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(1) Reversing Effects of Ginsenosides on LPS-induced Hepatic CYP3A11/3A4 Dysfunction Through the Pregnane X Receptor.[TOP]

Pubmed ID :30342195
Publication Date : //
Ginseng (Panax ginseng C. A. Meyer), a traditional Chinese medicine, is widely used in the adjunctive therapy of the liver diseases.

Authors : Sun Hai-Yan, Yan Yi-Jing, Li Yan-Hui, Lv Le,

(2) Anti-tumor activity and the mechanism of a green tea (Camellia sinensis) polysaccharide on prostate cancer.[TOP]

Pubmed ID :30342140
Publication Date : //
In this study, a homogeneous polysaccharide (GTP), with a molecular weight of 7.0 × 10 Da, was isolated from Green tea, which was only composed of glucose. The antitumor effects of GTP on prostate cancer (PC) cell line along with the possible mechanism was examined. First, we investigate the potential role of microRNA-93 (miR-93) in PC progression. Our results showed that miR-93 was significantly upregulated in human PC tissues and several PC cell lines, and its overexpression was correlated with poor survival in PC patients. Furthermore, functional analysis showed that miR-93 overexpression promoted the migration, invasion and proliferation of PC-3 cells transfected with miR-93 mimics, while its knockdown displayed an opposite result in DU145 cells following miR-93 inhibitor transfection. Additionally, in vivo tumorigenic studies on nude mice confirmed that miR-93 mimic treatment accelerated the growth of PC-3 xenograft tumors. As expected, GTP (25, 50 and 100 μg/ml) inhibited growth of PC-3 cells via inducing apoptosis, which was achieved by elevation of bax/bcl-2 ratio and caspae-3 protein expression, as well as a decrease of miR-93. Thus, miR-93 may be a potential therapeutic target by GTP for PC therapy.

Authors : Yang Ke, Gao Zhi-Yong, Li Tie-Qiu, Song Wei, Xiao Wei, Zheng Jue, Chen Hao, Chen Gui-Heng, Zou Hao-Yu,

(3) Successful intracranial delivery of trastuzumab by gene-therapy for treatment of HER2-positive breast cancer brain metastases.[TOP]

Pubmed ID :30342077
Publication Date : //
Trastuzumab is a monoclonal antibody which demonstrates efficacy for HER2 positive breast cancer patients. Recently, an increased incidence of brain metastasis in trastuzumab-treated patients has been reported. The reason for this may be the effectiveness of systemic trastuzumab allowing patients to survive longer thus providing time for brain metastases to develop, along with the lack of penetration of systemic therapies through the blood brain barrier. In recent years, several administration routes to the brain have been evaluated. Albeit advances in the field, there is still a need for improved delivery of therapeutic antibodies to the brain. To address this challenge, we have developed two gene therapy-based methods enabling continuous secretion of active trastuzumab in the brain.

Authors : Zafir-Lavie Inbal, Sherbo Shay, Goltsman Haim, Badinter Felix, Yieni Eilam, Ofek Paula, Miari Reem, Tal Osnat, Liran Atar, Shatil Tamar, Krispel Simi, Shapir Nir, Neil Garry A, Benhar Itai, Panet Amos, Fainaro Ronit Satchi,

(4) Sonodynamic Therapy on Intracranial Glioblastoma Xenografts Using Sinoporphyrin Sodium Delivered by Ultrasound with Microbubbles.[TOP]

Pubmed ID :30341739
Publication Date : //
Sonodynamic therapy (SDT) is a promising noninvasive method for cancer treatment. The anti-tumor effect of sinoporphyrin sodium (DVDMS)-mediated SDT on nude mice bearing intracranial U87 MG-Red-FLuc human glioblastoma was investigated. Focused ultrasound (FUS) with microbubbles (MBs) was utilized to open the blood-brain barrier for enhancing the delivery of the sonosensitizer DVDMS to the brain tumor first, and then the SDT treatment was performed. The in vitro study showed obvious cytotoxicity of DVDMS-mediated SDT (center frequency: 0.996 MHz, acoustic power: 1.7 W, pulse repletion frequency: 1 Hz, duty cycle: 30%, duration: 1 min) on U87 MG-Red-FLuc cells. The results indicated that more DVDMS accumulation in the tumor sites was induced by FUS with MBs by 3.43 folds of unsonicated ones. Longitudinal bioluminescence imaging illustrated that the intracranial glioblastoma progression in nude mice treated with SDT was retarded compared to the untreated group. The median survival time was prolonged to 30.25 days after SDT treatment by 27.37%. The anti-proliferation effect and cell apoptosis induction was further confirmed by immunohistochemical examinations. These results of the study suggested that SDT using the sonosensitizer DVDMS delivered by FUS with MBs may provide a new promising therapeutic strategy against glioblastoma.

Authors : Pi Zhaoke, Huang Yongpeng, Shen Yuanyuan, Zeng Xiaojun, Hu Yaxin, Chen Tie, Li Chenyang, Yu Hao, Chen Siping, Chen Xin,

(5) Low doses of widely consumed cannabinoids (cannabidiol and cannabidivarin) cause DNA damage and chromosomal aberrations in human-derived cells.[TOP]

Pubmed ID :30341733
Publication Date : //
Cannabidiol (CBD) and cannabidivarin (CBDV) are natural cannabinoids which are consumed in increasing amounts worldwide in cannabis extracts, as they prevent epilepsy, anxiety, and seizures. It was claimed that they may be useful in cancer therapy and have anti-inflammatory properties. Adverse long-term effects of these drugs (induction of cancer and infertility) which are related to damage of the genetic material have not been investigated. Therefore, we studied their DNA-damaging properties in human-derived cell lines under conditions which reflect the exposure of consumers. Both compounds induced DNA damage in single cell gel electrophoresis (SCGE) experiments in a human liver cell line (HepG2) and in buccal-derived cells (TR146) at low levels (≥ 0.2 µM). Results of micronucleus (MN) cytome assays showed that the damage leads to formation of MNi which reflect chromosomal aberrations and leads to nuclear buds and bridges which are a consequence of gene amplifications and dicentric chromosomes. Additional experiments indicate that these effects are caused by oxidative base damage and that liver enzymes (S9) increase the genotoxic activity of both compounds. Our findings show that low concentrations of CBD and CBDV cause damage of the genetic material in human-derived cells. Furthermore, earlier studies showed that they cause chromosomal aberrations and MN in bone marrow of mice. Fixation of damage of the DNA in the form of chromosomal damage is generally considered to be essential in the multistep process of malignancy, therefore the currently available data are indicative for potential carcinogenic properties of the cannabinoids.

Authors : Russo Chiara, Ferk Franziska, Mišík Miroslav, Ropek Nathalie, Nersesyan Armen, Mejri Doris, Holzmann Klaus, Lavorgna Margherita, Isidori Marina, Knasmüller Siegfried,

(6) The concept of the okadaic acid class of tumor promoters is revived in endogenous protein inhibitors of protein phosphatase 2A, SET and CIP2A, in human cancers.[TOP]

Pubmed ID :30341686
Publication Date : //
The okadaic acid class of tumor promoters, which are inhibitors of protein phosphatases 1 and 2A (PP1 and PP2A), induced tumor promotion in mouse skin, rat glandular stomach, and rat liver. Endogenous protein inhibitors of PP2A, SET and CIP2A, were up-regulated in various human cancers, so it is vital to review the essential mechanisms of tumor promotion by the okadaic acid class compounds, together with cancer progression by SET and CIP2A in humans.

Authors : Fujiki Hirota, Sueoka Eisaburo, Watanabe Tatsuro, Suganuma Masami,

(7) Loss of GRHL3 leads to TARC/CCL17-mediated keratinocyte proliferation in the epidermis.[TOP]

Pubmed ID :30341279
Publication Date : //
Identifying soluble factors that influence epidermal integrity is critical for the development of preventative and therapeutic strategies for disorders such as ichthyosis, psoriasis, dermatitis and epidermal cancers. The transcription factor Grainyhead-like 3 (GRHL3) is essential for maintaining barrier integrity and preventing development of cutaneous squamous cell carcinoma (SCC); however, how loss of this factor, which in the skin is expressed exclusively within suprabasal epidermal layers triggers proliferation of basal keratinocytes, had thus far remained elusive. Our present study identifies thymus and activation-regulated chemokine (TARC) as a novel soluble chemokine mediator of keratinocyte proliferation following loss of GRHL3. Knockdown of GRHL3 in human keratinocytes showed that of 42 cytokines examined, TARC was the only significantly upregulated chemokine. Mouse skin lacking Grhl3 presented an inflammatory response with hallmarks of TARC activation, including heightened induction of blood clotting, increased infiltration of mast cells and pro-inflammatory T cells, increased expression of the pro-proliferative/pro-inflammatory markers CD3 and pSTAT3, and significantly elevated basal keratinocyte proliferation. Treatment of skin cultures lacking Grhl3 with the broad spectrum anti-inflammatory 5-aminosalicylic acid (5ASA) partially restored epidermal differentiation, indicating that abnormal keratinocyte proliferation/differentiation balance is a key driver of barrier dysfunction following loss of Grhl3, and providing a promising therapeutic avenue in the treatment of GRHL3-mediated epidermal disorders.

Authors : Goldie Stephen J, Cottle Denny L, Tan Fiona H, Roslan Suraya, Srivastava Seema, Brady Rhys, Partridge Darren D, Auden Alana, Smyth Ian M, Jane Stephen M, Dworkin Sebastian, Darido Charbel,

(8) Catestatin as a Target for Treatment of Inflammatory Diseases.[TOP]

Pubmed ID :30337922
Publication Date : //
It is increasingly clear that inflammatory diseases and cancers are influenced by cleavage products of the pro-hormone chromogranin A (CgA), such as the 21-amino acids long catestatin (CST). The goal of this review is to provide an overview of the anti-inflammatory effects of CST and its mechanism of action. We discuss evidence proving that CST and its precursor CgA are crucial for maintaining metabolic and immune homeostasis. CST could reduce inflammation in various mouse models for diabetes, colitis and atherosclerosis. In these mouse models, CST treatment resulted in less infiltration of immune cells in affected tissues, although monocyte migration was increased by CST. Both and , CST can shift macrophage differentiation from a pro- to an anti-inflammatory phenotype. Thus, the concept is emerging that CST plays a role in tissue homeostasis by regulating immune cell infiltration and macrophage differentiation. These findings warrant studying the effects of CST in humans and make it an interesting therapeutic target for treatment and/or diagnosis of various metabolic and immune diseases.

Authors : Muntjewerff Elke M, Dunkel Gina, Nicolasen Mara J T, Mahata Sushil K, van den Bogaart Geert,

(9) Effect of polysaccharides from a Korean ginseng berry on the immunosenescence of aged mice.[TOP]

Pubmed ID :30337804
Publication Date : //
Korean ginseng has been widely evaluated to treat human diseases; however, most studies on Korean ginseng have focused on its root. In this study, polysaccharides [acidic-polysaccharide-linked glycopeptide (APGP) extracted with 90% ethanol and hot water] were prepared from Korean ginseng berries, and their effect on immunosenescence was explored.

Authors : Kim Miseon, Yi Young-Su, Kim Juewon, Han Sang Yun, Kim Su Hwan, Seo Dae Bang, Cho Jae Youl, Shin Song Seok,

(10) Dual Inhibition of Bcl-2/Bcl-xL and XPO1 is synthetically lethal in glioblastoma model systems.[TOP]

Pubmed ID :30337641
Publication Date : //
XPO1 has recently emerged as a viable treatment target for solid malignancies, including glioblastoma (GBM), the most common primary malignant brain tumor in adults. However, given that tumors become commonly resistant to single treatments, the identification of combination therapies is critical. Therefore, we tested the hypothesis that inhibition of anti-apoptotic Bcl-2 family members and XPO1 are synthetically lethal. To this purpose, two clinically validated drug compounds, the BH3-mimetic, ABT263, and the XPO1 inhibitor, Selinexor, were used in preclinical GBM model systems. Our results show that inhibition of XPO1 reduces cellular viability in glioblastoma cell cultures. Moreover, addition of ABT263 significantly enhances the efficacy of XPO1 inhibition on the reduction of cellular viability, which occurs in a synergistic manner. While selinexor inhibits the proliferation of glioblastoma cells, the combination treatment of ABT263 and selinexor results in substantial induction of cell death, which is accompanied by activation of effector- initiator caspases and cleavage of PARP. Mechanistically we find that XPO1 inhibition results in down-regulation of anti-apoptotic Mcl-1 and attenuates ABT263 driven Mcl-1 up-regulation. Consistently, siRNA mediated silencing of Mcl-1 sensitizes for ABT263 mediated cell death and partially for the combination treatment. By using a human patient-derived xenograft model of glioblastoma in mice, we demonstrate that the combination treatment of ABT263 and Selinexor reduces tumor growth significantly more than each compound alone. Collectively, these results suggest that inhibition of XPO1 and Bcl-2/Bcl-xL might be a potential strategy for the treatment of malignant glial tumors.

Authors : Shang Enyuan, Zhang Yiru, Shu Chang, Ishida Chiaki Tsuge, Bianchetti Elena, Westhoff Mike-Andrew, Karpel-Massler Georg, Siegelin Markus D,