Abstract
The aim of this study is to reveal the potential value of dynamin3 (DNM3) in colorectal cancer (CRC) evaluation of clinical diagnosis and prognosis. A total of 100 tissue samples were collected from 50 patients with stages I–IV, CRC tissues (n = 50) paired with non-cancerous adjacent colorectal tissues (n = 50). The expression levels of DNM3 were detected in 50 cases of CRC tissues and 50 cases of non-cancerous adjacent colorectal tissues by real-time fluorescent quantitative reverse transcription-polymerase chain reaction (RT-PCR). Immunohistochemical method (IHC) was conducted to semi-quantify the expression of DNM3 protein. Results showed that the relative expression of DNM3 mRNA in CRC tissues was 0.634-fold of that in non-cancerous adjacent colorectal tissues. The positive rate of DNM3 protein in CRC tissues (42.0%) was much lower than that in non-cancerous adjacent colorectal tissues (66.0%; P < 0.05). The expression level of DNM3 protein in CRC tissues was dependent on tumor size, degree of histological differentiation, and clinical stage (P < 0.05). The expression level of DNM3 mRNA in CRC tissues was significantly correlated with tumor size and pathology classification (P < 0.05). The research shows that detecting the expression of DNM3 helps in analyzing the tumor size, degree of histological differentiation, and clinical stage. Expression of DNM3 may be associated with good outcome in CRC.
Highlights
Colorectal cancer (CRC) is the third most common malignancy and the second most common cause of death from malignancy
reverse transcriptionpolymerase chain reaction (RT-PCR) and Immunohistochemical method (IHC) were used to detect the expression of DNM3 in colorectal cancer (CRC) and non-cancerous adjacent colorectal tissues
The results showed that the relative expression of DNM3 mRNA in CRC was 0.634-fold of that in non-cancerous adjacent colorectal tissues
Summary
Colorectal cancer (CRC) is the third most common malignancy and the second most common cause of death from malignancy. The WHO Cancer Research Center’s Globocan project estimated that there will be 1.8 million new cases of CRC and 880,000 deaths worldwide in 2018 [1]. The etiology of CRC is complex, and the exact molecular mechanism underlying its occurrence and development remains unclear. Tumor suppressor genes (TSGs) and their products have become the focus of research. An oncogene is a kind of gene that inhibits cell growth and has the potential to inhibit cancer. Studies showed that inactivation of multiple TSGs occurs during the development of CRC, and the inactivation mechanism includes loss of gene fragments, hypermethylation of gene promoters, and amplification of proto-oncogenes [2,3]
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