Suppressors of cytokine signaling 1 (SOCS1) is a member of SOCS family and acts as negative regulators of cytokine signaling by direct inhibition of receptor-associated janus kinases. The clinical significance and biological function of SOCS1 in variant tumor tissues and at variant tumor stages is still controversial. The aim of our study is to confirm the expression status of SOCS1 in triple-negative breast cancer (TNBC) tissues and cell lines, and explore the clinical value and biological function of SOCS1 in TNBC. In microarray data sets (GDS2250 and GDS817), we observed SOCS1 was overexpressed in TNBC tissues and cell line compared with normal mammary tissues and mammary epithelial cell line, or non-TNBC tissues and cell line. Furthermore, SOCS1 mRNA and protein overexpression were confirmed in TNBC tissues and cell lines compared with normal mammary tissues and mammary epithelial cell lines or non-TNBC tissues and cell lines. SOCS1 protein overexpression was obviously associated with advanced clinical stage, large tumor size, more lymph node metastasis, present distant metastasis, and malign histological grade. Downregulation of SOCS1 expression suppressed TNBC cells proliferation and promoted cell apoptosis. In conclusion, SOCS1 is associated with clinical progression in TNBC patients and acts as an oncogenic role in regulating TNBC cells proliferation and apoptosis. © 2018 IUBMB Life, 70(4):320-327, 2018.
The aim of the present study is to study the expressions of suppressor of cytokine signaling (SOCS)-1 in the tumor tissues and adjacent normal tissues of patients with breast cancer. The study was also planned to investigate the association of SOCS-1 gene expression with patients' clinical pathology, molecular subtype and prognosis. A total of 60 cases of frozen and paraffin-embedded specimens of tumor tissues and corresponding adjacent normal tissues of patients with breast cancer were selected. Reverse transcription-quantitative polymerase chain reaction (RT-qPCR) was used to detect the expression levels of SOCS-1 messenger RNA (mRNA) in the patients' tumor tissues and adjacent normal tissues. The immunohistochemical method was applied to detect the expressions of SOCS-1 proteins in the patients' breast cancer tissues and adjacent normal tissues. Moreover, the correlations of SOCS-1 protein expressions in breast cancer tissues with patients' pathological parameters, molecular subtypes and prognosis were analyzed in combination with the clinical data. The results of RT-qPCR showed that the SOCS-1 mRNA expression in breast cancer tissues was significantly lower than that in adjacent normal tissues (p<0.01). The immunohistochemical results indicated that the positive expression rate of the SOCS-1 proteins in breast cancer tissues (23.33%) was remarkably lower than that in adjacent normal tissues (88.33%) (p<0.01). The low expression of SOCS-1 in breast cancer tissues was related to lymph node metastasis and clinical staging. The positive expression rates of the luminal A SOCS-1 proteins were the highest (47.62%) (p<0.01). The 5-year overall survival rate of the breast cancer patients was 63.33% (38/60). The univariate survival analysis revealed that the patients with low expression of SOCS-1 had poorer prognosis. In conclusion, the low expression of SOCS-1 plays a key role in the pathogenesis of breast cancer; in particular, it is associated with the lymph node metastasis and clinical staging of the tumor; so, the SOCS-1 expression in breast cancer tissues can be regarded as an important reference for the prognostic estimation of breast cancer.
Purpose: The purpose of this study was to investigate the effects of miR-29a on papillary thyroid cancer (PTC) and its underlying mechanisms. Methods: Primary tumor tissues and adjacent tissues of 69 patients with PTC were obtained. Human thyroid cell line Nthy-ori3-1 and PTC cell lines K1, BCPAP, TPC-1 were cultured. K1 cells were transfected and divided into following groups: blank group (without any treatment), miR-29a mimics group, control mimics group, miR-29a inhibitor group, control inhibitor group, DPP4 siRNA group, control siRNA group and miR-29a inhibitor + DPP4 siRNA group. qRT-PCR and Western blot were used to detect miR-29a and DPP4 expression. 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) and transwell assay were performed to detect cells proliferation, migration, and invasion. A nude mice xenograft experiment was performed. Results: miR-29a was significantly downregulated in PTC tissues, K1 and TPC-1 cells ( P <0.01). DPP4 was significantly upregulated in the miR-29a inhibitor group and significantly downregulated in the miR-29a mimics group ( P <0.01). DPP4 was the target gene of miR-29a. miR-29a significantly inhibited K1 cell proliferation, invasion, migration and PTC growth in nude mice by targeting DPP4 ( P <0.01). Conclusion: miR-29a inhibits proliferation, migration, and invasion of PTC by targeting DPP4, which might provide a new target for clinical treatment of PTC.
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