic targets are urgently needed to improve the clinical prognosis and outcomes of PAAD patients
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