Copper sulfide along with morphologydependent photodynamic along with photothermal antibacterial routines

OBJECTIVE Diabetic nephropathy (DN) is one of the most representative diabetic microangiopathy complications. So far, there have been no satisfactory therapeutic strategies, and the injection of stem cells provides a target for DN therapy. PATIENTS AND METHODS Urine-derived stem cells (USCs) were obtained from 9 healthy men. 24 mice were randomly and equally divided into control group, DN model group, DN+hUSC group (treated with USCs for 3 times). Hematoxylin-eosin (HE) and Masson staining were used to detect histological changes of kidney injury. Creatinine and blood urea nitrogen (BUN) were measured to assess renal function. Besides, myofibroblast accumulation, macrophage infiltration, cell proliferation, and oxidative stress were detected by immunohistochemical analysis. RESULTS Compared with DN model group, DN+hUSC group showed lower function loss, cell infiltration, and oxidative stress, as well as less renal fibrosis, histological damage, and cell proliferation. CONCLUSIONS USC can alleviate inflammation and oxidative stress, reduce renal interstitial fibrosis, improve renal tissue structure and protect renal function through paracrine effect.OBJECTIVE Glioma is a common aggressive cancer and a major public health problem worldwide, with high incidence, recurrence, and mortality. Circular RNA (circRNA) has been reported to be involved in glioma, but the role of circ_0079593 in glioma is still unclear. selleck inhibitor MATERIALS AND METHODS The real-time quantitative polymerase chain reaction (RT-qPCR) was performed to quantify the expression levels of circ_0079593, miR-499a-5p, and karyopherin alpha 2 (KPNA2) in glioma tissues or cells. The protein expression level of KPNA2 was assessed by Western blot. 3-(4, 5-dimethylthiazol-2-yl)-2,5-diphenyl-2H-tetrazol-3-ium bromide (MTT), flow cytometry, and transwell assays were conducted to evaluate proliferation, apoptosis, migration and invasion of glioma cells, respectively. The relationship between miR-499a-5p and circ_0079593 or KPNA2 was analyzed by bioinformatics database and confirmed by Dual-Luciferase reporter analyses, respectively. The effects of circ_0079593 silencing in vivo were measured by a xenograft experiment. RESULTS Circ_0079593 and KPNA2 were elevated in glioma tissues and cells. Loss-of functional experiments revealed that knockdown of circ_0079593 hampered the progression of glioma by repressing proliferation, motility and inducing apoptosis in vitro and declining tumor growth in vivo. Similarly, suppression of KPNA2 impeded the process of glioma by inhibiting proliferation, motility and increasing apoptosis. MiR-499a-5p, interacting with KPNA2, was a target gene of circ_0079593. In addition, overexpression of KPNA2 could reverse the effects of circ_0079593 knockdown on proliferation, apoptosis, migration and invasion of glioma cells. Mechanistically, circ_0079593 mediated proliferation, motility and apoptosis of glioma cells by regulating KPNA2 expression via sponging miR-499a-5p. CONCLUSIONS Circ_0079593 stimulated the pathological process of glioma via acting as competing endogenous RNA to sponge miR-499a-5p.OBJECTIVE The specific roles of long noncoding RNAs (lncRNAs) have been found in human cancers, including retinoblastoma (RB). However, the function of lncRNA-NORAD has not been reported in RB. Therefore, the regulatory mechanism of lncRNA-NORAD was investigated in the development of RB. PATIENTS AND METHODS The experimental tissues were collected from 24 RB patients and 6 patients with ruptured globes. The average age of all patients was 2.78 years (range, 2 months to 11 years). The mRNA and protein expression was measured by Real Time-quantitative Polymerase Chain Reaction (RT-qPCR) and Western blot analysis. The functional mechanism of NORAD was assessed by Cell Counting Kit-8 (CCK-8), transwell, and Dual-Luciferase reporter assays. RESULTS Upregulation of NORAD and downregulation of miR-136-5p were found in RB. Functionally, knockdown of NORAD and miR-136-5p overexpression restrained RB cell viability, invasion, and migration. In addition, NORAD acts as a ceRNA of miR-136-5p in RB. MiR-136-5p was found to directly target PBX3. Furthermore, knockdown of PBX3 inhibited the progression of RB. More importantly, the NORAD/miR-136-5p axis is involved in RB progression by mediating PBX3. CONCLUSIONS LncRNA NORAD, serving as a ceRNA of miR-136-5p, accelerates RB progression by upregulation of PBX3.OBJECTIVE Recent researches have proved that circular RNAs (circRNAs) play important roles in many diseases. Thyroid cancer is one of the most common malignant tumors worldwide. Therefore, the aim of this study was to investigate the role of circ-ABCB10 in thyroid cancer. PATIENTS AND METHODS Circ-ABCB10 expression in 40 paired thyroid cancer tissues and adjacent normal tissues was monitored by Real Time-quantitative Polymerase Chain Reaction (RT-qPCR). Subsequently, circ-ABCB10 was silenced or overexpressed in thyroid cancer cells. Function assays were conducted to explore the role of circ-ABCB10 in the proliferation and invasion of thyroid cancer in vitro. Furthermore, RT-qPCR and Western blot assay were performed to elucidate the potential underlying mechanism. RESULTS Circ-ABCB10 expression was significantly higher in thyroid cancer tissues than that in adjacent tissues. The growth ability of thyroid cancer cells was significantly inhibited after circ-ABCB10 silence. However, the growth ability of thyroid cancer cells was remarkably promoted after circ-ABCB10 was overexpressed in vitro. Similarly, the invasion of thyroid cancer cells was significantly inhibited or promoted after circ-ABCB10 silence or overexpression, respectively. Besides, the expression of KLF6 was markedly up-regulated by the silence of circ-ABCB10. However, KLF6 expression was down-regulated by overexpression of circ-ABCB10. CONCLUSIONS Circ-ABCB10 was first identified as a novel oncogene in thyroid cancer. Furthermore, it significantly enhanced the proliferation and invasion of thyroid cancer by targeting KLF6. Our findings suggested that circ-ABCB10 could be used as a potential therapeutic target in thyroid cancer.OBJECTIVE Current conclusions on the potential influence of the single nucleotide polymorphism (SNP) of Matrix metalloproteinase-2 (MMP)-2-1306 C>T on Breast cancer (BCa) susceptibility remain controversial. This study aims to accurately clarify their relation. MATERIALS AND METHODS The relevant literature on the relation between genetic variation of MMP-2 and BCa susceptibility was searched in PubMed, Web of School, VIP, and CNKI published before March 2019. The keywords used were as follows "MMP-2, breast/mammary cancer/carcinoma/tumor" or "SNPs of MMP-2, breast/mammary cancer/carcinoma/tumor". Odds ratio (OR) and 95% CI of extracted data from eligible literature were calculated. RESULTS A total of 7 studies involving 1823 BCa patients and 1899 healthy controls were included. All control genes were consistent with HWE (p>0.05). Different genetic models were utilized to clarify the potential influence of MMP-2-1306 C>T (rs243865) on BCa susceptibility. No significant correlation was identified between the SNP of MMP-2-1306 C>T and BCa susceptibility based on the calculated OR and 95% CI in different genotypes CC vs. CT&TT p=0.54, OR=0.88 (95% CI=0.58-1.33); TT vs. CC&CT p=0.67, OR=1.07 (95% CI=0.79-1.44); CC vs. TT p=0.73, OR=0.95 (95% CI=0.70-1.29); C Allele vs. T Allele p=0.93, OR=1.02 (95% CI=0.70-1.47). CONCLUSIONS The SNP of MMP-2-1306 C>T did not correlate to the susceptibility to BCa.OBJECTIVE To investigate the effect of MiR-221 on proliferation and apoptosis of laryngeal carcinoma cells through the PI3K/AKT signaling pathway. MATERIALS AND METHODS LipofectamineTM 2000 liposomes were used to transfer MiR-221 analogue, MiR-221 NC into Hep-2 cells of laryngeal carcinoma. Real-time fluorescence quantitative polymerase chain reaction (PCR) method was used to detect the expression of MiR-221, MTT method was used to detect the proliferation of cells, flow cytometry was used to detect cell cycle, Western blotting was used to detect the expression of apoptosis proteinase-1 (Apaf-1) and cyclin-dependent kinase (CDK1, CDK2) protein and the activation of phosphatidylinositol 3 kinase (PI3K)/protein kinase B (AKT). RESULTS Compared with MiR-221 NC group, the expression of MiR-221 in MiR-221 analogue group was up-regulated (p less then 0.01), the cell proliferation rate was decreased (p less then 0.01), the cell cycle was stagnated in the G1 phase (p less then 0.01), the expression levels of Cyclin A, CDK1, CDK2, PI3K, and p-AKT were significantly down-regulated (p less then 0.01), and the expression levels of Bax and Apaf-1 were significantly up-regulated (p less then 0.01). CONCLUSIONS MiR-221 analogues can significantly inhibit the proliferation and induce apoptosis of Hep-2 cells in laryngeal cancer, and this is achieved by blocking the PI3K/AKT signaling pathway, which also indicates that MiR-221 affects the proliferation and apoptosis of laryngeal cancer cells through the PI3K/AKT signaling pathway.OBJECTIVE This study aimed to investigate whether long-chain non-coding ANCR is involved in the progression of non-small cell LCa (NSCLC) and its possible molecular mechanisms. PATIENTS AND METHODS Quantitative Real Time-Polymerase Chain Reaction (qRT-PCR) was applied to examine ANCR expression in 48 cases of NSCLC and adjacent normal tissues. In addition, ANCR level in patients of different tumor staging was analyzed. The Kaplan-Meier method was applied to analyze the interplay between ANCR expression and the prognosis of patients with NSCLC. Subsequently, qRT-PCR was performed to detect ANCR level in LCa cell lines. After knocking down ANCR in A549 cells, ANCR and E-Ca mRNA expression were examined by qRT-PCR, while the expression levels of epithelial-mesenchymal transition (EMT)-related proteins were detected by Western blot. At the same time, cell viability and migration ability were analyzed through cell counting kit-8 (CCK-8) and cell wound healing assay, respectively. RNA immunoprecipitation (RIP) testsion of ANCR. The qRT-PCR study verified that ANCR was highly expressed in the LCa cell line A549. After knocking down ANCR in A549 cells, ANCR and E-Ca mRNA levels were found conspicuously decreased, and so were the expression levels of EMT-related proteins, as well as the cell viability and migration ability. The RIP assay result indicated that ANCR can indeed bind to EZH2. E-Ca mRNA expression was elevated after the knockdown of EZH2 in A549 cells. In addition, the result of CHIP test demonstrated that EZH2 could combine with E-Ca. Simultaneous down-regulation of ANCR and E-Ca in A549 cells could reverse the influence of knocking down ANCR alone on cell viability and migration ability. CONCLUSIONS Long-chain non-coding RNA ANCR was highly expressed in NSCLC tissues and could enhance the viability and malignancy of NSCLC cells by inhibiting the expression of E-Ca, thereby promoting the progression of NSCLC.OBJECTIVE Recent studies have proved that long non-coding RNAs (lncRNAs) play important roles in many diseases, especially malignancies. The aim of this study was to investigate the exact role of lncRNA HOXA-AS2 (Hoxa cluster antisense RNA 2) in the development of non-small cell lung cancer (NSCLC). PATIENTS AND METHODS Quantitative Real Time-Polymerase Chain Reaction (qRT-PCR) was utilized to detect HOXA-AS2 expression in NSCLC patients. The Wound healing assay and transwell assay were conducted to explore the function of HOXA-AS2 on NSCLC metastasis. Furthermore, the mechanism assays were used to explore the interaction between HOXA-AS2 and microRNA-145-3p (miR-145-3p). RESULTS HOXA-AS2 expression level in NSCLC tissues was significantly higher than adjacent tissues. HOXA-AS2 expression was negatively correlated with disease-free survival of NSCLC patients. Moreover, the functional assays showed that the migration and invasion of NSCLC cells were significantly inhibited after HOXA-AS2 in vitro silence. Furthermore, the luciferase reporter gene assay also revealed that miR-145-3p was a direct target of HOXA-AS2 in NSCLC.