The multiple myeloma is a malignant clonal tumor of bone marrow plasma cells that is incurable and inevitably recurrent. The mechanisms of progression include tumor cell metastasis, immune escape, resistance to apoptosis, and malignant proliferation. The cysteine-rich secreted acidic protein is closely related to the growth, development, remodeling, and repair of cells and tissues. In our study, we divided myeloma patients and patients with other blood diseases into groups and measured the cysteine-rich secreted acidic protein (SPARC) content in the serum of different groups of patients as well as the prognostic differences. The U266 cells were transfected with interfering vectors and overexpressed SPARC vectors to determine the physiological functions of MM cells. Our results showed that SPARC was highly expressed in MM and the survival rate of the high SPARC expression group was lower than that of the low expression group. Interfering SPARC vectors inhibited cancer cell proliferation, migration, and invasion and promoted apoptosis. Overexpression of SPARC vectors promoted cancer cell development. SPARC affected the patient’s disease development by regulating the biological behavior of the MM cells.

Background: To explore the biological effects and potential molecular mechanisms of long non-coding RNA (lncRNA) gastric carcinoma proliferation enhancing transcript 1 (GHET1) in acute myeloid leukemia (AML). Methods: Fluorescence in situ hybridization was performed to determine the location of GHET1. Quantitative polymerase chain reaction (qPCR) was performed to verify RNA expression. GHET1 overexpression and knockdown were achieved by transfection of the expression vector or short hairpin RNA. Western blotting, qPCR, Cell Counting Kit-8 assay, JC-1 staining, and flow cytometry were performed to measure GHET1 function. The dual luciferase reporter assay was performed to confirm the relationship between microRNA 105 (mir-105) and Ras-related protein Rap-2B ( RAP2B ). Results: GHET1 was localized in the nucleus of NB4 cell lines. GHET1 expression was elevated in AML cell lines compared with normal bone marrow mononuclear cells. GHET1 knockdown led to inhibition of proliferation and promoted the differentiation and apoptosis of AML cell lines. Furthermore, GHET1 directly bound to miR-105 and downregulated miR-105 expression. MiR-105 overexpression suppressed proliferation and induced the differentiation and apoptosis of AML cell lines. In addition, RAP2B was confirmed to be a target gene of miR-105 and an inverse correlation was shown between their expression levels in AML cell lines; when miR-105 increased, Rap-2B level decreased and vice versa . Conclusion: This study demonstrated that the GHET1/miR-105/ Rap2B axis may be a critical signaling pathway involved in AML progression.