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#29036264   2017/10/16 Save this To Up

Immature colon carcinoma transcript-1 promotes proliferation of gastric cancer cells.

Gastric cancer is the fourth most common malignant tumor and has been considered as one of the leading causes of cancer-related death worldwide. The identification of the molecular mechanism during gastric cancer progression is urgently needed, which will help to develop more effective treatment strategies. As a component of the human mitoribosome, immature colon carcinoma transcript-1 (ICT1) might be involved in tumor formation and progression. However, its biological function and the corresponding mechanism in gastric cancer have been poorly characterized. To study the mechanism of ICT1 in gastric cancer, we first investigated the mRNA levels of ICT1 in human normal and gastric cancer tissues using datasets from the publicly available Oncomine database. The results showed that ICT1 is overexpressed in gastric cancer tissues. Then in order to study the role of ICT1 in gastric cancer, two shRNAs were used to silence ICT1 in MGC80-3 and AGS cells. Functional analysis showed ICT1 knockdown significantly inhibited the proliferation of gastric cancer cells and induced apoptosis. Further, mechanistic study demonstrated that ICT1 silencing induced cell-cycle arrest at G2/M phase via the suppression of cyclin A2 and cyclin B1. In addition, ICT1 silencing also increased cleaved caspase-3 and activated PARP in gastric cancer cells. These findings suggest that ICT1 may play a crucial role in promoting gastric cancer proliferation in vitro.

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#29036189   2017/10/16 Save this To Up

Inhibition of CUG-binding protein 1 and activation of caspases are critically involved in piperazine derivative BK10007S induced apoptosis in hepatocellular carcinoma cells.

Though piperazine derivative BK10007S was known to induce apoptosis in pancreatic cancer xenograft model as a T-type CaV3.1 a1G isoform calcium channel blocker, its underlying antitumor mechanism still remains unclear so far. Thus, in the present study, the antitumor mechanism of BK10007S was elucidated in hepatocellular carcinoma cells (HCCs). Herein, BK10007S showed significant cytotoxicity by 3-[4,5-2-yl]-2,5-diphenyltetra-zolium bromide (MTT) assay and anti-proliferative effects by colony formation assay in HepG2 and SK-Hep1 cells. Also, apoptotic bodies and terminal deoxynucleotidyl transferase (TdT) dUTP Nick End Labeling (TUNEL) positive cells were observed in BK10007S treated HepG2 and SK-Hep1 cells by 4',6-diamidino-2-phenylinodole (DAPI) staining and TUNEL assay, respectively. Consistently, BK10007S increased sub G1 population in HepG2 and SK-Hep1 cells by cell cycle analysis. Furthermore, Western blotting revealed that BK10007S activated the caspase cascades (caspase 8, 9 and 3), cleaved poly (ADP-ribose) polymerase (PARP), and downregulated the expression of cyclin D1, survivin and for CUG-binding protein 1 (CUGBP1 or CELF1) in HepG2 and SK-Hep1 cells. Conversely, overexpression of CUGBP1 reduced cleavages of PARP and caspase 3, cytotoxicity and subG1 population in BK10007S treated HepG2 cells. Overall, these findings provide scientific evidences that BK10007S induces apoptosis via inhibition of CUGBP1 and activation of caspases in hepatocellular carcinomas as a potent anticancer candidate.

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#29035884   2017/10/16 Save this To Up

Protective Effects of Pretreatment with Quercetin Against Lipopolysaccharide-Induced Apoptosis and the Inhibition of Osteoblast Differentiation via the MAPK and Wnt/β-Catenin Pathways in MC3T3-E1 Cells.

Quercetin, a flavonoid found in onions and other vegetables, has potential inhibitory effects on bone resorption in vivo and in vitro. In our previous study, we found that quercetin treatment reversed lipopolysaccharide (LPS)-induced inhibition of osteoblast differentiation through the mitogen-activated protein kinase (MAPK) pathway in MC3T3-E1 cells. In this study, we investigated the underlying mechanisms of pretreatment with quercetin on apoptosis and the inhibition of osteoblast differentiation in MC3T3-E1 cells induced by LPS.

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#29035827   2017/10/16 Save this To Up

Ginsenoside Rg3 enhances the anti-proliferative activity of erlotinib in pancreatic cancer cell lines by downregulation of EGFR/PI3K/Akt signaling pathway.

Erlotinib has shown activity in the management of pancreatic cancer. However, the benefit of EGFR blockade is limited due to EGFR independent PI3K/Akt signaling pathway. Studies have reported that Ginsenoside Rg3 strongly inhibited PI3K-Akt signaling pathway of many carcinomas. We aimed to investigate the activity of Ginsenoside Rg3 to sensitize erlotinib in treating pancreatic cancer in vitro and in vivo. Human pancreatic cancer cell lines BxPC-3 and AsPC-1 were used. Cell proliferation and colony formation assay, Annexin V/PI apoptosis analysis, Western blot analysis, immunohistochemistry and in vivo study were carried out. Ginsenoside Rg3 enhanced the anti-proliferative effects of erlotinib in BxPC-3 and AsPC-1 pancreatic cancer cells and xenograft. Ginsenoside Rg3 enhanced erlotinib-induced apoptosis and increased caspase-3,9 and PARP cleavage expression levels. Erlotinib/Ginsenoside Rg3 treatment decreased the levels of p-EGFR, p-PI3K, and p-Akt expression significantly. Ginsenoside Rg3 could enhance the efficacy of erlotinib to inhibit the proliferation of pancreatic cancer cells via induction of apoptosis and downregulation of the EGFR/PI3K/AKT pathway.

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#29035685   2017/10/16 Save this To Up

Mechanistic effect of human umbilical cord blood derived-mesenchymal stem cells on the submandibular salivary gland in ovariectomized rats.

To reveal the effect of human umbilical cord blood-derived mesenchymal stem cells (hUCB-MSCs) on the submandibular gland after bilateral ovariectomy, 21 adult Sprague-Dawley female rats were divided equally into three groups: sham-operated group (SHAM), ovariectomized group (OVX) and OVX received repeated intravenous injection of hUCB-MSCs group (OVX + hUCB-MSCs). RT-PCR for AQP3, AQP4, AQP5 and BMP6 gene expression was determined. The cellular localization and expression of anti-human CD105 anti-human CD34, anti-proliferating nuclear antigen (PCNA), anti-single stranded DNA(ssDNA), anti-Caspase 3, anti-aquaporin 1(AQP1) and anti-α smooth muscle actin(α-SMA) were determined immunohistochemically. In the OVX group, a significant decrease in AQP3, AQP4, and BMP6 gene expression, as well as the acinar area %, was detected while GCTs areas % showed a significant increase. A significant decrease of positive area % of anti-AQP1 and anti-α SMA was noted. In the hUCB-MSCs treated group, a significant increase in AQP3, AQP4 and BMP6 gene expression and an obvious improvement in the structure of the sub-mandibular gland were demonstrated. The acinar and GCTs areas%, as well as the different measured markers, were around normal.

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#29035676   2017/10/16 Save this To Up

The Molecular Mechanism and Neuroprotective Effect of Dihydrocapsaicin-Induced Mild Hypothermia After Cardiopulmonary Resuscitation in Rats.

To investigate the molecular mechanism of dihydrocapsaicin (DHC)-induced mild hypothermia in rats, and to compare its protective effect on the central nervous system with that of a conventional method of inducing hypothermia, 24 healthy male Sprague Dawley rats were randomly divided into four groups based on the following conditions: control group, cardiopulmonary resuscitation (CPR) group, body surface cooling group, and DHC group. Tracheal clipping was used to mimic asphyxia arrest. Rats were assessed for their neurological deficit scores. After sacrifice, immunohistochemical staining was used to examine caspase-3 expression in the cerebral cortex and TRPV1 (transient receptor potential vanilloid subfamily, member 1) expression in the hypothalamus. Terminal TdT-mediated dUTP-biotin nick end labeling (TUNEL) staining was used to evaluate cell apoptosis in the cerebral cortex. Furthermore, intracellular Ca(2+) concentration in the hypothalamus and arginine vasopressin (AVP) concentration in ventral septal tissues were also detected in these four groups. Results of our study showed that neurological deficit scores in the DHC group were significantly higher than those in the CPR and body surface cooling groups (p < 0.05). Caspase-3 expression in the cerebral cortex of control group rats was significantly lower than that in other three groups (p < 0.05). Hypothalamic TRPV1 expression, hypothalamic intracellular Ca(2+) concentration, and AVP concentration in the ventral septum in the DHC group were significantly higher than that in the other three groups (p < 0.05). Within these three groups, there were significantly fewer apoptotic cells in the DHC and body surface cooling group rats than in the CPR group rats (p < 0.05). DHC has the neuroprotective effect. DHC induced mild hypothermia and reduces apoptosis through a mechanism whereby DHC activates TRPV1 on hypothalamic cells to cause a large Ca(2+) influx, which alters corresponding physiological functions and causes the release of AVP to induce hypothermia.

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#29035583   2017/10/16 Save this To Up

Resveratrol Suppresses Growth and Migration of Myelodysplastic Cells by Inhibiting the Expression of Elevated Cyclin D1 (CCND1).

Myelodysplastic syndromes (MDS) are a group of heterogeneous diseases characterized by poorly formed blood cells. We wanted to elucidate the underlying molecular mechanism to better determine pathogenesis, prognosis, diagnosis, and treatment for patients with MDS. We compared gene expression levels between normal and MDS tissue samples by immunohistochemical analysis. We studied the proliferation, survival, and migration of MDS cells using the EDU assay, colony formation, and transwell assays. We assessed the apoptotic rate and cell cycle status using flow cytometry and Hoechst staining. Finally, we evaluated RNA and protein expressions using polymerase chain reaction and Western blots, respectively. We found that resveratrol suppressed SKM-1 (an advanced MDS cell line) proliferation in a dose-dependent manner. Consistent with this finding, the EDU and colony formation assays also showed that resveratrol inhibited SKM-1 growth. Moreover, flow cytometry and Hoechst 33258 staining demonstrated that resveratrol induced apoptosis and a change in cell cycle status in SKM-1 cells, while the transwell assay showed that resveratrol reduced the migratory ability of SKM-1 cells. Resveratrol also decreased the expression of CCND1 (a gene that encodes the cyclin D1 protein) and increased expressions of KMT2A [lysine (K)-specific methyltransferase 2A] and caspase-3, suggesting that resveratrol exerts its effect by regulating CCND1 in SKM-1 cells. In addition, a combination of resveratrol and the PI3K/AKT inhibitor LY294002 exhibited a stronger inhibitory effect on the SKM-1 cells, compared with resveratrol alone. Our study proved that resveratrol suppresses SKM-1 growth and migration by inhibiting CCND1 expression. This finding provides novel insights into the pathogenesis of MDS and might help develop new diagnosis and treatment for patients with MDS.

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#29035012   2017/10/16 Save this To Up

Regulatory Effects of Black Rice Extract on Helicobacter pylori Infection-Induced Apoptosis.

Black rice extract (BRE) contains cyanidin 3-O-glucoside (C3G), an anthocyanin, as the major component. In this study, we found that BRE inhibited the mRNA and protein expression of genes encoding cytotoxin-associated protein A (cagA) and vacuolating protein A (vacA) in Helicobacter pylori 60190 strain.

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#29034805   2017/10/16 Save this To Up

In vitro investigation of the effect of matrix molecules on the behavior of colon cancer cells under the effect of geldanamycin derivative.

The chaperone-binding drug, 17-allylamino-17-demethoxygeldanamycin, has recently come into clinical use. It is a derivative of geldanamycin, an ansamycin benzoquinone antibiotic with anti-carcinogenic effect. Understanding the effect of this drug on the cancer cells and their niche is important for treatment. We applied 17-allylamino-17-demethoxygeldanamycin to colon cancer cell line (Colo 205) on matrix molecules to investigate the relationship of apoptosis with terminal deoxynucleotidyl transferase dUTP nick end labeling immunocytochemistry and related gene expression. We used laminin and collagen I for matrix molecules and vascular endothelial growth factor for angiogenic structure. We also examined apoptosis-related signaling pathway including mitochondrial proteins, cytochrome c, Bcl-2, caspase-9, Apaf-1 expression using real-time polymerase chain reaction. There was clear effect of 17-allylamino-17-demethoxygeldanamycin that killed more cells on tissue culture plastic compared to matrix molecules. The IC50 value was 0.58 µg/mL for tissue culture plastic compared with 0.64 µg/mL for laminin and 0.75 µg/mL for collagen I. The analyses showed that more cells on matrix molecules underwent apoptosis compared to that on tissue culture plastic. Apoptosis-related gene expression was similar in which Bcl-2 expression decreased and proapoptotic gene expression of the cells on matrix molecules increased compared to that on tissue culture plastic. However, the application of 17-allylamino-17-demethoxygeldanamycin was more effective for the cells on collagen I compared to the cells on laminin. There was also a decrease in angiogenesis as shown by the vascular endothelial growth factor staining. This was more pronounced by coating of the tissue culture plastic with matrix molecules. Our results supported the anti-cancer effect of 17-allylamino-17-demethoxygeldanamycin, and this effect depended on matrix molecules. This effect occurs through apoptosis, and related genes were also altered. All these genes may serve for novel target under the effect of matrix substrate. However, correct interpretation of the results requires further studies.

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#29034737   2017/10/16 Save this To Up

Anti-allergic inflammatory effect of vanillic acid through regulating thymic stromal lymphopoietin secretion from activated mast cells.

Vanillic acid, which is well known as a benzoic acid derivative, has been used as a flavouring agent. Currently, we ascertained the therapeutic potential action of vanillic acid on allergic inflammatory reaction in human mast cell line, HMC-1. Treatment with vanillic acid resulted in a significant decrease in levels of thymic stromal lymphopoietin and pro-inflammatory cytokines compared to phorbol 12-myristate 13-acetate and calcium ionophore A23187 (PMACI)-treated HMC-1 cells. In PMACI-stimulated cells, treatment with vanillic acid also dramatically inhibited activities of caspase-1 and nuclear factor-kB (p65). Furthermore, treatment with vanillic acid suppressed phosphorylation of mitogen-activated protein kinases in PMACI-treated HMC-1 cells. Taken together, these findings suggest that vanillic acid has a beneficial effect on allergic inflammatory disorders.

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