Kidney cancer is a malignant tumor of the urinary system. Although the 5-year survival rate of patients with kidney cancer has increased by ~30% in recent years due to the early detection of low-grade tumors using more accurate diagnostic methods, the global incidence of kidney cancer continues to increase every year. Therefore, identification of novel and efficient candidate genes for predicting the prognosis of patients with kidney cancer is important. The present study aimed to investigate the role of SEC61 translocon subunit-γ (SEC61G) in kidney cancer. The Cancer Genome Atlas database was screened to obtain the expression profile of SEC61G and identify its association with kidney cancer prognosis. Furthermore, the
in vitro
effect of SEC61G knockdown on kidney cancer cell proliferation, migration, invasion and apoptosis was investigated using a Cell Counting Kit-8 assay, wound healing assay, Transwell assay and flow cytometry. The results demonstrated that compared with healthy tissues, SEC61G was upregulated in human kidney tumor tissues, which was associated with poor prognosis. In addition, SEC61G knockdown significantly inhibited kidney cancer cell proliferation, migration and invasion compared with the negative control (NC) group. Furthermore, E-cadherin expression was significantly upregulated, and N-cadherin and β-catenin expression levels were significantly downregulated in SEC61G-knockdown kidney cancer cells compared with the NC group. In addition, compared with the NC group, SEC61G knockdown significantly promoted cell apoptosis in a caspase-dependent manner. The aforementioned results suggested that SEC61G might serve as a proto-oncogene to promote kidney tumor progression. Therefore, the present study provided a novel candidate gene for predicting the prognosis of patients with kidney cancer.
Purpose Castleman's disease(CD) is a rare angiofollicular lymph node hyperplasia. It is difficult to diagnose CD preoperatively due to its occurrence in multiple regions. It is reported that CD generally occurred in the mediastinum and there were very few reports which mentioned adrenal area. We report a case of Castleman's disease in the adrenal area. Methods We reviewed the patient's hospitalization records, including clinical manifestations, diagnostic tools, management, and outcomes. Histopathological examination was the method for diagnosis. Result In this case report, we present a case of CD that occurred in the adrenal area. The patient was initially diagnosed with adrenal tumor by CT. After operation, histopathological examination showed unicentric CD of the hyaline vascular type. Discussion Castleman's disease rarely occurs in adrenal, which is easily neglected and misdiagnosed. Histopathological examination is the gold standard in the diagnosis of CD, and surgical excision is effective in the treatment of unicentric CD.
MicroRNAs (miRs) are small non-coding RNA molecules that regulate gene expression at the post-transcriptional level. Aberrant expression of miR-9 has been reported to be involved in the tumorigenesis and progression of various malignancies. However, its role in prostate cancer (PC) has not been completely clarified. In the present study, miR-9 expression was examined in different PC cell lines, patient tissues and a mouse model. Cell Counting Kit-8 and BrdU immunofluorescence assays were performed to assess the effect of miR-9 on the viability of PC cells, while Transwell and wound-healing assays were utilized to evaluate the migration and invasion of PC cells expressing miR-9. Furthermore, a dual-luciferase reporter assay was performed to verify whether mitogen-activated protein kinase kinase kinase 3 (MEKK3) was a direct target of miR-9. The results demonstrated significant downregulation of miR-9 expression in different PC cell lines and 31 human PC tissues, as compared with that in a normal prostate cell line and adjacent normal tissues, respectively. By contrast, upregulation of MEKK3 was confirmed in human PC tissue samples, with its level inversely associated with miR-9 expression. Overexpression of miR-9 in six different PC cell lines (DU145, LNCaP, 22Rv1, PC-3, C4-2B and VCaP) reduced the cell viability and migration. Furthermore, it was demonstrated that the 3'-untranslated region of MEKK3 was a target of miR-9, and that MEKK3 overexpression prevented the inhibitory effects of miR-9 on the viability, migration and invasion of PC cells. miR-9 overexpressing tumor cells also exhibited growth delay in comparison with control tumor cells in vivo. Taken together, the current study findings provided novel insights into the underlying molecular mechanisms of PC oncogenesis, which may support the development of new therapeutic approaches for the treatment of PC.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.