ABSTRACT
The roles of microRNA (miRNA/miR)-383-5p have been reported in several malignancies, including breast cancer, gastric cancer, ovarian cancer and lung adenocarcinoma. However, its function in diffuse large B-cell lymphoma (DLBCL) remains unclear. Thus, the present study aimed to investigate the role of miR-383-5p in DLCBL. Reverse transcription-quantitative PCR analysis was performed to detect miR-383-5p expression in 80 paired tissue samples from patients with DLBCL and control subjects, as well as related cancer cell lines. Kaplan-Meier survival analysis was performed, and the prognostic value of miR-383-5p was determined via Cox regression analysis. Furthermore, the association between miR-383-5p expression and the clinicopathological characteristics of patients with DLBCL was investigated. The Cell Counting Kit-8, crystal violet staining and Transwell assays were performed to assess the effects of miR-383-5p on cell proliferation and invasion, respectively. The results demonstrated that miR-383-5p expression was upregulated in human DLBCL tissues and cell lines. In addition, miR-383-5p expression was closely associated with clinical stage and extranodal invasion in patients with DLBCL. Notably, high miR-383-5p expression was able to predict a favorable clinical prognosis in patients with DLBCL. Furthermore, overexpression of miR-383-5p significantly inhibited the proliferation and invasion of DLBCL cells, the effects of which were reversed following miR-383-5p knockdown. Taken together, the results of the present study suggest that miR-383-5p may predict favorable prognosis, and thus may be used as a prognostic biomarker for patients with DLBCL. In addition, miR-383-5p appears to play critical roles in inhibiting the proliferation and invasion of DLBCL cells, and thus may be used as a potential therapeutic target in patients with DLBCL.
ABSTRACT
BACKGROUND: Small nucleolar RNA host gene 12 (SNHG12) expression is associated with multiple cancers, including renal cell carcinoma, prostate cancer, cervical cancer, nasopharyngeal carcinoma, colorectal cancer, and hepatocellular carcinoma. However, SNHG12 biological function is unclear in diffuse large B-cell lymphoma (DLBCL). METHODS: SNHG12 expression and associated clinicopathological characteristics were evaluated in DLBCL tissues. CCK-8 and transwell assay were used to analyze the in vitro role of SNHG12 in DLBCL progression. The xenograft model was used to explore the in vivo role of SNHG12 in DLBCL growth. The physical interaction between SNHG12 and miR-195 was confirmed using bioinformatics analysis and a dual luciferase assay. RESULTS: SNHG12 expression was upregulated in DLBCL tissues and correlated with patients' prognosis. SNHG12 downregulation inhibited cell growth, migration, and invasion of DLBCL cells in vitro, while its overexpression promoted these cellular processes. Moreover, SNHG12 knockdown repressed tumorigenesis of DLBCL cells in vivo. Further experiments demonstrated that miR-195 is a target of SNHG12 in DLBCL and that their expression negatively correlates in DLBCL. SNHG12 functioned as a competing endogenous RNA for miR-195 in DLBCL cells and miR-195 upregulation abolished the effects of SNHG12 on of DLBCL progression. CONCLUSION: SNHG12 predicts poor clinical outcome and serves as a novel oncogene in DLBCL via miR-195 sponging. We also suggest that SNHG12 can be used as a potential therapeutic candidate for DLBCL patients.
ABSTRACT
OBJECTIVE: To analyze the expression characteristics of leukemia stem cell (LSC) antigen in acute myeloid leukemia (AML) and to explore the correation of LSC-specific antigens with the subtypes, cytogenetics and clinical efficacy of AML. METHODS: A total of 61 newly diagnosed patients with AML (except M3) hospltalized in Department of Hematology of our hopital were selected from January 2013 to March 2016. The immun phenotypes and expression of Tim-3, CD96 and CD123 on leucamia cells were detected by direct immunofluorescenct flow cytometry. 61 patients were divided into positive expression and megative expression groups according to expression of Tim-3, CD96 and CD123; the correlation of LSC antigen expression level with high WBC count, chromosome and therapeutic efficacy was analyzed. RESULTS: Among 61 newly diagnosed patients with AML (except M3), the expression rate of Tim-3, CD96 and CD123 was 52.45%, 44.26% and 55.73% respectively. The expression rates of Tim-3, CD96 and CD123 between the AML subtypes and total patients was not stetistically different (P>0.05). The high WBC count occurred more easily in AML (except MS) patients with positive expression of Tim-3, CD96 and CD123, but compared with AML patients with negative espression, the difference was not statstically significant (P>0.05). The proportion of chromosone karyotype with poor prognosis detected in patients with positive expression of Tim-3 and CD96 was higher than that in patients with negative expreesion (P<0.05); while the preoprtion of chromosome karyotype with poor prognosis detected in patients with positive and negative expression of CD123 was not significantly different (P>0.05). After 2 courses of chemotherapy, the complete remission (CR) rate in patients with positive expression of Tim-3, CD96 and CD123 was significantly lower than that in patients with negative expression of Tim-3, CD96 and CD123 (P<0.05), the comparison of OS time in patients with positive and negative expression of Tim-3 and CD96 showed the statistical difference (P>0.05), while the difference of OS time in patients with positive and negative expression of CD123 was not significant (P>0.05). CONCLUSION: The expression levels of Tim-3, CD96 and CD123 in newly diagnosed AML (except M3) sybtype patients are not significantly different form those in total patients. The high WBC count ocours more easily in patients with positive expression of Tim-3, CD96 and CD123. After 2 course of chemotherapy, the CR rate in patients with positive expression of Tim-3, CD96 and CD123 was significantly lower than that in patients with negative expression. The proportion of chromsome karyotype with poor prognosis detected in patients with positive expression of Tim-3 and CD96 is high, moreover, OS time in patients with positive expression of Tim-3 and CD96 is shorter than that in patients with negative expression.
