The aim of this study was to detect the expression of micro ribonucleic acid (miR)-335-5p in the liver tissues of patients with liver cancer, and to explore its effect on liver cancer and mechanism using Huh7 human liver cancer cells.

Liver tissues were collected from patients with liver cancer. The expression of miR-335-5p in tissues was detected via quantitative reverse transcription-polymerase chain reaction (qRT-PCR). Subsequently, Huh7 cells were transfected with miR-335-5p in vitro. After overexpressing miR-335-5p, changes in the expression of octamer-binding transcription factor 4 (Oct4) gene were observed via qRT-PCR. Furthermore, the proliferation of Huh7 cells and the protein expressions of protein kinase B (Akt) and phosphorylated Akt (p-Akt) were detected using cell counting kit (CCK)-8 assay and Western blotting (WB), respectively.

Compared with Control group, the expression of miR-335-5p increased significantly in the liver tissues of liver cancer patients (p<0.01). In comparison with those in negative group, the messenger RNA (mRNA) expression of Oct4 and the proliferation rate of Huh7 cells were both significantly inhibited in miR-335-5p group (p<0.01, p<0.05). After overexpression of miR-335-5p, the protein expression level of p-Akt decreased remarkably (p<0.01).

MiR-335-5p directly binds to the 3' untranslated region (3'UTR) of Oct4 mRNA to restrain the phosphorylation of Akt, thereby inhibiting Huh7 cell proliferation.
MiR-335-5p directly binds to the 3' untranslated region (3'UTR) of Oct4 mRNA to restrain the phosphorylation of Akt, thereby inhibiting Huh7 cell proliferation.
As the research of circular RNAs (circRNAs) in human malignant tumors has been increasing, multiple circRNAs have been discovered to be engaged in the modulation of the liver cancer cell functions. This study aims at exploring how circSOX4 affects the progression of hepatocellular carcinoma (HCC).

CircSOX4 levels in HCC tissue samples were detected by quantitative real-time polymerase chain reaction (qRT-PCR) analysis, and the relationship between circSOX4 expression and HCC patients' prognosis was analyzed. CircSOX4 expression was knocked down by transfection of small interfering RNA. The effects of circSOX4 on cell functions including proliferation, invasiveness and migration ability were examined by cell counting kit-8 (CCK-8), transwell, cell wound healing test and flow cytometry experiments, respectively. The target RNA of circSOX4 was predicted through searching bioinformatics website, and the binding between the two was verified through Luciferase assay.

CircSOX4 was abnormally highly expressed either in HCC tissues or in cell lines, which was positively correlated with the poor prognosis of HCC patients. https://www.selleckchem.com/products/poziotinib-hm781-36b.html Transfection of small interfering RNA against circSOX4 in HCC cells resulted in inhibited migration and proliferation of HCC cells, while an increase in cell apoptosis. Bioinformatics analysis revealed that microRNA-432 contained the binding site pairing to circSOX4 3'UTR, and their binding relationship was confirmed by Luciferase assay. Their expression levels were negatively correlated. In addition, downregulation of microRNA-432 can partially reverse the effect of silenced circSOX4 on regulating apoptosis, proliferation and migration of HCC cells.

CircSOX4, highly expressed in HCC, indicates a poor prognosis. CircSOX4 may mediate the progression of HCC by binding to microRNA-432.
CircSOX4, highly expressed in HCC, indicates a poor prognosis. CircSOX4 may mediate the progression of HCC by binding to microRNA-432.
To study the role of long-chain non-coding RNA (lncRNA) DUXAP8 in ovarian cancer (OCa) and the underlying potential mechanism.

The expression pattern of DUXAP8 in ovarian cancer was analyzed using the GEPIA database. Quantitative real-time polymerase chain reaction (qRT-PCR) was applied to determine the expression of DUXAP8 in OCa tissues; at the same time, OCa cell lines were cultured to complete functional experiments, including cell counting kit-8 (CCK-8), plate cloning experiments and transwell experiments to evaluate the effects of DUXAP8 on the proliferative and migration ability of OCa cell lines. Bioinformatics analysis and Dual-Luciferase reporter genes were used to determine the binding and expression of DUXAP8 to its downstream key gene microRNA-29a-3p in OCa cells. In addition, co-transfection technology and cell function recovery experiments were used to verify the important role of the DUXAP8/microRNA-29a-3p regulatory network in OCa.

DUXAP8 was abnormally highly up-regulated in OCa tissues and cell lines, besides, its expression was related to poor prognosis of patients. CCK-8 and plate cloning experiments showed that knockdown of DUXAP8 in OCa cells can significantly inhibit the proliferation of OCa cells. Transwell results suggested that knockdown of DUXAP8 can significantly inhibit OCa cell migration. In addition, it was found that DUXAP8 can bind and negatively regulate the expression of microRNA-29a-3p in OCa. Functional experiments in OCa cells also revealed that microRNA-29a-3p was a key downstream gene that mediated the regulation of DUXAP8 on OCa function.

DUXAP8 has abnormally high expression in OCa and can lead to malignant progression of the tumor.
DUXAP8 has abnormally high expression in OCa and can lead to malignant progression of the tumor.
To study the protective effect and mechanism of intravenously administered bone marrow mesenchymal stem cells (BMSCs) on renal failure in diabetic mice.

BMSCs were obtained from the bone marrow of mice, identified by flow cytometry and tri-line differentiation test. Diabetic model (DM) mice were established using STZ and infused with mice BMSCs intravenously, followed by the analysis of fasting blood glucose and proteinuria levels, renal tissue damage by optical microscope and electron microscope, and PI3K/AKT signaling protein expression in kidney by Western blot and endocrine function by immunofluorescence staining.

DM mice exhibited gradually increased albumin excretion rate with time, and the MSC-treated diabetic mice presented significantly reduced proteinuria levels. HE staining indicated that MSC administration mitigated renal damage as proved by smaller tubular dilatation, reduced glomerulosclerosis and trace protein cylinders, and recovered kidney ultrastructure as shown by improved mesangial dilatation and podocyte loss. Further, BMSCs treatment activated PI3K/AKT signaling, which was downregulated in diabetic mice. However, MSC administration failed to improve pancreatic endocrine function in DM mice.

Intravenous administration of MSCs can effectively prevent renal failure in diabetic mice by activating PI3K/AKT signaling pathway.
Intravenous administration of MSCs can effectively prevent renal failure in diabetic mice by activating PI3K/AKT signaling pathway.
Paget disease of the breast (PDB) is a rare form of cutaneous breast cancer. Up to date, no randomized studies evaluated the different management strategies. This systematic review investigates the role of radiotherapy and its best technical profile in the treatment of this disease, with great attention to doses and fractionation regimens.

A systematic search was performed on PubMed, Embase and Scopus in order to detect case reports, case series and prospective as well as retrospective clinical studies describing histologically proven PDB and providing information about pertinent radiation treatments. Searching strategy followed PRISMA (Preferred Reporting Items for Systematic Reviews and Meta-Analysis) guidelines.

Inclusion criteria were met by six papers, dealing with radiation treatments performed postoperatively and in exclusive settings. No evaluations were performed on preoperative radiotherapy.

Actually, the standard treatment of PDB reflects oncological principles of breast carcinoma therapy, including the role of breast-preserving surgery. The traditional radiotherapic dose is 50 Gy, with daily fractionation of 2 Gy. Adjuvant radiotherapy following breast preserving surgery represents the current standard of care; prospective studies could be of help in defining the role of exclusive radiotherapy, hypofractionated schemes and smaller target volumes.
Actually, the standard treatment of PDB reflects oncological principles of breast carcinoma therapy, including the role of breast-preserving surgery. The traditional radiotherapic dose is 50 Gy, with daily fractionation of 2 Gy. Adjuvant radiotherapy following breast preserving surgery represents the current standard of care; prospective studies could be of help in defining the role of exclusive radiotherapy, hypofractionated schemes and smaller target volumes.
Due to the decrease of estrogen and estrogen receptor (ER) in postmenopausal women, they have a higher risk of intervertebral disc degeneration (IDD) than men. This study aims to explore how ERα and ERb interact with CCN5 and protect IDD.

We used Chromatin immunoprecipitation (ChIP) and Luciferase reporter assay to determine whether the ERα/b protein binds to CCN5 promoter and activates its expression. We used TNF-α to induce nucleus pulposus (NP) cell degeneration to simulate the IDD process. The change of the expression of ERα/β and CCN5 was measured in the degenerated NP cells. To understand the function of ERα/β in the NP cells degeneration, we upregulated the ERα/b gene expression by vector transfection or 17b-estradiol (E2) stimulation. Besides, we also used the CCN5 gene-silenced NP cells by siRNA transfection as a comparison to determine the role of CCN5. We tested the cell proliferation and principal components of the extracellular matrix (ECM) to value the degree of NP cell degeneration.

ERα and ERβ protein can bind to the same promoter regions of CCN5 and activate its expression, respectively. TNF-α degraded NP cells with a reduction of cell proliferation, collagen II, ACAN, ERα, ERβ, and CCN5 expression, and increased collagen I/III, and MMP-13 expression. Upregulated ERα or ERβ resulted in the maintains of CCN5 and alleviated the NP cell degeneration. Besides, 17β-E2 supplement increased the ERα, ERβ, and CCN5 expression, as well as stable NP cells phenotype. However, it was partly abolished by the silencing of CCN5.

Upregulation of ERα and ERβ protects the NP cell degeneration during IDD through the activation of CCN5 by binding to its promoter.
Upregulation of ERα and ERβ protects the NP cell degeneration during IDD through the activation of CCN5 by binding to its promoter.
To evaluate changes in pH and Flow Rate (FR) of the Unstimulated Whole Saliva (UWS) in a sample of pregnant women in different gestational periods.

After collecting demographic data and medical histories, as well as conducting an oral examination, a sample of pregnant women were instructed on how to prepare prior to the sample collection. At a time between 11.00 and 12.00 a.m., they were subjected to salivary collection (spitting method, time 5 minutes); the measurement of FR was carried out using a professionally calibrated precision scale and the pH with a portable pH meter.

The average FR of the women's detected sample (0.40 ± 0.20 ml/min) was lower than that of non-pregnant women (0.48 ± 0.15 ml/min) of the same age (p <0.05). We observed an increase (p <0.001) of FR in the first trimester (0.56 ± 0.20 ml/min) compared to second (0.34 ± 0.14 ml/min) and third (0.31 ± 0.14 ml/min) trimester. The salivary pH of pregnant women was lower than the one detected in the non-pregnant women's sample (p <0.