Abstract. The purpose of this study is to evaluate the potential synergic effect of BRAF V600E mutation and multifocality on central lymph nodes metastasis (CLNM) in the patients with unilateral papillary thyroid carcinoma (PTC). We enrolled 413 patients with unilateral PTCs who accepted prophylactic unilateral or bilateral central lymph node dissection (LND). Univariate and multivariate analyses were made to determine the association between related factors and CLNM. Then, all patients were divided into 4 groups based on their status of BRAF V600E mutation and multifocality. Relative excess risk of interaction (RERI), attributable proportion (AP) of interaction and synergy index (SI) were applied to evaluate the interactive effect of these two factors on CLNM. Results showed that BRAF V600E mutation and multifocality were independent risk factors for CLNM. A further study revealed that unilateral PTCs accompanying multifocality with BRAF V600E mutation had the highest incidence of CLNM compared with other subgroups. Besides, RERI was 4.323 (95% CI = 1.276-7.369), AP was 0.523 (95% CI = 0.364-0.682) and SI was 2.469 (95% CI = 1.607 to 3.794), indicating a significant additive interaction of BRAF V600E mutation and multifocality on CLNM. The present study has confirmed that BRAF V600E mutation and multifocality are risk factors for CLNM in unilateral PTC. Additionally, unilateral PTC patients accompanying multifocality with BRAF V600E mutation may have an increased risk of CLNM in clinically negative CLNM.
Background The effect of circular RNAs (circRNAs) is widely studied in various human cancers, including breast cancer (BC). Herein, circUSPL1 has been recognized as a new regulator for BC progression. However, the detailed biological function and molecular mechanism of circUSPL1 in BC remain vague. Methods The expression level of circUSPL1, miR‐1296‐5p and metastasis associated 1 (MTA1) was examined by quantitative reverse transcription PCR. BC cell proliferation, migration, invasion, apoptosis and aerobic glycolysis were analyzed by colony formation assay, 5‐ethynyl‐2′‐deoxyuridine assay, wound healing assay, transwell assay, flow cytometry and glycolysis corresponding kits, respectively. The protein level of Bcl‐2, Bax, HK2, GLUT1 and MTA1 was evaluated by western blot analysis. The relationship of miR‐1296‐5p and circUSPL1 or MTA1 was affirmed using dual‐luciferase reporter or RIP assays. A murine xenograft model was conducted to analyze the tumor growth in vivo. Results CircUSPL1 and MTA1 expression level was increased, but miR‐1296‐5p was particularly reduced in BC tissues and cells. CircUSPL1 deficiency significantly inhibited BC cell proliferation, migration, invasion, glycolysis, and promoted cell apoptosis. In addition, circUSPL1 directly targeted miR‐1296‐5p, and downregulation of miR‐1296‐5p eliminated the inhibitory action of circUSPL1 knockdown. Additionally, overexpression of miR‐1296‐5p repressed cell malignant properties, while the suppressive effects were overturned by MTA1 elevation. Lastly, silencing of circUSPL1 inhibited tumor growth by sponging miR‐1296‐5p and regulating MTA1. Conclusion CircUSPL1 deficiency repressed BC cell malignant phenotypes through reducing MTA1 via targeting miR‐1296‐5p, which might provide a theoretical basis for BC treatment.
To investigate the effects of signal transducer and activator of transcription 3 (STAT3) combined with cisplatin (CDDP) on the growth of human Wilms tumour (WT) SK-NEP-1 cell subcutaneous xenografts in nude mice and the possible mechanisms. Human WT SK-NEP-1 cells were subcutaneously transplanted to establish the BALB/c nude mice xenograft model. Mice were randomly divided into five groups: blank control group, adenovirus control group (NC group), STAT3 group, CDDP group and STAT3 plus CDDP group (combination group). Tumour volume and tumour weight were observed during the therapeutic process. The expression levels of STAT3, glucose regulatory protein 78 (GRP78) and BCL2-associated X protein (BAX) were evaluated by immunohistochemical analysis. Compared with the STAT3 group or CDDP group, the tumour weight and volume was significantly reduced in the combination group (P<0.05). No statistical significance was found in NC group compared with the blank control group (P > 0.05). Immunohistochemical analysis showed that STAT3, GRP78 and BAX protein levels in the combination group were significantly higher than those in STAT3 group and CDDP group (P<0.05). Exogenous STAT3 and CDDP may synergistically inhibit the xenograft tumour growth through up-regulation of BAX protein via GRP78.
LncRNA FOXP4-AS1 expresses at a higher level in gastric carcinoma cells and can promote proliferation and other biological behaviors. However, the effect of FOXP4-AS1 on mammary cancer cells has not yet been elucidated. Therefore, this article explores the influence of lncRNA FOXP4-AS1 on the proliferation and other biological processes of mammary cancer MDA-MB-231 cells via its regulation of miRNA-655-3p. Firstly, nanoPCR was used to quantify the expression of FOXP4-AS1 and miRNA-655-3p in mammary cancer tissues and adjacent tissues. Compared to the adjacent tissues, the expression level of FOXP4-AS1 in mammary cancer tissue was significantly increased, while that of miRNA-655-3p was substantially reduced. Then, si-FOXP4-AS1, miRNA-655-3p mimics, si-FOXP4-AS1 + anti-miRNA-655-3p were transfected into human mammary cancer MDA-MB-231 cells. The transfection of si-FOXP4-AS1 or miRNA-655-3p mimics considerably reduced cell viability and the protein levels of Ki-67 and MMPs. The transfection of si-FOXP4-AS1 or miRNA-655-3p mimics could reduce cell migration and invasion. The dual-luciferase reporter assays revealed that FOXP4-AS1 could target miRNA-655-3p. The co-transfection of si-FOXP4-AS1 and anti-miRNA-655-3p increased cell viability, migration, and invasion; the same co-transfection also elevated the protein levels of Ki-67 and MMPs. In conclusion, this study suggests that knocking down FOXP4-AS1’s expression can reduce mammary cancer cells’ ability to proliferate and execute other biological processes by targeting the expression of miRNA-655-3p.
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