ABSTRACT
Osteosarcoma is a highly malignant tumor that occurs in the bone. Previous studies have shown that multiple microRNAs (miRNAs) regulate the development of osteosarcoma. This study aimed to explore the role of miR-629-5p and its target gene, caveolin 1 (CAV1), in osteosarcoma development. To analyze the expression of miR-629-5p and CAV1 mRNA in osteosarcoma tissues and cell lines, qRT-PCR analysis was performed. Dual-luciferase reporter experiments were subsequently performed to validate the relationship between CAV1 and miR-629-5p. CCK8 assay was used to measure osteosarcoma cell proliferation, and wound-healing assay was performed to study their migratory phenotype. Our findings revealed that miR-629-5p was overexpressed in osteosarcoma tissues and cells, and thereby enhanced cell proliferation and migration. Further, we validated that miR-629-5p targets CAV1 mRNA directly. CAV1 expression, which was negatively correlated with miR-629-5p expression, was found to be downregulated in osteosarcoma tissue samples. Moreover, our data showed that an increase in CAV1 level led to a decline in osteosarcoma cell proliferation and migration, which could be rescued by miR-629-5p upregulation. Overall, our study confirmed that miR-629-5p promoted osteosarcoma proliferation and migration by directly inhibiting CAV1.
Subject(s)
Humans , Bone Neoplasms/genetics , Osteosarcoma/genetics , MicroRNAs/genetics , Gene Expression Regulation, Neoplastic , Cell Movement/genetics , Cell Line, Tumor , Cell Proliferation/genetics , Caveolin 1/geneticsABSTRACT
Background: The receptor for advanced glycation end-product (RAGE) was one of the signal transduction receptors. RAGE interacted with various signaling molecules which were involved in human disease processes including tumorigenesis. Previous reports have indicated that RAGE/high-mobility group box 1 (HMGB1) could regulate autophagy in different carcinomas. However, the functional role of RAGE/ HMGB1 in the regulation of clear cell renal cell carcinoma (ccRCC) autophagy remained unrevealed. Methods: Western blot, quantitative real-time polymerase chain reaction (qRT-PCR) and immunofluorescence were used in the present study. Results: In this study, we demonstrated that the levels of RAGE/HMGB1 and autophagic protein LC3, Beclin-1, PI3K were much higher in ccRCC samples than those of in adjacent normal tissues. RAGE and autophagic protein expression was regulated with RAGE/HMGB1 in human RCC cell lines. Conclusion: Our results implicated that RAGE and autophagy played important roles in ccRCC, and RAGE/HMGB1 might serve as a novel therapeutic target for future ccRCC treatment
ABSTRACT
The effect of bisacodyl on the treatment of rats with slow transit constipation (STC) was studied. Forty-five female Wister rats were divided into control group, STC group, and STC bisacodyl group. The immunohistochemical method was used to determine interstitial cells of Cajal (ICC) and the expression of c-Kit protein. Body mass and the number of defecations were significantly decreased in the STC group compared with the control group on the 100th day after diphenoxylate administration, while dry weight of feces was significantly increased and the intestinal transit time was prolonged. There were significant differences in the number of defecations, dry weight of feces, and intestinal transit time among the three groups. The number of defecations was higher, dry weight of feces was lower, and intestinal transit time was shorter in the STC bisacodyl group compared to the STC group. In addition, ICC basement membrane dissolution occurred in the colon wall of the STC group. The connection between ICC and surrounding cells was destroyed, and the nucleus shrunken to different degrees. Moreover, c-Kit expression in the STC group was significantly lower than the control group. The connection between ICC and surrounding cells in the STC bisacodyl group was significantly stronger than the STC group, and the number of ICC and the expression of c-Kit were increased. Bisacodyl could reduce the severity of STC in rats by increasing the number of ICC and the expression of c-Kit.