No abstract

No abstract

No abstract

BackgroundDiffuse large B-cell lymphoma (DLBCL) is the most common subtype of non-Hodgkin's lymphoma (NHL), which can involve various types of mature B-cells. The incidence of DLBCL has been increased, additional research is required to identify novel and effective prognostic and therapeutic molecules. Fc receptor-like 1 (FCRL1) act as an activation co-receptor of human B-cells. Aberrant expression of this molecule has been reported in a number of B-cell-related disorders. Moreover, the clinical signi cance and prognosis value of FCRL1 in DLBCL not completely identi ed. MethodsIn this study, the expression levels of FCRL1 was determined in thirty patients with DLBCL and 15 healthy controls (HCs). In addition, the correlation between FCRL1 expressions with clinicopathological variables of DLBCL patients were examined. Then, the potential roles of FCRL1 in proliferation, apoptosis, and cell cycle distribution of B-cells from DLBCL patients were determined using ow cytometry analysis, after knockdown of this marker using retroviral short hairpin RNA interference. Quantitative real time-PCR, western blotting, and enzyme-linked immunosorbent assay were also used to identify the possible effects of FCRL1 knockdown on expression levels of BCL-2, BID, BAX, intracellular signaling pathway PI3K/p-Akt, and p65 nuclear factor-kappa B (NF-κB) in B-cells of DLBCL. ResultsStatistical analysis revealed higher levels of FCRL1 expression in B-cells of DLBCL patients compared to HCs at both protein and mRNA levels. A positive correlation observed between the expression of FCRL1 with some clinicopathological parameters of DLBCL patients. In addition, FCRL1 knockdown signi cantly decreased cell proliferation and stimulated apoptosis as well as G1 cell cycle arrest in B-cells of DLBCL patients. The levels of p65 NF-κB and PI3K/p-Akt expression markedly reduced after knockdown of FCRL1 expression. ConclusionsThese results suggested FCRL1 as a potential novel biomarker for prognosis and/or a possible effective therapeutic target for treatment of patients with DLBCL.

Background:The p28 is a small-sized cell-penetrating peptide derived from bacterial protein azurin and can function as a cancerspecific anti-proliferative agent. It can penetrate cancer tissues easily without involving the immune system, and increase the intracellular concentration of p53. Objectives: In this study, we have expressed and purified recombinant p28, then evaluated its anti-proliferative and pro-apoptotic effects on Raji cancer cell line. Methods: The p28 gene was amplified and cloned into pTZ57R cloning vector and was sequenced subsequently. Afterward, it was transformed into E. coli BL21 bacterial host by using pET-28a expression vector. Peptide purification was carried out using Ni-NTA chromatography system. Bradford, SDS-PAGE, and western blotting assays were applied to assess the concentration and expression level of the recombinant peptide. The proficiency of p28 in inhibition of tumor growth and induction of apoptosis in cancerous cells was investigated by evaluating the Raji and HEK-293 cells treated with different concentrations of p28. Results: The overexpression of the p28 peptide in the bacterial host was confirmed by SDS-PAGE and western blotting. Moreover, Bradford assay revealed desirable concentrations of the recombinant p28 before and after dialysis. The MTT and PE-Annexin V apoptosis assays indicated the specific function of p28 in impeding the proliferation of cancerous cells and triggering the apoptosis. Conclusions: The p28 induces apoptosis in cancerous cells but not in normal control cells. In summary, p28 is a non-immunogenic small peptide that can penetrate cancerous cells preferentially, impede the cell proliferation, and induce the apoptosis. Overall, these findings suggest p28 as a promising anticancer drug.