The identification of cancer stem cells (CSCs) has improved the understanding of tumor occurrence and development. According to CSC theory, colorectal carcinoma (CRC) may be derived from these few cells. Thus, markers for CSCs may lead to the identification of CSCs and investigation of the correlation with various clinicopathological features and survival time in human CRC patients. Aldehyde dehydrogenase 1 (ALDH1) and CD133 (also known as Prominin-1 or AC133) were involved in the current study. The aim of the present study was to identify CSCs through markers of CSCs and to explore the value of the CSC markers, ALDH1 and CD133, in human CRC. The correlation between ALDH1 and CD133 protein expression and the various clinicopathological parameters were investigated through immunohistochemistry (IHC). In addition, the Kaplan-Meier method was used to estimate patients’ overall survival. Correlation of the survival differences between ALDH1- or CD133-positive expression and negative controls was analyzed by the log-rank test. Furthermore, the correlation between the expression of ALDH1 and CD133 was assessed by Spearman’s rank correlation. A marked correlation between the differentiation degree and expression of ALDH1 in tumor cells was demonstrated, but not with CD133 expression. In addition, it was demonstrated that low-stage tumors exhibit a higher expression of ALDH1 or CD133 staining compared with high-stage tumors. Meanwhile, CD133 expression was associated with lymph node metastasis-positive cases, but ALDH1 expression was not. Furthermore, compared with negative cases, ALDH1-positive patients exhibited a poor prognosis. However, no significant difference was identified between CD133-positive and -negative cases in terms of survival time. Overall, the results of the present study indicated that ALDH1 and CD133 may serve as useful markers of CSC to predict disease prognosis and clinicopathological characteristics of human CRC.
Since the identification of cancer stem cells (CSCs) a new understanding of tumor occurrence and development has evolved. According to the stem cell (SC) theory, colorectal carcinoma (CRC) SCs may be derived from mutations in normal intestinal cells. CSCs can be defined by their cell of origin (SCs or early progenitor cells). Thus, through a shared stem cell marker between CSCs and SCs, it is possible to investigate the association between its expression and the various clinicopathological features in patients with CRC. Aldehyde dehydrogenase 1 (ALDH1) is an appropriate marker. The present study was performed to examine the role of ALDH1 in CRC. Through indirect fluorescence antibody staining, the association between ALDH1 protein expression and various clinicopathological parameters was investigated. Furthermore, enzyme‑linked immunosorbent assay (ELISA) was used to investigate the differing content of ALDH1 between CRC tissues and normal colorectal tissues. The results revealed that ALDH1 expression was markedly associated with tumor stage, Dukes' stage and the level of tumor cell differentiation. Using ELISA, it was demonstrated that there was a greater level of ALDH1 in CRC tissue than in normal colorectal tissue. Therefore, ALDH1 levels can be used as a useful parameter for pathological evaluation of tissue histology and to predict disease prognosis.
Nesfatin-1 is a novel anorexigenic peptide that possesses antihyperglycemic and cardiovascular effects. We hypothesized that nesfatin-1 has a beneficial protective effect against diabetic cardiomyopathy (DC). We investigated the therapeutic effect of nesfatin-1 on diabetes-associated cardiac dysfunction in the high-fat diet (HFD)/streptozotocin (STZ)-induced diabetic mouse model. We found that the cardiac nesfatin-1 level was lower in diabetic mice than in normal mice. Nesfatin-1 treatment (180 mg/kg/day for two weeks) improved insulin sensitivity and mitigated diabetic dyslipidemia. Nesfatin-1 ameliorated the diabetes-related myocardial hypertrophy and heart dysfunction, as revealed by the reduced hypertrophy index, heart rate, mean arterial pressure (MAP), creatine kinase (CK)-MB, and aspartate aminotransferase (AST) levels. Nesfatin-1 exerted antioxidant and anti-inflammatory activity in diabetic mice, as shown by decreased reactive oxygen species (ROS), oxidative lipid product malondialdehyde (MDA) levels, increased superoxide dismutase (SOD) and glutathione (GSH), decreased cardiac and plasma interleukin-1 β (IL-1β) and tumor necrosis factor-α (TNF-α) levels. Mechanistically, we found that nesfatin-1 inhibited the cardiac p38-MAPK pathway activation and subsequent glucagon-like peptide-1 (GLP-1) level. Collectively, our data shows nesfatin-1 exerted protective effects against diabetic cardiomyopathy. Our study suggests that nesfatin-1 therapy has therapeutic implications against diabetic cardiomyopathy.
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