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T cells expressing NKG2D chimeric antigen receptors efficiently eliminate glioblastoma and cancer stem cells.

Traditional therapies fail to cure most glioblastoma patients and the 5-year survival rate is less than 10%, highlighting need for new therapeutic approaches. The natural killer group 2 member D ligands (NKG2DLs) are highly expressed in glioblastomas and are considered promising targets for chimeric antigen receptor (CAR) T-cell therapy. The aim of this study was to investigate the effect of NKG2D-expressing CAR-T cells on glioblastomas and glioblastoma stem cells.

2403 related Products with: T cells expressing NKG2D chimeric antigen receptors efficiently eliminate glioblastoma and cancer stem cells.

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IL-29 Exhibits Anti-Tumor Effect on Pan-48 Pancreatic Cancer Cells by Up-regulation of P21 and Bax.

Pancreatic cancer is the most lethal cancer of the digestive system. IL-29 is a new member of the IFNλ family and well-known for its strong antiviral activity. However, its direct effect on pancreatic cancer is still unclear. This study was performed to investigate if IL-29 has any direct effect on Pan-48 pancreatic cancer cells.

2667 related Products with: IL-29 Exhibits Anti-Tumor Effect on Pan-48 Pancreatic Cancer Cells by Up-regulation of P21 and Bax.

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MicroRNA-325-3p protects the heart after myocardial infarction by inhibiting RIPK3 and programmed necrosis in mice.

Receptor-interacting serine-threonine kinase 3 (RIPK3)-mediated necroptosis has been implicated in the progression of myocardial infarction (MI), but the underlying mechanisms, particularly whether microRNAs (miRNAs) are involved, remain largely unknown.

2826 related Products with: MicroRNA-325-3p protects the heart after myocardial infarction by inhibiting RIPK3 and programmed necrosis in mice.

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Hispidulin exhibits neuroprotective activities against cerebral ischemia reperfusion injury through suppressing NLRP3-mediated pyroptosis.

Ischemia/reperfusion (I/R) injury is the major cause of neurological deficit following stroke. Our previous study showed neuroprotective effects of hispidulin against cerebral ischemia reperfusion injury (IRI). In this study, we further examined the involvement of pyroptosis in this neuroprotective function.

1029 related Products with: Hispidulin exhibits neuroprotective activities against cerebral ischemia reperfusion injury through suppressing NLRP3-mediated pyroptosis.

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Anti-Proliferation and Pro-Apoptotic Effects of Diosmetin via Modulating Cell Cycle Arrest and Mitochondria-Mediated Intrinsic Apoptotic Pathway in MDA-MB-231 Cells.

BACKGROUND Breast cancer is one of the most malignant tumors worldwide. The natural flavonoid diosmetin has been reported to exhibit various pharmacological activities, including anti-cancer effects. This study aimed to investigate the anti-breast cancer effects of diosmetin on MDA-MB-231 cells and to explore the underlying molecular mechanisms of cell apoptosis. MATERIAL AND METHODS The MDA-MB-231 cells were incubated with diosmetin for 24 h. Then, cell viability and lactate dehydrogenase (LDH) leakage were detected using CCK-8 and LDH assay kits, respectively. Inverted fluorescence microscopy and flow cytometry were used to measure the mitochondrial membrane potential (MMP) and intracellular reactive oxygen species (ROS). Cell apoptosis and cell cycle were determined by flow cytometry. The expressions of apoptosis and cell cycle-related genes were determined by Western blotting and qRT-PCR. RESULTS The results revealed that diosmetin exerts significant cytotoxic effects on MDA-MB-231 cells, as indicated by decreased cell viability, increased intracellular ROS accumulation and LDH release, as well as cell cycle arrest in G0/G1 phase, inducing mitochondrial dysfunction and apoptosis. Moreover, diosmetin treatment significantly downregulated the expression levels of Bcl-2 and Cyclin D1, and upregulated that of p53, Bax, caspase 3, cleaved caspase 9, and cleaved caspase 3. CONCLUSIONS These findings demonstrate that diosmetin has anti-proliferative and pro-apoptotic activities against MDA-MB-231 cells via cell cycle arrest and the mitochondria-mediated intrinsic apoptotic pathway. Our results extend the understanding of the anti-tumor mechanism of diosmetin and suggest that it may be of use as an active natural agent for the prevention or treatment of human breast cancer.

1917 related Products with: Anti-Proliferation and Pro-Apoptotic Effects of Diosmetin via Modulating Cell Cycle Arrest and Mitochondria-Mediated Intrinsic Apoptotic Pathway in MDA-MB-231 Cells.

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Mirt2 functions in synergy with miR-377 to participate in inflammatory pathophysiology of Sjögren's syndrome.

The interaction of long non-coding RNAs (lncRNAs)-microRNAs (miRs) exerts crucial functions in mediating inflammatory reaction. It is still unclear whether myocardial infarction associated transcript 2 (Mirt2)-miR-377 mediates the inflammatory pathogenesis in Sjögren's syndrome (SS). The inflammatory lesion model was established by stimulating salivary gland epithelial cells (SGECs) by interferon gamma (IFN-γ). Mirt2- and/or miR-377-transfected SGECs, as well as their negative controls, were applied to investigate the biological functions in inflammation. Cell viability and apoptosis were examined using commercial kits. Western blot was applied to quantify protein level, and enzyme-linked immuno sorbent assay (ELISA) was used to value the secretion of cytokines. The up-regulation of Mirt2 was observed in IFN-γ-treated SGECs. Mirt2 overexpression restored the expression of miR-377 which was repressed by IFN-γ. However, miR-377 silence abolished the protective effect on cell viability, inhibitory effect on apoptosis and prohibitive role in pro-inflammatory factors. Mirt2 diminished the phosphorylated expression of crucial regulators while miR-377 silence restored the phosphorylation in IFN-γ-treated SGECs. Mirt2 was elevated in IFN-γ-treated SGECs and then up-regulated miR-377 in response to inflammatory lesions. Mechanically, in synergy with miR-377 Mirt2 blocked IFN-γ-evoked activation of NF-κB and JAK/STAT signalling pathway.

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LINC00305 represses miR-124 expression to trigger inflammatory insults in the presence of lipopolysaccharide.

The anti-inflammatory function of microRNA-124 (miR-124) has been a matter of extensive studies in the last few years. Although LINC00305 regulates biological activities by acting as a miR sponge, it is still unexplored whether LINC00305 is involved in inflammation by regulating miR-124. Cell viability and apoptosis were evaluated with commercial kits, cell counting kit-8 (CCK-8) and Annexin V-fluorescein isothiocyanate (FITC) kit, respectively. LINC00305, miR-124 and mRNA levels were quantified by quantitative reverse transcription PCR (qRT-PCR). Protein level was assessed with Western blot assay and enzyme-linked immunosorbent assay (ELISA). The expression of LINC00305 was up-regulated by lipopolysaccharide (LPS). LINC00305 overexpression further suppressed the cell viability, promoted apoptosis and induced inflammation in LPS-treated ATDC5 cells while its silence enhanced the cell viability, inhibited apoptosis and ameliorated inflammation. miR-124 was negatively regulated by LINC00305 and its overexpression abolished the effects of LINC00305 in the presence of LPS. LINC00305 further triggered the Notch/nuclear factor kappa B (NF-κB) signalling pathway in LPS-treated ATDC5 cells and this activation was abrogated when ATDC5 cells overexpressed miR-124. LINC00305 might emerge as a novel suppressor for miR-124. LINC00305-caused miR-124 silence compromises ATDC5 cell viability and ultimately results in inflammatory insults by activating Notch/NF-κB pathway.

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MicroRNA‑217 inhibition relieves cerebral ischemia/reperfusion injury by targeting SIRT1.

MicroRNAs (miRs) have been proposed to be involved in the pathological processes of cerebral ischemia/reperfusion (CIR) injury. The present study aimed to investigate the potential role and molecular mechanisms of miR‑217 in the regulation of neuronal survival in CIR injury. To perform the investigation, an in vitro cellular model of CIR injury was established by treating neurons with oxygen‑glucose deprivation and reoxygenation (OGD/R). miR‑217 levels in neurons were detected using reverse transcription‑quantitative PCR. The association between miR‑217 and sirtuin 1 (SIRT1) was identified using TargetScan and validated in a dual‑luciferase reporter assay. Cell viability and apoptosis were measured using a Cell Counting Kit‑8 assay and flow cytometry, respectively. The release of lactate dehydrogenase, and the production of proinflammatory factors and oxidative stress biomarkers were analyzed by ELISAs and using specific assay kits. It was revealed that miR‑217 was significantly upregulated in OGD/R‑treated neurons. SIRT1 was a direct target of miR‑217, and was downregulated in neurons following OGD/R treatment. Downregulation of miR‑217 significantly ameliorated OGD/R‑induced neuronal injury, inflammatory responses and oxidative stress. The effects of miR‑217 inhibitor on OGD/R treated neurons were attenuated by SIRT1 knockdown. Additionally, western blotting revealed that the SIRT1/AMP‑activated protein kinase‑α/NF‑κB pathway was partially involved in the regulation of OGD/R‑induced neuronal injury by miR‑217. In conclusion, the data of the present study indicated that the downregulation of miR‑217 protected neurons against OGD/R‑induced injury by targeting SIRT1.

1320 related Products with: MicroRNA‑217 inhibition relieves cerebral ischemia/reperfusion injury by targeting SIRT1.

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The cytotoxic and oxidative effects of restorative materials in cultured human gingival fibroblasts.

The aim of this study was to evaluate the cytotoxic and oxidative effects of the most commonly used dental restorative materials on human gingival fibroblast cells (HGFCs). HGFCs were obtained from healthy individuals. The tested restorative materials were a microhybrid resin based composite, a compomer resin, a glass ionomer cement, and an amalgam alloy. One hundred eight cylindirical samples, 10 mm in diameter and 2 mm in height, were prepared according to ISO 10993-12:2002 specifications ( = 9 in the tested subgroups). Freshly prepared and aged samples in artificial saliva at 37 °C (7 and 21 d) were placed into well plates and incubated. Wells without dental materials were constituted as the control group. After 72 h incubation period, cytotoxicity was determined using the neutral red (NR) assay. Oxidative alterations were assessed using total antioxidant capacity (TAC) and total oxidant status (TOS) assay kits. Data were analyzed using the ANOVA and LSD post hoc tests. All tested materials led to significant decreases in the cell viability rates (33-73%) compared to the control group. Glass ionomer and resin composite were found to be more cytotoxic than amalgam alloy and compomer. The highest TAC level was observed in glass ionomer after seven-day aging and these changes prevented an increase in TOS levels. Increases in TAC levels after seven-day aging in all groups exhibited significant differences with freshly prepared samples ( < 0.05). In all material groups, TOS levels of freshly prepared samples differed statistically and significantly from samples aged for 7 and 21 d ( < 0.05). The data obtained suggested that all the tested materials exhibited cytotoxic and pro-oxidant features. Freshly prepared samples caused higher TOS levels. However, oxidant status induced by materials decreased over time.

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Microvesicles Derived from Transforming Growth Factor-β1-Stimulated Hepatic Stellate Cells Aggravate Hepatocellular Injury.

Hepatic stellate cells (HSCs) are liver-specific cells playing critical roles in liver physiological and pathophysiological processes. Transforming growth factor-β1 (TGF-β1) is an inflammatory cytokine secreted by both hepatocytes and HSCs. We have previously shown that microvesicles (MVs) derived from quiescent HSCs protect hepatocyte functions. In this study, we investigated the effects of MVs released from TGF-β1-stimulated HSCs (HSC-MVs) on xenobiotic-injured hepatocytes. Two hepatocyte cell lines (BRL-3A and HL-7702) were treated with -acetyl--aminophenol or HO to build the injury models. Different concentrations of HSC-MVs were used to coculture with injured hepatocytes. MTT, Hochest33258 staining, and flow cytometry were used to determine their effects on the viability and apoptosis of hepatocytes. Liver injury indicators, alanine aminotransferase (ALT) and aspartate amino transferase (AST), were assessed by enzyme-linked immune sorbent assay kits. The phosphoinositide 3-kinase (PI3K) activator (740Y-P) and extracelluar signal regulated kinase (Erk)1/2 activator (platelet-derived growth factor-BB) were used for pathway analysis. The expression levels of p-PI3K/PI3K, p-Akt/Akt, and activated caspase-3 were measured by western blot. Results showed that (i) HSC-MVs dose dependently impaired the viability of hepatocytes in both injury models, (ii) moreover, HSC-MVs dose dependently increased the apoptosis in those cell models, (iii) HSC-MVs also elevated the levels of ALT and AST in the coculture media, and (iv) these effects were accompanied by a decrease in p-PI3K/PI3K and p-Akt/Akt, which could be partially abolished by 740Y-P. Meanwhile, the proapoptotic effect of HSC-MVs was associated with p-Erk1/2/Erk1/2 downregulation and activated caspase-3 upregulation, and could be inhibited by Erk1/2 activation. Our findings demonstrate that HSC-MVs are involved in inflammatory hepatocytes injury probably through the PI3K/Akt, Erk1/2, and caspase-3 pathways.

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