The Long Non-coding RNA LINC01705 Regulates the Development of Breast Cancer by Sponging miR-186-5p to Mediate TPR Expression as a Competitive Endogenous RNA.

Long non-coding RNAs (lncRNAs) may be a regulatory factor of tumorigenesis. However, it is unclear what its biomechanisms are in breast cancer. In this study, different lncRNAs were detected in breast cancer through microarray analysis (GSE119233) and LINC01705 was selected for further study. qRT-PCR was then utilized for the detection of LINC01705 expression in breast cancer cells. A transwell assay, flow cytometry, 5-ethynyl-2'-deoxyuridine (EdU), a cell counting Kit-8 (CCK-8), and a wound-healing assay were performed to determine cell migration, invasion, apoptosis, and proliferation in breast cancer, respectively. For the identification of potential targets of LINC01705, dual-luciferase reporter gene and bioinformatics assays were conducted. Moreover, for the clarification of their interaction and roles in the regulation of the occurrence of breast cancer, Western blotting and RIP assays were conducted. Our findings revealed high LINC01705 expression in breast cancer tissues relative to adjacent non-cancerous tissues (n = 40, P < 0.001). Overexpression of LINC01705 notably enhanced cell migration and proliferation in breast cancer. In addition, LINC01705 positively regulated the translocated promoter region, nuclear basket protein (TPR) through competition with miR-186-5p. In conclusion, our results suggest that LINC01705 is implicated in the progression of breast cancer via competitively binding to miR-186-5p as a competing endogenous RNA (ceRNA), thereby regulating TPR expression.

[Diagnosis and treatment of breast lumps in children].

OBJECTIVE: To summarize the diagnosis and treatment of breast lumps in children. METHODS: The clinical data of 61 children with breast lumps, 20 with physiological breast masses, 5 male and 15 female, aged 1 - 14, 38 with benign tumors, 1 male and 37 female, aged 10 - 14, 3 with malignant tumors, aged 7 months, and 10 and 13 years. diagnosed and treated 2001 - 2006 were analyzed. RESULTS: The 20 cases of physiological masses did not undergo any treatment and were followed up for 2 years. The masses disappear by itself within one year in 17 cases, disappear within 2 years in 2 cases, and remained the same size in 1 case. The 38 cases with benign tumors all underwent resection, 36 cases were cured and 2 cases recurred. Recurrence was not seen in 2 of the 3 cases of malignant breast tumors, and the patient of leiomyosarcoma died one year after the operation. CONCLUSION: Physiological breast masses in children needn't treatment; mostly enjoy spontaneous cure. The outcomes of benign breast tumors in children are good after operation. Malignant breast tumor is rare, and it is still difficult to predict its prognosis now.

[Correlation between expression of metastasis-associated gene 1 and matrix metalloproteinase 9 and invasion and metastasis of breast cancer].

OBJECTIVE: To investigate the expression of metastasis-associated gene 1 (MTA1) and matrix metalloproteinase 9 (MMP-9) gene in breast carcinoma and the relationship between the expression of these genes and the invasion of breast cancer. METHODS: Fluorescence quantitative PCR technique was used to detect the mRNA expression of MTA1 and MMP-9 gene among 56 human breast cancer samples. RESULTS: The mRNA expression rate of MTA1 was higher in 83.9% (47/56) of the primary breast cancer tissues compared with the matched normal breast tissues. The mRNA expression of MMP-9 was higher in 85.7% (48/56) of the primary breast cancer tissues compared to the matched normal breast tissues. The over-expression of MTA1 and that of the MMP-9 gene were significantly related with the degree of differentiation, clinical stage, and lymph node metastasis of breast cancer (all P < 0.05). The positive ratio of MTA1 gene is tightly associated with that of MMP-9 gene (P < 0.05). CONCLUSION: The united detection of MTA1 and MMP-9 gene expression predicts the invasion and metastasis of breast cancer and supplies evidence for clinical therapy and judgment of prognosis. MTA1 and MMP-9 will become new targets for gene therapy.