OBJECTIVE: Janus kinase (JAK)- signal transducer and activator of transcription (STAT) signaling pathway participates in regulating cell proliferation, differentiation, and apoptosis, and related to lymphoma. Suppressors of cytokine signaling 3 (SOCS3) is a negative regulator of the JAK-STAT signaling pathway. SOCS3 reduction and miR-155 up-regulation are associated with lymphoma pathogenesis. Bioinformatics analysis showed the complementary binding site between miR-155 and SOCS3. This study aimed to investigate the role of miR-155 in regulating SOCS3/JAK-STAT signaling pathway and affecting diffuse large B cell lymphoma (DLBCL) cell proliferation and apoptosis. PATIENTS AND METHODS: DLBCL tumor sample was collected from the patients in our hospital. Lymphatic tissue derived from reactive lymphoid hyperplasia patients were selected as control. MicroRNA-155 (MiR-155) and SOCS3 expressions were detected. Dual luciferase assay was used to verify the targeted relationship between miR-155 and SOCS3. OCI-LY10 cells were cultured in vitro and divided into five groups, including miR-NC, miR-155 inhibitor, pIRES2-Blank, pIRES2-SOCS3, and miR-155 + pIRES2-SOCS3 groups. SOCS3, p-JAK1, p-JAK2, p-STAT3, and Survivin expressions were tested. Cell apoptosis and proliferation were detected by flow cytometry. RESULTS: MiR-155 expression significantly increased, while SOCS3 level declined in DLBCL tissue compared with control. MiR-155 targeted regulated SOCS3 expression. MiR-155 inhibitor and/or pIRES2-SOCS3 transfection markedly up-regulated SOCS3 expression, reduced p-JAK1, p-JAK2, p-STAT3, and Survivin levels, attenuated cell proliferation, and enhanced cell apoptosis in OCI-LY10 cells. CONCLUSIONS: Down-regulation of miR-155 inhibited DLBCL cell proliferation and facilitated apoptosis through up-regulating SOCS3 expression to suppress JAK-STAT3 signaling pathway.
OBJECTIVE: Janus kinase (JAK)- signal transducer and activator of transcription (STAT) signaling pathway participates in regulating cell proliferation, differentiation, and apoptosis, and related to lymphoma. Suppressors of cytokine signaling 3 (SOCS3) is a negative regulator of the JAK-STAT signaling pathway. SOCS3 reduction and miR-155 up-regulation are associated with lymphoma pathogenesis. Bioinformatics analysis showed the complementary binding site between miR-155 and SOCS3. This study aimed to investigate the role of miR-155 in regulating SOCS3/JAK-STAT signaling pathway and affecting diffuse large B cell lymphoma (DLBCL) cell proliferation and apoptosis. PATIENTS AND METHODS: DLBCL tumor sample was collected from the patients in our hospital. Lymphatic tissue derived from reactive lymphoid hyperplasiapatients were selected as control. MicroRNA-155 (MiR-155) and SOCS3 expressions were detected. Dual luciferase assay was used to verify the targeted relationship between miR-155 and SOCS3. OCI-LY10 cells were cultured in vitro and divided into five groups, including miR-NC, miR-155 inhibitor, pIRES2-Blank, pIRES2-SOCS3, and miR-155 + pIRES2-SOCS3 groups. SOCS3, p-JAK1, p-JAK2, p-STAT3, and Survivin expressions were tested. Cell apoptosis and proliferation were detected by flow cytometry. RESULTS:MiR-155 expression significantly increased, while SOCS3 level declined in DLBCL tissue compared with control. MiR-155 targeted regulated SOCS3 expression. MiR-155 inhibitor and/or pIRES2-SOCS3 transfection markedly up-regulated SOCS3 expression, reduced p-JAK1, p-JAK2, p-STAT3, and Survivin levels, attenuated cell proliferation, and enhanced cell apoptosis in OCI-LY10 cells. CONCLUSIONS: Down-regulation of miR-155 inhibited DLBCL cell proliferation and facilitated apoptosis through up-regulating SOCS3 expression to suppress JAK-STAT3 signaling pathway.