1.Effects of highly active anti-retroviral therapy on the viral reservoir in prostate tissue of human immunodeficiency virus/acquired immunodeficiency syndrome patients
Lixin FAN ; Xiongcai ZHOU ; Xunrong ZHU ; Chaoxiong DONG ; Kunpeng LIU ; Chengsong LI ; Zhihua WANG ; Xiaosheng LI
Chinese Journal of Infectious Diseases 2021;39(2):70-73
Objective:To investigate the status of viral reservoirs in prostate tissue of patients with human immunodeficiency virus/acquired immunodeficiency syndrome (HIV/AIDS), and to investigate the effect of highly active anti-retroviral therapy (HAART) on HIV-1 DNA in prostate tissue of HIV/AIDS patients.Methods:Twelve patients with HIV infection and hyperplasia of prostate who required surgical treatment and admitted to Guangzhou Eighth People′s Hospital from July 2017 to October 2019 were included. Blood and prostate specimens of these patients were collected, and HIV-1 RNA in plasma, CD4 + T lymphocyte count in peripheral blood and HIV-1 DNA level in prostate tissue were tested respectively. The independent sample t test or Mann-Whitney U test was used for statistical analysis. Results:Among the 12 patients, the CD4 + T lymphocytes was (519.8±121.5)/μL and HIV-1 DNA in the prostate tissue was 2 602 (365, 10 700) copies/10 6cells in six patients who had not started HAART. The CD4 + T lymphocytes was (182.8±69.7)/μL and the HIV-1 DNA in the prostate tissue was 144 (36, 563) copies/10 6cells in the six patients who underwent HAART for over six months. There were statistically significant differences in CD4 + T lymphocytes and HIV-1 DNA in the prostate tissue between the two groups ( t=-5.889 and Z=-2.082, respectively, both P<0.05). Conclusion:Prostate tissue can be used as an HIV-1 virus repository with or without HAART, and the size of the prostate tissue virus repository can be reduced by HAART after immune reconstitution.
2.Expression and mechanism of microRNA-613 in breast cancer
Kepeng ZHU ; Xunrong XIAO ; Yi LUO ; Wen YI ; Junming YIN ; Chuan YANG ; Guocheng DU
Chinese Journal of Clinical Oncology 2019;46(14):718-722
ABSTRACT Objective: To investigate the expression and mechanism of microRNA (miRNA)-613 in breast cancer. Methods: A total of 91 specimens of breast cancer tissue were collected from Nanchong Central Hospital between May 2017 and May 2018. Quantitative real-time PCR (qRT-PCR) was used to estimate miRNA-613 expression levels in breast cancer and adjacent tissues and breast cancer ( cells MDA-MB-231, MDA-MB-468, and MCF-7) and normal breast epithelial (HBL-100) cell lines. Based on these data, the relationship between miRNA-613 expression and clinicopathological characteristics and prognosis in breast cancer patients were analyzed using the cancer genome atlas (TCGA) database. A dual-luciferase reporter assay was used to detect the binding of miRNA-613 to the 3'UTR of SOX9. Effects on cell proliferation and cell invasion and migration upon transfection of MDA-MB-231 cells with miRNA-613 mimics were detected by the CCK-8 assay and Transwell invasion and migration assays, respectively. In addition, Western blot was used to estimate the expression levels of SOX9, β-catenin, E-cadherin, and Vimentin in the transfected cells. Results: The expression of miRNA-613 in breast cancer tissues was significantly lower than that in adjacent tissues (P<0.05) and was found to be closely related to TNM stage and lymph node metastasis (P<0.05). TCGA survival data showed that miRNA-613 expression was not related to the overall survival rate of breast cancer patients (P>0.05 ). The expression of miRNA-613 in breast cancer cell lines was significantly lower than that in the normal breast epithelial cell line (P<0.05). Similarly, the expression of miRNA-613 in highly invasive metastatic breast cancer cell lines (MDA-MB-231 and MDA-MB-468) was significantly lower than that in the metastatic breast cancer cell line MCF-7 with lower invasion ability (P<0.05). The dual-luciferase reporter assay showed that miRNA-613 could specifically bind to the 3'UTR of SOX9. Upregulation of miRNA-613 expression could inhibit the proliferation, invasion, and migration of MDA-MB-231 cells (P<0.05). This was associated with the downregulated expression of SOX9, β-catenin, and Vimentin (P<0.05) and upregulation of E-Cadherin expression (P<0.05). Conclusions: The expression of miRNA-613 was decreased in breast cancer tissues and cell lines. MiRNA-613 may inhibit the proliferation, invasion, and metastasis of breast cancer cells and epithelial-mesenchymal transition by regulating the SOX9 and Wnt/β-catenin signaling pathways.