ABSTRACT
We mainly corroborated the potential mechanism of DLX1 and miR-129-5p in prostate cancer cells. DLX1 was upregulated in cancer cells according to qRT-PCR assay. We evaluated the functional changes of the transfected cells via Transwell assay, CCK-8 assay and wound healing assay. DLX1 was confirmed as a cancer promoter. In addition, qRT-PCR showed down-regulated miR-129-5p expression in prostate cancer. We further used dual-luciferase reporter detection to elucidate the targeting between these two genes. The inhibition of miR-129-5p on tumour was verified. Besides, co-transfection of oe-DLX1 and miR-129-5p mimics attenuated this inhibition. These data demonstrated functions of DLX1/miR-129-5p axis in prostate cancer: miR-129-5p hindered the biological functions of cancer cells via inhibiting DLX1 expression. We provide a novel biomarker for prostate cancer.
Subject(s)
MicroRNAs , Prostatic Neoplasms , Cell Line, Tumor , Cell Movement , Humans , Male , MicroRNAs/genetics , Prostatic Neoplasms/genetics , Signal TransductionABSTRACT
The present study aimed to establish a mouse model of patient-derived castration-resistant prostate cancer (CRPC) xenograft tumors, and to evaluate the effects of various doses of metformin on phospholipase Cε (PLCε) expression and the neurogenic locus notch homolog protein 1 (Notch1)/hairy and enhancer of split 1 and androgen receptor (AR) signaling pathways via western blotting and reverse transcription-quantitative PCR. Additionally, phorbol 12-myristate 13-acetate was used to activate PLC, and Jagged1 was used as a Notch activator to verify whether metformin could suppress CRPC development via the PLCε/Notch1/AR pathways. The results confirmed that metformin may serve critical roles in CRPC by significantly inhibiting the occurrence, growth and proliferation of CRPC tumors by decreasing PLCε/Notch1 expression and AR nucleation.
ABSTRACT
To probe into the efffects of miR-101-3p via regulating CUL4B within PI3K/AKT/mTOR signaling pathway on progression of prostate cancer (PCA). Western blot and qRT-PCR were adopted to detect CUL4B and miR-101-3p expressions in 75 cases with PCA . The cellular strains of PCA (LNCaP and PC3) were chose as the objects to check the targeting correlation between CUL4B and miR-101-3p through dual-luciferase reporter experiments. LNCaP cells and PC3 cells were randomly divided into the blank group, miR-101-3p mimic group, siRNA negative control (NC) group, CUL4B siRNA group and CUL4B siRNA plus the miR-101-3p inhibitor group. Cellular bioactivity measurement was done via Cell-Light EDU, MTT, Annexin-V-FITC/PI, scratch-heal experiments and invasion tests of Transwell. MiR-101-3p expression was decreased more signally in tumor tissues than in normal tissues adjacent to the cancer. MiR-101-3p inhibited cellular proliferating, migrating and invasion. Nevertheless, it promoted cellular apoptosis, up-regulated apoptotic proteins as well as down-regulated anti-apoptotic proteins. CUL4B siRNA and miR-101-3p simulation were similar in terms of their outcomes. Nonetheless, these results could be reversed through the miR-101-3p inhibitor. Besides, CUL4B siRNA and the simulation halted a serious of PI3K signal in PCA cells. MiR-101-3p expression was down-regulated in PCA patients. CUL4B was upregulated in PCA patients. Moreover, miR-101-3p suppressed cellular invasion, migration, proliferation and led to cellular apoptosis, which might be related to the PI3K/AKT/mTOR signaling pathway suppression. Finally, we found, MiR-101-3P suppressed PCA progression via aiming for CUL4B, which may offer the new molecular target for PCA clinical treatment.
Subject(s)
Cullin Proteins , MicroRNAs , Prostatic Neoplasms , Signal Transduction/genetics , Cell Line, Tumor , Cullin Proteins/genetics , Cullin Proteins/metabolism , Humans , Male , MicroRNAs/genetics , MicroRNAs/metabolism , Middle Aged , Phosphatidylinositol 3-Kinases/genetics , Phosphatidylinositol 3-Kinases/metabolism , Prostatic Neoplasms/genetics , Prostatic Neoplasms/metabolism , Prostatic Neoplasms/pathology , Proto-Oncogene Proteins c-akt/genetics , Proto-Oncogene Proteins c-akt/metabolism , TOR Serine-Threonine Kinases/genetics , TOR Serine-Threonine Kinases/metabolismABSTRACT
BACKGROUND: Advances in micro-percutaneous nephrolithotomy (PCNL) for kidney stones have made it an alternative approach to the retrograde intrarenal surgery (RIRS) approach. Nevertheless, the superiority of micro-PCNL over RIRS is still under debate. The results are controversial. OBJECTIVES: The purpose of this study was to systematically evaluate the clinical results in patients presenting with kidney stones treated with micro-PCNL or RIRS. METHODS: A literature search was done for electronic databases to identify researches that compared micro-PCNL and RIRS till December 2019. The clinical outcome included complications, stone-free rates (SFRs), hemoglobin reduction, length of hospital stay, and operative time. RESULTS: Five articles were included in our study. The pooled results revealed no statistical difference in the rate of complications (OR = 0.99, 95% CI = 0.57-1.74, p = 0.99), length of hospital stay (MD = -0.29, 95% CI = -0.82 to 0.24, p = 0.28), and operative time (MD = -6.63, 95% CI = -27.34 to 14.08, p = 0.53) between the 2 groups. However, significant difference was present in hemoglobin reduction (MD = -0.43, 95% CI = -0.55 to 0.30, p < 0.001) and the SFRs (OR = 0.59, 95% CI = 0.36-0.98, p = 0.04) when comparing RIRS with micro-PCNL. CONCLUSIONS: Compared with micro-PCNL to treat kidney stones, RIRS is associated with better stone clearance and bearing higher hemoglobin loss. As the advantages of both technologies have been shown in some fields, the continuation of well-designed clinical trials may be necessary.