Anti-CCND1 monoclonal antibody, clone FQS3352

Background: Multiple myeloma (MM) primarily origins from terminally differentiated B cells. The Cyclin D1 (CCND1) gene polymorphism is located on the long arm of chromosome 11 in exon 4, and coding of the Cyclin D1 protein is reported in MM. This study aimed at investigating the relationship between CCND1 polymorphism and MM in northern part of Iran. Materials and Methods: This case-control study was performed on 87 patients with MM (case group) and 70 healthy individuals (control group). The population was selected from Touba Clinic, the largest referral center in Mazandaran province, Iran. Data analysis was done in SPSS software version 19. Results: The participants were aged 18-83 years (mean age: 53.8 +/- 16.7 years), including 72 (45.9%) males and 85 (54.1%) females. The adjusted odds ratio (aOR) for GG genotype was found to be significant (aOR = 4.28, confidence interval [CI] 95% = 1.21-15.13). In addition, the presence of G allele compared to allele A increased the odds ratio (OR) of MM (OR = 2.28, CI 95% = 1.45-3.57). The age and sex aOR by age and sex was 2.08, CI 95% = 1.10-3.93. Conclusion: The current study elucidated that, unlike most previous surveys on Cyclin D1 G870A gene polymorphism that associated AA genotype with various types of malignancies, the GG genotype is a risk factor for MM.

BackgroundEmerging evidence indicates that Long non-coding RNAs (LncRNAs) and microRNAs (miRNAs) play crucial roles in tumor progression, including hepatocellular carcinoma (HCC). However, whether there is a crosstalk between LncRNA pituitary tumor-transforming 3 (PTTG3P) and miR-383 in HCC remains unknown. This study is designed to explore the underlying mechanism by which LncRNA PTTG3P sponges miR-383 during HCC progression.MethodsqPCR and Western blot were used to analyze LncRNA PTTG3P, miR-383 and other target genes' expression. CCK-8 assay was performed to examine cell proliferation. Annexin V-PE/PI and PI staining were used to analyze cell apoptosis and cell cycle distribution by flow cytometry, respectively. Transwell migration and invasion assays were used to examine cell migration and invasion abilities. An in vivo xenograft study was performed to detect tumor growth. Luciferase reporter assay and RNA pull-down assay were carried out to detect the interaction between miR-383 and LncRNA PTTG3P. RIP was carried out to detect whether PTTG3P and miR-383 were enriched in Ago2-immunoprecipitated complex.ResultsIn this study, we found that PTTG3P was up-regulated in HCC tissues and cells. Functional experiments demonstrated that knockdown of PTTG3P inhibited cell proliferation, migration and invasion, and promoted cell apoptosis, acting as an oncogene. Mechanistically, PTTG3P upregulated the expression of miR-383 targets Cyclin D1 (CCND1) and poly ADP-ribose polymerase 2 (PARP2) by sponging miR-383, acting as a competing endogenous RNA (ceRNA). The PTTG3P-miR-383-CCND1/PARP2 axis modulated HCC phenotypes. Moreover, PTTG3P also affected the PI3K/Akt signaling pathway.ConclusionThe data indicate a novel PTTG3P-miR-383-CCND1/PARP2 axis in HCC tumorigenesis, suggesting that PTTG3P may be used as a potential therapeutic target in HCC.