Abstract
Aim. To investigate the correlation between Sirtuin 3 (SIRT3) expression and the clinical outcome of patients with colon cancer. Methods. The tumor specimens from 127 patients with colon cancer were obtained for SIRT3 immunohistochemical staining. Patients were followed up. In in vitro study, SIRT3 gene was inhibited to observe the effects of SIRT3 on the biological behavior of cultured colon cells. Results. The SIRT3 expression level was found to be significantly associated with the lymph node metastasis (P < 0.001) and tumor stages (P < 0.001). The colon cancer-specific survival was 64.6% among patients with high SIRT3 expressions and 88.6% among patients with low SIRT3 expressions (log-rank P = 0.016). The overall survival was 80.2% among patients with low SIRT3 expressions and 55.9% among patients with high SIRT3 expressions (log-rank P = 0.002). In vitro study showed that silencing of SIRT3 gene inhibited the proliferation, invasion, and cells migration but increased the apoptosis in the cultured colon cell lines. Conclusion. This study provides evidence supporting that SIRT3 is closely associated with the clinical outcomes of colon cancer. SIRT3 may be considered as a marker for colon cancer.
Highlights
Colon cancer is a worldwide health problem with 655,000 deaths per year [1, 2]
High Sirtuin 3 (SIRT3) expression was seen in 71 patients and low SIRT3 expression was seen in 56 patients
We found that there was no significant correlation between the expression level of SIRT3 and patients’ age (P = 0.415), gender (P = 0.052), and tumor size (P = 0.312); higher SIRT3 expression level was found to be significantly associated with tumor stages (P < 0.001) and lymph node metastasis (P < 0.001) but not transvascular metastasis (P < 0.001)
Summary
Colon cancer is a worldwide health problem with 655,000 deaths per year [1, 2]. In China, colon cancer remains a major cause of cancer-related death [3, 4]. Despite the development of new treatment in recent decades, the five-year survival rate of advanced colon cancer patients remains very poor because of insensitivity to chemotherapy and more prone to recurrence [5,6,7]. Some studies revealed that SIRT3 is a tumor promoter that prompts tumorigenesis. In oral squamous cell carcinoma (OSCC) cell lines, downregulation of SIRT3 inhibited OSCC cell growth and proliferation and increased OSCC cell sensitivity to radiation and cisplatin treatments in vitro [14]. Studies have shown that SIRT3 downregulation reduced tumor burden in vivo [14]. Some studies showed that SIRT3 may be a tumor suppressor [14]. SIRT3 inhibits hepatocellular carcinoma cell growth through reducing Mdm2-mediated p53 degradation [16]. The function of SIRT3 varies in normal and tumor tissues and may be cell- and tumor-type specific
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