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MOUSE ANTI HUMAN FIBROBLASTS_EPITHELIAL CELLS

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[#ABS10507] MOUSE ANTI HUMAN FIBROBLASTS_EPITHELIAL CELLS

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ABS10507 | MOUSE ANTI HUMAN FIBROBLASTS_EPITHELIAL CELLS, 0.2 mg
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(1) Geodorum densiflorum rhizome lectin inhibits Ehrlich ascites carcinoma cell growth by inducing apoptosis through the regulation of BAX, p53 and NF-κB genes expression.[TOP]

Pubmed ID :30521911
Publication Date : //
A lectin with a molecular mass of 12 ± 1 kDa was isolated for the first time from Geodorum densiflorum (Lam.) rhizome (GDL). The lectin exhibited hemagglutination activity both in mice and human erythrocytes which was inhibited by 4-nitrophenyl-β-D-glucopyranoside among the tested 26 sugars. The lectin was heat stable and showed its full activity in the pH range from 5.0 to 9.0. The lectin did not lose its activity in the presence of urea but the activity lost significantly when treated with EDTA. Divalent cation Ca and Mg also partially inhibited the activity of the lectin The lectin strongly agglutinated Ehrlich ascites carcinoma (EAC) and inhibited the cells growth by 60% at 160 μg/ml protein concentration but unable to inhibit the growth of HeLa cells in vitro. The growth inhibition was due to the induction of apoptosis in the EAC cells which was confirmed by annexin-V and caspase-3 substrate and finally by apoptosis-related genes expression. An intensive expression of anti-apoptotic Bcl-X gene was observed only in untreated EAC cells while pro-apoptotic Bak and Bax genes expressed only in GDL treated EAC cells with the remarkable increase of the p53 gene expression. In the treated EAC cells NFκB expression was down regulated.

Authors : Ahsanul Kabir K M, Amin Ruhul, Hasan Imtiaj, Asaduzzaman A K M, Khatun Hamida, Kabir Syed Rashel,



(2) Glucuronorhamnoxylan from Capsosiphon fulvescens inhibits the growth of HT-29 human colon cancer cells in vitro and in vivo via induction of apoptotic cell death.[TOP]

Pubmed ID :30521889
Publication Date : //
Colorectal cancer is the third most diagnosed cancer and a leading cause of cancer death. Dissatisfaction with currently available anti-colorectal cancer drugs caused by unwanted side effects and low efficacy necessitates new therapeutic agents. In the present study, a sulfated glucuronorhamnoxylan polysaccharide (named SPS-CF) purified from a green alga Capsosiphon fulvescens was evaluated for its anti-cancer activity in vitro and in vivo against colorectal cancer. The SPS-CF treatment resulted in a dose-dependent inhibition of the HT-29 human colon cancer cell growth up to 40% at 500 μg/mL. This inhibitory activity was shown to be mediated by upregulation of the cleavage of caspase-8, -9, -3 and poly (ADP-ribose) polymerase (PARP), induction of DNA fragmentation, and disruption of mitochondrial membrane potential (MMP), demonstrating that SPS-CF causes apoptotic death of HT-29 cancer cells though activation of caspase-dependant pathway. Administration of SPS-CF to BALB/c-nude mice bearing HT-29 cell-xenograft tumor also reduced the tumor growth. The results of this study demonstrated that the SPS-CF effectively inhibits the colorectal tumor growth both in vitro and in vivo by induction of apoptotic death of tumor cells, suggesting that it can be a potent ingredient for health-beneficial foods or anti-cancer agents to prevent or ameliorate human colon cancer.

Authors : Choi Ji Won, Lee Jisun, Kim Seong Cheol, You SangGuan, Lee Chang Won, Shin Juhee, Park Yong Il,



(3) Subdominance and poor intrinsic immunogenicity limit humoral immunity targeting influenza HA-stem.[TOP]

Pubmed ID :30521496
Publication Date : //
Both natural influenza infection and current seasonal influenza vaccines primarily induce neutralising antibody responses against highly diverse epitopes within the "head" of the viral hemagglutinin (HA) protein. There is increasing interest on redirecting immunity towards the more conserved HA-stem or stalk as a means to broaden protective antibody responses. Here we examined HA-stem-specific B cell and T-follicular helper (Tfh) cell responses in the context of influenza infection and immunisation in mouse and monkey models. We found that during infection the stem domain was immunologically subdominant to the head in terms of serum antibody production and antigen-specific B and Tfh responses. Similarly, we found HA-stem immunogens were poorly immunogenic compared to the full-length HA with abolished sialic acid binding activity, with limiting Tfh elicitation a potential constraint to the induction or boosting of anti-stem immunity by vaccination. Finally, we confirm that currently licensed seasonal influenza vaccines can boost pre-existing memory responses against the HA-stem in humans. An increased understanding of the immune dynamics surrounding the HA-stem is essential to inform the design of next-generation influenza vaccines for broad and durable protection.

Authors : Tan Hyon-Xhi, Jegaskanda Sinthujan, Juno Jennifer A, Esterbauer Robyn, Wong Julius, Kelly Hannah G, Liu Yi, Tilmanis Danielle, Hurt Aeron C, Yewdell Jonathan W, Kent Stephen J, Wheatley Adam K,



(4) Antibody-assisted delivery of a peptide-drug conjugate for targeted cancer therapy.[TOP]

Pubmed ID :30521347
Publication Date : //
A number of cancer-targeting peptide-drug conjugates (PDCs) have been explored as alternatives to antibody-drug conjugates (ADCs) for targeted cancer therapy. However, the much shorter circulation half-life of PDCs compared with ADCs in vivo has limited their therapeutic value and thus their translation into the clinic, highlighting the need to develop new approaches for extending the half-life of PDCs. Here, we report a new strategy for targeted cancer therapy of a PDC based on a molecular hybrid between an anti-hapten antibody and a hapten-labeled PDC. An anti-cotinine antibody (Abcot) was used as a model anti-hapten antibody. The anticancer drug SN38 was linked to a cotinine-labeled aptide specific to extra domain B of fibronectin (cot-APTEDB), yielding the model PDC, cot-APTEDB-SN38. The cotinine-labeled PDC showed specific binding to and cytotoxicity toward an EDB-overexpressing human glioblastoma cell line (U87MG) and also formed a hybrid complex (HC) with Abcot in situ, designated HC[cot-APTEDB-SN38/Abcot]. In glioblastoma-bearing mice, in situ HC[cot-APTEDB-SN38/Abcot] significantly extended the circulation half-life of cot-APTEDB-SN38 in blood, and enhanced accumulation and penetration within the tumor and, ultimately, inhibition of tumor growth. These findings suggest that the present platform holds promise as a new, targeted delivery strategy for PDCs in anticancer therapy.

Authors : Kim Hyungjun, Hwang Do Been, Choi Minsuk, Lee Soyoung, Kang Sukmo, Lee Yonghyun, Kim Sunghyun, Chung Junho, Jon Sangyong,



(5) Effects of cannabinoids in Amyotrophic Lateral Sclerosis (ALS) murine models: A systematic review and meta-analysis.[TOP]

Pubmed ID :30520038
Publication Date : //
Amyotrophic Lateral Sclerosis (ALS) is a neurodegenerative disorder that results from motor neuron damage. Cannabinoids have been proposed as treatments for ALS due to their anti-excitotoxicity, anti-oxidant, and anti-inflammatory effects. Pre-clinical studies in mice models of ALS have been published using a range of cannabinoid formulations and doses. To date, there has been no rigorous evaluation of these trials to assess a potential cannabinoid treatment effect. This review and meta-analysis was undertaken to provide evidence for or against a treatment effect of cannabinoids in murine ALS models. Evidence of a treatment effect in mice may provide motivation for trials in human ALS. We identified a total of 10 studies; 9 studies using cannabinoid treatment in transgenic SOD1-G93A ALS-model mice and 1 study in TDP-43 transgenic mice. 8 of the 9 studies that used SOD1-G93A mice expressed similarly high copy numbers of the transgene whilst one study used a low-copy number line. Outcomes evaluated were survival time and disease progression. The latter was measured by motor function and bodyweight decline. Meta-analysis of the mean difference in survival time across the 7 studies showed an increase in survival of 3.84 days (95% CI 0.35 to 7.32 days; P =0.031) for cannabinoid treated compared to control SOD1-G93A mice. It was not possible to conduct meta-analyses for motor function decline or weight loss. However, 8 of 9 studies reported significant improvements in measures of motor function decline and 1 reported non-significant improvements. Weight loss was significantly attenuated in 4 of 5 studies reporting this measure whilst the other study reported a non-significant attenuation. This review provides some evidence for the efficacy of cannabinoids in prolonging survival time in an ALS mouse model. A delay in disease progression is also suggested following cannabinoid treatment though it was not possible to consolidate the results from reviewed studies. However, studies have moderate to high risk of bias and are highly heterogeneous. Although this review provides some evidence to support the conduct of a cannabinoid trial in human ALS, more standardized studies on specific cannabinoids are necessary before supporting therapeutic potential of cannabinoids in treating patients with ALS. This article is protected by copyright. All rights reserved.

Authors : Urbi Berzenn, Owusu Maame Amma, Hughes Ian, Katz Matthew, Broadley Simon, Sabet Arman,



(6) is a novel hypothalamic gene upregulated by a high-fat diet and leptin in mice.[TOP]

Pubmed ID :30519364
Publication Date : //
Energy homeostasis is regulated by the hypothalamus but fails when animals are fed a high-fat diet (HFD), and leptin insensitivity and obesity develops. To elucidate the possible mechanisms underlying these effects, a microarray-based transcriptomics approach was used to identify novel genes regulated by HFD and leptin in the mouse hypothalamus.

Authors : Sergi Domenico, Campbell Fiona M, Grant Christine, Morris Amanda C, Bachmair Eva-Maria, Koch Christiane, McLean Fiona H, Muller Aifric, Hoggard Nigel, de Roos Baukje, Porteiro Begona, Boekschoten Mark V, McGillicuddy Fiona C, Kahn Darcy, Nicol Phyllis, Benzler Jonas, Mayer Claus-Dieter, Drew Janice E, Roche Helen M, Muller Michael, Nogueiras Ruben, Dieguez Carlos, Tups Alexander, Williams Lynda M,



(7) Oxymatrine Synergistically Potentiates the Antitumor Effects of Cisplatin in Human Gastric Cancer Cells.[TOP]

Pubmed ID :30519359
Publication Date : //
Cisplatin (CDDP) has been extensively used for gastric cancer (GC) treatment but limited by drug resistance and severe toxicity. The chemo-sensitizers that enhance its efficiency and overcome its limitation are urgently needed. Oxymatrine (OMT), a primary active ingredient from the dry roots of Sophora favescens, has shown powerful anti-cancer property with little side-effect. In this study, we explored the chemo-sensitization of OMT to potentiate the anti-tumor effect of CDDP. GC cell lines were dealt with OMT and/or CDDP and then subjected to different experimental methods. We found that OMT could significantly potentiate the CDDP-caused BGC-823 and SGC7901 cells viability loss, and OMT acts synergistically with CDDP. The combinative treatment could arrest cell cycle in G0/G1 phase by increasing p21, p27 and decreasing cyclin D1, and induced apoptosis by ROS generation and AKT/ERK inactivation. Inhibition of ROS respectively reversed the cell death induced by OMT and/or CDDP, suggesting the pivotal roles of ROS in the process. Moreover, OMT enhanced the antitumor effects of CDDP in nude mice bearing BGC823 tumor xenografts Taken together, this study highlights that the co-treatment with OMT and CDDP exerted synergistic antitumor effects in GC cells, and that these effects may be mediated by ROS generation and inactivation of the AKT/ERK pathways.

Authors : Liu Yan, Qin Lei, Bi Tingting, Dai Wei, Liu Wei, Gao Quangen, Shen Genhai,



(8) ALS-Associated E478G Mutation in Human OPTN (Optineurin) Promotes Inflammation and Induces Neuronal Cell Death.[TOP]

Pubmed ID :30519240
Publication Date : //
Amyotrophic Lateral Sclerosis (ALS) is a group of neurodegenerative disorders that featured with the death of motor neurons, which leads to loss of voluntary control on muscles. The etiologies vary among different subtypes of ALS, and no effective management or medication could be provided to the patients, with the underlying mechanisms incompletely understood yet. Mutations in human (Optineurin), particularly E478G, have been found in many ALS patients. In this work, we report that NF-κB activity was increased in knockout () MEF (mouse embryonic fibroblast) cells expressing OPTN of different ALS-associated mutants especially E478G. Inflammation was significantly activated in mice infected with lenti-virus that allowed overexpression of mutation in the motor cortex, with marked increase in the secretion of pro-inflammatory cytokines as well as neuronal cell death. Our work with both cell and animal models strongly suggested that anti-inflammation treatment could represent a powerful strategy to intervene into disease progression in ALS patients who possess the distinctive mutations in gene.

Authors : Liu Zhengzhao, Li Hongming, Hong Chungu, Chen Menglu, Yue Tao, Chen Chunyuan, Wang Zhenxing, You Qing, Li Chuanyin, Weng Qinjie, Xie Hui, Hu Ronggui,



(9) Osthole sensitizes with radiotherapy to suppress tumorigenesis of human nasopharyngeal carcinoma in vitro and in vivo.[TOP]

Pubmed ID :30519095
Publication Date : //
Radiotherapy is one of the most comment and useful treatment for nasopharyngeal carcinoma (NPC), but the radioresistance remains a major obstacle. Osthole, a natural coumarin derivative, has been shown to have anti-tumor and anti-inflammatory activity. However, the relationship between osthole and NPC treatment, especially for radiotherapy, is still elusive.

Authors : Peng Lin, Huang Yi-Teng, Chen Jian, Zhuang Yi-Xuan, Zhang Fan, Chen Jiong-Yu, Zhou Li, Zhang Dong-Hong,



(10) Cisplatin-induced immune modulation in ovarian cancer mouse models with distinct inflammation profiles.[TOP]

Pubmed ID :30518877
Publication Date : //
The backbone of ovarian cancer treatment is platinum-based chemotherapy and aggressive surgical debulking. New therapeutic approaches using immunotherapy via immune checkpoint blockade, which have demonstrated clinical efficacy in other tumor types, have been less promising in ovarian cancer. To increase their clinical efficacy, checkpoint inhibitors are now being tested in clinical trials in combination with chemotherapy. Here, we evaluated the impact of cisplatin on tumor immunogenicity and its in vivo roles when used alone or in combination with anti-PD-L1, in two novel murine ovarian cancer cell models. The 2F8 and its platinum-resistant derivative 2F8cis model, display distinct inflammatory profiles and chemotherapy sensitivities, and mirror the primary and recurrent human disease, respectively. Acute and chronic exposure to cisplatin enhances tumor immunogenicity by increasing calreticulin, MHC class I, antigen presentation and T-cell infiltration. Cisplatin also upregulates PD-L1 expression in vitro and in vivo, demonstrating a dual, paradoxical immune modulatory effect and supporting the rationale for combination with immune checkpoint blockade. One of the pathways activated by cisplatin treatment is the cGAS/STING pathway. Chronic cisplatin treatment led to upregulation of cGAS and STING proteins in 2F8cis compared to parental 2F8 cells, while acute exposure to cisplatin further increases cGAS and STING levels in both 2F8 and 2F8cis cells. Overexpression of cGAS/STING modifies tumor immunogenicity by upregulating PD-L1, MHC I and calreticulin in tumor cells. Anti-PD-L1 alone in a platinum-sensitive model or with cisplatin in a platinum-resistant model increases survival. These studies have high translational potential in ovarian cancer.

Authors : Grabosch Shannon, Bulatovic Mirna, Zeng Feitianzhi, Ma Tianzhou, Zhang Lixin, Ross Malcolm, Brozick Joan, Fang YuSi, Tseng George, Kim Eun, Gambotto Andrea, Elishaev Esther, P Edwards Robert, Vlad Anda M,