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Notch signaling triggered via the ligand DLL4 impedes M2 macrophage differentiation and promotes their apoptosis.

Notch signaling controls many cellular processes, including cell fate determination, cell differentiation, proliferation and apoptosis. In mammals, four Notch receptors (Notch 1-4) can interact with five distinct ligands [Jagged1, Jagged2, Delta-like 1 (DLL1), DLL3, and DLL4]. We previously reported that Notch activation is modulated in endothelial cells and monocytes during inflammation and showed that inflammation upregulates DLL4 on endothelial cells. DLL4 promotes differentiation of blood monocytes into proinflammatory M1 macrophages. Here, we further investigated the ability of DLL4 to interfere with the polarization of blood monocytes into immunosuppressive M2 macrophages.

2470 related Products with: Notch signaling triggered via the ligand DLL4 impedes M2 macrophage differentiation and promotes their apoptosis.

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Long noncoding RNA Lnc‑EGFR promotes cell proliferation and inhibits cell apoptosis via regulating the expression of EGFR in human tongue cancer.

Tongue cancer remains a difficult disease to overcome. Long noncoding RNAs (LncRNAs) have been shown to serve significant roles in the diagnosis and treatment of tongue cancer. Herein, the present study aimed to investigate the role of a newly‑discovered Lnc, Lnc‑EGFR in tongue cancer. The results showed that the transcript level of Lnc‑EGFR was upregulated in patients with tongue cancer and in cultured tongue cancer cell lines. Consistently, expression of EGFR was also elevated selectively in cancerous tissues and malignant cell lines. Knockdown of Lnc‑EGFR inhibited the clonogenic ability and cell viability of human tongue cancer cell lines UM1 and CAL‑27, as evidenced by colony formation assays, and cell proliferation assays. Furthermore, depletion of Lnc‑EGFR in UM1 and CAL‑27 cells increased cell apoptosis by upregulating the activities of caspase‑3, and caspase‑9, but not caspase‑8. Lnc‑EGFR knockdown‑mediated inhibition of clonogenic ability and cell viability was rescued by overexpression of EGFR by adding EGFR recombinant protein into both cell lines. Likewise, Lnc‑EGFR knockdown‑induced cell apoptosis was reversed by co‑treatment with recombinant EGFR protein in UM1 and CAL‑27 cells. All of these results suggested the oncogenic potential of Lnc‑EGFR, which was achieved by positive regulation of EGFR in human tongue cancer.

1076 related Products with: Long noncoding RNA Lnc‑EGFR promotes cell proliferation and inhibits cell apoptosis via regulating the expression of EGFR in human tongue cancer.

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Neural Stem Cell Transplantation Is Associated with Inhibition of Apoptosis, Bcl-xL Upregulation, and Recovery of Neurological Function in a Rat Model of Traumatic Brain Injury.

Traumatic brain injury (TBI) is a common disease that usually causes severe neurological damage, and current treatment is far from satisfactory. The neuroprotective effects of neural stem cell (NSC) transplantation in the injured nervous system have largely been known, but the underlying mechanisms remain unclear, and their limited sources impede their clinical application. Here, we established a rat model of TBI by dropping a weight onto the cortical motor area of the brain and explored the effect of engrafted NSCs (passage 3, derived from the hippocampus of embryonic 12- to 14-d green fluorescent protein transgenic mice) on TBI rats. Moreover, RT-PCR and Western blotting were employed to investigate the possible mechanism associated with NSC grafts. We found rats with TBI exhibited a severe motor and equilibrium dysfunction, while NSC transplantation could partly improve the motor function and significantly reduce cell apoptosis and increase B-cell lymphoma-extra large (Bcl-xL) expression at 7 d postoperation. However, other genes including Bax, B-cell lymphoma 2, Fas ligand, and caspase3 did not exhibit significant differences in expression. Moreover, to test whether Bcl-xL could be used as a therapeutic target, herpes simplex virus (HSV) 1 carrying Bcl-xL recombinant was constructed and injected into the pericontusional cortices. Bcl-xL overexpression not only resulted in a significant improvement in neurological function but also inhibits cell apoptosis, as compared with the TBI rats, and exhibits the same effects as the administration of NSC. The present study therefore indicated that NSC transplantation could promote the recovery of TBI rats in a manner similar to that of Bcl-xL overexpression. Therefore, Bcl-xL overexpression, to some extent, could be considered as a useful strategy to replace NSC grafting in the treatment of TBI in future clinical practices.

1260 related Products with: Neural Stem Cell Transplantation Is Associated with Inhibition of Apoptosis, Bcl-xL Upregulation, and Recovery of Neurological Function in a Rat Model of Traumatic Brain Injury.

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Generation of apoptosis-resistant HEK293 cells with CRISPR/Cas mediated quadruple gene knockout for improved protein and virus production.

Apoptosis has important functions during pathophysiologic processes. However, from a biopharmaceutical point of view, active apoptosis of host cells is undesirable during viral packaging or protein expression, because it decreases the efficiency of viral or protein production. Here we used the CRISPR/Cas technique to knock out four pro-apoptotic genes, Caspase3, Caspase6, Caspase7 and AIF1, in HEK293 cells, and successfully produced an apoptosis-resistant cell line. Furthermore, this cell line showed higher expression levels of pro-apoptotic proteins and higher packaging efficiency for the virus carrying these proteins than control HEK293 cells. This study not only produced an apoptosis-resistant cell line that is useful in producing apoptosis-inducing proteins or viruses expressing these proteins, but also provides a methodology to build other apoptosis-resistant cell lines.

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CD44-shRNA recombinant adenovirus inhibits cell proliferation, invasion, and migration, and promotes apoptosis in HCT116 colon cancer cells.

The cell-surface glycoprotein CD44 is closely associated with cell proliferation, tumor invasion, and metastasis. Previous studies have reported that knockdown of CD44 with short hairpin RNA (shRNA) reduced cell proliferation and migration, and induced apoptosis. However, more efficient means of delivering small interference RNA are still necessary. We developed an in vitro model of CD44-shRNA recombinant adenovirus (Ad-CD44-shRNA) and evaluated its ability to alter tumor invasion, migration, and apoptosis in human colon cancer cells. An shRNA against CD44 was used for knockdown of CD44 expression, and recombinant adenovirus was constructed using AD293 cells. The Ad-CD44-shRNA-treated HCT116 colon cancer cells showed a significant decrease in cell proliferation, migration, and invasion, while apoptosis was increased. The Ad-CD44-shRNA also decreased the phosphorylation of Akt and GSK-3β. The levels of Bcl-2 and Bcl-xL expression were downregulated, whereas the expression levels of Bax, cleaved caspase‑3 and -9, and PARP were increased in Ad-CD44-shRNA-treated colon cancer cells. These results support the feasibility of an adenovirus-mediated RNA interference therapy targeting human colon cancer via the CD44 as a potential future therapeutic intervention.

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Recombinant human soluble thrombomodulin protects against brain injury in a CVST rat model, via downregulation of the HMGB1-RAGE axis.

Cerebral venous sinus thrombosis (CVST) is a distinct cerebrovascular disorder, and ~50% of CVST patients progress to cerebral venous infarction, resulting in elevation of cerebral venous pressure. Anticoagulation is the standard initial treatment and is associated with a reduced relative risk of mortality and dependency. Recombinant human soluble thrombomodulin (rhs‑TM) is a promising therapeutic natural anticoagulant comparable to antithrombin, tissue factor pathway inhibitor, and activated protein C. The present study aimed to investigate the protective effects of rhs‑TM in a CVST rat model, and identify any underlying mechanisms. Rats were treated with rhs‑TM intravenously prior to CVST. Following neurological function evaluation, animals were sacrificed and brain water content and infarct volume were assessed. Brain tissue was collected from the infarcted segments and mRNA and protein expression levels of high mobility group box 1 (HMGB1), receptor for advanced glycation end products (RAGE), tumor necrosis factor (TNF)‑α, interleukin (IL)‑1β, IL‑6, caspase‑3, B‑cell lymphoma‑2 and Bcl‑2 associated X were analyzed by reverse transcription-quantitative polymerase chain reaction and western blot analysis. rhs‑TM significantly prevented neurological deficits in locomotor function and reduced infarct volume. The expression levels of HMGB1‑RAGE were upregulated in the infarcted segments of rat brains following CVST. Pretreatment with rhs‑TM inhibited the HMGB1‑RAGE axis, alleviating the expression levels of the proinflammatory cytokines, TNF‑α, IL‑1β and IL‑6; however, expression levels of the apoptosis-associated genes and proteins remained unaffected. The results of the present study indicated that rhs‑TM protects against CVST in the rat model via inhibition of the HMGB1‑RAGE axis and inflammation, but not via apoptosis.

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Expression of HIF-1α ODD domain fused canine caspase 3 by EGFR promoter-driven adenovirus vector induces cytotoxicity in canine breast tumor cells under hypoxia.

Adenovirus (Ad) vectors are widely used in cancer gene therapies. However, compared to human patients, relatively limited information is available on gene transduction efficiency or cell-specific cytotoxicity in canine tumor cells transduced with Ad vectors. Since epidermal growth factor receptor (EGFR) is highly expressed on canine breast tumor cells, we sought to develop an Ad vector based on the RGD fiber-mutant adenovirus vector (AdRGD) that expresses canine caspase 3 under the control of EGFR promoter. The aims of this study were to achieve high transduction efficiency with transgene expression restricted to canine breast tumor cells. Using EGFR promoter-driven AdRGD, we were able to restrict transgene expression to canine breast tumor cells with no evidence of expression in normal cells. Canine breast tumor cells transduced with EGFR promoter-driven AdRGD carrying canine caspase 3 gene showed cytotoxic activity. We constructed a second AdRGD vector that expressed oxygen-dependent degradation (ODD)-caspase 3 under the control of the EGFR promoter; the fusion protein contains a core part of the ODD domain of hypoxia inducible factor-1 alpha (HIF-1α) fused to caspase 3. Transduction of canine breast tumor cells with EGFR promoter-driven AdRGD expressing ODD-caspase 3 induced a higher rate of cell death under hypoxic conditions compared with under normoxia. The results indicate that the EGFR promoter-driven AdRGD vectors will be of value for tumor-specific transgene expression and safe cancer gene therapy in dogs.

2249 related Products with: Expression of HIF-1α ODD domain fused canine caspase 3 by EGFR promoter-driven adenovirus vector induces cytotoxicity in canine breast tumor cells under hypoxia.

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Involvement of endoplasmic reticulum stress and p53 in lncRNA MEG3-induced human hepatoma HepG2 cell apoptosis.

Long non-coding RNAs (lncRNAs) play important roles in diverse biological processes. Although downregulation of lncRNA maternally expressed gene 3 (MEG3) has been identified in several types of cancers, little is known concerning its biological role and regulatory mechanism in hepatoma. Our previous studies demonstrated that MEG3 induces apoptosis in a p53-dependent manner. The aim of the present study was to determine whether endoplasmic reticulum (ER) stress is involved in MEG3‑induced apoptosis. Recombinant lentiviral vectors containing MEG3 (Lv‑MEG3) were constructed and transfected into HepG2 cells. A 3‑(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay, RT‑PCR, flow cytometry, western blot analysis, immunofluorescence and immunohistochemistry were applied. Transfected HepG2 cells were also transplanted into nude mice, and the tumor growth curves were determined. The results showed that the recombinant lentivirus of MEG3 was transfected successfully into the HepG2 cells and the expression level of MEG3 was significantly increased. Ectopic expression of MEG3 inhibited HepG2 cell proliferation in vitro and in vivo, and also induced apoptosis. Ectopic expression of MEG3 increased ER stress‑related proteins 78‑kDa glucose‑regulated protein (GRP78), inositol‑requiring enzyme 1 (IRE1), RNA‑dependent protein kinase‑like ER kinase (PERK), activating transcription factor 6 (ATF6), C/EBP homologous protein (CHOP), caspase‑3, as well as p53 and NF‑κB expression accompanied by NF‑κB translocation from the cytoplasm to the nucleus. Furthermore, inhibition of NF‑κB with Bay11‑7082 decreased p53 expression in the MEG3‑transfected cells. These results indicate that MEG3 inhibits cell proliferation and induces apoptosis, partially via the activation of the ER stress and p53 pathway, in which NF‑κB signaling is required for p53 activation in ER stress.

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miR-29a up-regulation in AR42J cells contributes to apoptosis via targeting TNFRSF1A gene.

To investigate the expression of miR-29a in rat acute pancreatitis and its functional role in AR42J cell apoptosis.

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Infection by Cx43 adenovirus increased chemotherapy sensitivity in human gastric cancer BGC-823 cells: not involving in induction of cell apoptosis.

There is a lower basal expression of Connexin43 (Cx43) in human gastric cancer BGC-823 cells. In the present study, BGC-823 cells were transfected with recombinant Cx43 adenovirus plasmid vector, and we explored the influences of Cx43 expression on cell proliferation, chemo-sensitivity, colony forming ability, invasion ability and apoptosis. Moreover, we also determined the expression of Pgp, Cx43, as well as apoptosis-related proteins (bcl-2, bax, caspase3 and caspase 9).

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