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  Subjects -> BIOLOGY (Total: 2989 journals)
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    - BIOLOGY (1427 journals)
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BIOLOGY (1427 journals)

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Journal Cover Biochemistry and Cell Biology
  [SJR: 0.859]   [H-I: 76]   [14 followers]  Follow
    
   Hybrid Journal Hybrid journal (It can contain Open Access articles)
   ISSN (Print) 0829-8211 - ISSN (Online) 1208-6002
   Published by NRC Research Press Homepage  [21 journals]
  • MeCP2 and CTCF: enhancing the cross-talk of silencers
    • Authors: Juan Ausió, Philippe T. Georgel
      Pages: 593 - 608
      Abstract: Biochemistry and Cell Biology, Volume 95, Issue 6, Page 593-608, December 2017.
      This paper provides a brief introductory review of the most recent advances in our knowledge about the structural and functional aspects of two transcriptional regulators: MeCP2, a protein whose mutated forms are involved in Rett syndrome; and CTCF, a constitutive transcriptional insulator. This is followed by a description of the PTMs affecting these two proteins and an analysis of their known interacting partners. A special emphasis is placed on the recent studies connecting these two proteins, focusing on the still poorly understood potential structural and functional interactions between the two of them on the chromatin substrate. An overview is provided for some of the currently known genes that are dually regulated by these two proteins. Finally, a model is put forward to account for their possible involvement in their regulation of gene expression.
      Citation: Biochemistry and Cell Biology
      PubDate: 2017-08-10T07:00:00Z
      DOI: 10.1139/bcb-2017-0147
       
  • Hydrogen peroxide regulates angiogenesis-related factors in tumor cells
    • Authors: Ana Jerónimo, Gonçalo Rodrigues, Filipe Vilas-Boas, Gabriel G. Martins, Ana Bagulho, Carla Real
      Pages: 1 - 7
      Abstract: Biochemistry and Cell Biology, e-First Articles.
      Tumor angiogenesis is required for tumor development and growth, and is regulated by several factors including ROS. H2O2 is a ROS with an important role in cell signaling, but how H2O2 regulates tumor angiogenesis is still poorly understood. We have xenografted tumor cells with altered levels of H2O2 by catalase overexpression into zebrafish embryos to study redox-induced tumor neovascularization. We found that vascular recruitment and invasion were impaired if catalase was overexpressed. In addition, the overexpression of catalase altered the transcriptional levels of several angiogenesis-related factors in tumor cells, including TIMP-3 and THBS1. These two anti-angiogenic factors were found to be H2O2-regulated by two different mechanisms: TIMP-3 expression in a cell-autonomous manner; and, THBS1 expression that was non-cell-autonomous. Our work shows that intracellular H2O2 regulates the expression of angiogenic factors and the formation of a vessel network. Understanding the molecular mechanisms that govern this multifunctional effect of H2O2 on tumor angiogenesis could be important for the development of more efficient anti-angiogenic therapies.
      Citation: Biochemistry and Cell Biology
      PubDate: 2017-08-17T07:00:00Z
      DOI: 10.1139/bcb-2017-0083
       
  • Knockdown of Snail inhibits epithelial–mesenchymal transition of human
           laryngeal squamous cell carcinoma Hep-2 cells through the vitamin D
           receptor signaling pathway
    • Authors: Xue Zhao, Dan Yu, Jingpu Yang, Kai Xue, Yan Liu, Chunshun Jin
      Pages: 1 - 7
      Abstract: Biochemistry and Cell Biology, e-First Articles.
      It has been well documented that Snail plays a decisive role in various tumors. However, the direct effect of Snail on laryngeal squamous cell carcinoma (LSCC) has not been elaborated. In this study, we firstly detected the expression of Snail in 14 samples of patients with LSCC and found that its content was high in cancer tissues compared with adjacent tissues. Then we established LSCC Hep-2 cells with Snail silencing and validated the knockdown efficiency by Western blotting and real-time PCR. Results showed that silencing of Snail significantly inhibited the ability of adhesion, migration, and invasion of Hep-2 cells. Further study revealed that knockdown of Snail suppressed the epithelial–mesenchymal transition (EMT) process of Hep-2 cells, as evidenced by downregulation of matrix metallopeptidase (MMP)-2, MMP-9, integrin subunit beta 1 (ITGβ1), β-catenin, vimentin, N-cadherin, and fibronectin and upregulation of vitamin D receptor (VDR) and E-cadherin. Additionally, transfection with the small interfering RNA of VDR reversed the effect induced by Snail silencing in Hep-2 cells. Taken together, these results demonstrate that knockdown of Snail can inhibit the EMT process of LSCC cells through the VDR signaling pathway in vitro.
      Citation: Biochemistry and Cell Biology
      PubDate: 2017-08-14T07:00:00Z
      DOI: 10.1139/bcb-2017-0039
       
  • Human bone marrow mesenchymal stem cells suppress the proliferation of
           hepatic stellate cells by inhibiting the ubiquitination of p27
    • Authors: Liang Wang, Guang Bai, Fei Chen
      Pages: 1 - 6
      Abstract: Biochemistry and Cell Biology, e-First Articles.
      Bone marrow mesenchymal stem cells (BMSCs) have considerable therapeutic potential for the treatment of end-stage liver disease. Previous studies have demonstrated that BMSCs secrete growth factors and cytokines that inactivate hepatic stellate cells (HSCs), which inhibited the progression of hepatic fibrosis. The aim of this study was to determine the mechanism by which BMSCs suppress the function of HSCs in fibrosis. Our results showed that co-culture of BMSCs and HSCs induced cell cycle arrest at the G10/G1 phase and cell apoptosis of HSCs, which finally inhibited the cell proliferation of HSCs. Consistent with the cell cycle arrest, co-culture of BMSCs and HSCs increased the abundance of the cell cycle protein p27. Mechanistically, we further uncovered that following the co-culture with BMSCs, the expression level of the E3 ligase S-phase kinase-associated protein 2 (SKP2) that is responsible for the ubiquitination of p27 was decreased, which attenuated the ubiquitination of p27 and increased the stability of p27 in HSCs. Collectively, our results indicated the potential involvement of the SKP2–p27 axis for the inhibitory effect of BSMCs on the cell proliferation of HSCs.
      Citation: Biochemistry and Cell Biology
      PubDate: 2017-07-26T07:00:00Z
      DOI: 10.1139/bcb-2017-0127
       
  • Regulation of the insulin–Akt signaling pathway and glycolysis during
           dehydration stress in the African clawed frog Xenopus laevis
    • Authors: Cheng-Wei Wu, Shannon N. Tessier, Kenneth B. Storey
      Pages: 1 - 9
      Abstract: Biochemistry and Cell Biology, e-First Articles.
      Estivation is an adaptive stress response utilized by some amphibians during periods of drought in the summer season. In this study, we examine the regulation of the insulin signaling cascade and glycolysis pathway in the African clawed frog Xenopus laevis during the dehydration stress induced state of estivation. We show that in the brain and heart of X. laevis, dehydration reduces the phosphorylation of the insulin growth factor-1 receptor (IGF-1R), and this is followed by similar reductions in the phosphorylation of the Akt and mechanistic target of rapamycin (mTOR) kinase. Interestingly, phosphorylation levels of IGF-1R and mTOR were not affected in the kidney, and phosphorylation levels of P70S6K and the ribosomal S6 protein were elevated during dehydration stress. Animals under estivation are also susceptible to periods of hypoxia, suggesting that glycolysis may also be affected. We observed that protein levels of many glycolytic enzymes remained unchanged during dehydration; however, the hypoxia response factor-1 alpha (HIF-1α) protein was elevated by greater than twofold in the heart during dehydration. Overall, we provide evidence that shows that the insulin signaling pathway in X. laevis is regulated in a tissue-specific manner during dehydration stress and suggests an important role for this signaling cascade in mediating the estivation response.
      Citation: Biochemistry and Cell Biology
      PubDate: 2017-07-14T07:00:00Z
      DOI: 10.1139/bcb-2017-0117
       
  • Petroleum ether extract of Njavara rice (Oryza sativa) bran upregulates
           the JAK2–STAT3-mediated anti-inflammatory profile in macrophages and
           aortic endothelial cells promoting regression of atherosclerosis
    • Authors: Pushpan K. Chithra, Ananthasankaran Jayalekshmy, Antony Helen
      Pages: 1 - 11
      Abstract: Biochemistry and Cell Biology, e-First Articles.
      “Njavara” (Oryza sativa L.) is a unique rice variety grown in Kerala that is reported to have significantly higher antioxidant, anti-inflammatory, chemical indices, and bioactive components compared with staple rice varieties. However, the role of NBE in reversing the atherosclerosis development remains unclear. The present study aimed to elucidate the role of NBE in promoting atherosclerotic regression. Male New Zealand white breed rabbits were divided into three groups. Group I was the control, group II was the regression control, and group III was NBE treated (100 mg/kg body mass). Serum and tissue lipids, CRP, antioxidant enzyme activities, mRNA, and protein expression of genes of RTC and mRNA expression of cytokines were studied. The current study showed that hypercholesterolemic rabbits treated with NBE decreased the serum and tissue lipids concentrations, ApoB expression, and CRP levels and enhanced the activities of antioxidant enzymes and PON1expression, JAK2, STAT3, ABCA1, and ApoA. Our results indicate that NBE attenuates proinflammatory cytokine production (IL-1β), enhanced expression and interactions of ABCA1/ApoA1 leading to JAK2/STAT3 activation in macrophages switching to an anti-inflammatory milieu in the system, and enhanced expression of IL-10 and decreased expression of ApoB, indicating that treatment with NBE facilitates plaque regression.
      Citation: Biochemistry and Cell Biology
      PubDate: 2017-07-12T07:00:00Z
      DOI: 10.1139/bcb-2017-0090
       
  • Danshen attenuates osteoarthritis-related cartilage degeneration through
           inhibition of NF-κB signaling pathway in vivo and in vitro
    • Authors: Xilin Xu, Hang Lv, Xiaodong Li, Hui Su, Xiaofeng Zhang, Jun Yang
      Pages: 1 - 8
      Abstract: Biochemistry and Cell Biology, e-First Articles.
      Danshen (Salvia miltiorrhiza) is a traditional Chinese medicine herb that can alleviate the symptoms of osteoarthritis (OA) (Söder et al. 2006) in animals. However, the underlying mechanisms remain poorly understood and require further investigation. In this study, rabbits with experimentally induced OA were given an intra-articular injection of danshen (0.7 mL/day) for 5 weeks. In addition to attenuating the cartilage degeneration of OA in the rabbits, danshen decreased the expression and activity of matrix metalloproteinase 9 (MMP-9) and MMP-13, and increased the expression of their natural inhibitors: tissue inhibitor of matrix metalloproteinase 1 (TIMP-1) and TIMP-2. Apoptosis in osteoarthritic cartilage tissues was attenuated by danshen, accompanied with increased expression of B cell lymphoma 2 (Bcl-2) and decreased levels of Bcl-2-associated X protein (Bax). Further, danshen inhibited the nuclear accumulation of nuclear factor kappa-B (NF-κB) p65 in osteoarthritic cartilage. The therapeutic effects of danshen in vivo were comparable to that of sodium hyaluronate, which is a drug used clinically for the treatment OA. In vitro, sodium nitroprusside (SNP) was used to stimulate apoptosis in primary rabbit chondrocytes. We found that the SNP-induced apoptosis was mitigated by danshen. BAY11-7028, an inhibitor of the NF-κB pathway, augmented danshen’s anti-apoptotic effects in cells exposed to SNP. When these results are considered together, they indicate that danshen alleviates the cartilage injury in rabbit OA through inhibition of the NF-κB signaling pathway.
      Citation: Biochemistry and Cell Biology
      PubDate: 2017-06-29T07:00:00Z
      DOI: 10.1139/bcb-2017-0025
       
  • Modulation of procaspase-7 self-activation by PEST amino acid residues of
           the N-terminal prodomain and intersubunit linker
    • Authors: Juliano Alves, Miguel Garay-Malpartida, João M. Occhiucci, José E. Belizário
      Pages: 1 - 10
      Abstract: Biochemistry and Cell Biology, e-First Articles.
      Procaspase-7 zymogen polypeptide is composed of a short prodomain, a large subunit (p20), and a small subunit (p10) connected to an intersubunit linker. Caspase-7 is activated by an initiator caspase-8 and -9, or by autocatalysis after specific cleavage at IQAD198↓S located at the intersubunit linker. Previously, we identified that PEST regions made of amino acid residues Pro (P), Glu (E), Asp (D), Ser (S), Thr (T), Asn (N), and Gln (Q) are conserved flanking amino acid residues in the cleavage sites within a prodomain and intersubunit linker of all caspase family members. Here we tested the impact of alanine substitution of PEST amino acid residues on procaspase-7 proteolytic self-activation directly in Escherichia coli. The p20 and p10 subunit cleavage were significantly delayed in double caspase-7 mutants in the prodomain (N18A/P26A) and intersubunit linker (S199A/P201A), compared with the wild-type caspase-7. The S199A/P201A mutants effectively inhibited the p10 small subunit cleavage. However, the mutations did not change the kinetic parameters (kcat/KM) and optimal tetrapeptide specificity (DEVD) of the purified mutant enzymes. The results suggest a role of PEST-amino acid residues in the molecular mechanism for prodomain and intersubunit cleavage and caspase-7 self-activation.
      Citation: Biochemistry and Cell Biology
      PubDate: 2017-06-28T07:00:00Z
      DOI: 10.1139/bcb-2016-0220
       
  • Jatropha-6(17),11E-diene class derivatives induce apoptosis effects in
           OVCAR-3 and Caov-4 ovarian cancer cell lines via a mitochondrial pathway
    • Authors: Behzad Bahmani, Mohammad Keyvanloo Shahrestanaki, Mustafa Ghanadian, Sima Hajiahmadi, Mahmoud Aghaei
      Pages: 1 - 12
      Abstract: Biochemistry and Cell Biology, e-First Articles.
      We investigated the molecular mechanism of apoptosis induced by novel jatropha-6(17),11E-diene class derivatives, compounds A, B, and C that were extracted from Euphorbia osyridea Boiss, in the ovarian cancer cell lines Caov-4 and OVCAR-3. The OVCAR-3 and Caov-4 cell lines were treated with different concentrations of these compounds. Cytotoxicity was evaluated using MTT, clonogenic survival assay, and flow cytometry assays. The production of reactive oxygen species (ROS), mitochondrial membrane potential (ΔΨm), and the activity of caspase 3 and 9 were evaluated. Compounds A, B, and C reduced cell viability in a dose-dependent manner (P < 0.05). The IC50 values were calculated as 46.27 ± 3.86, and 38.81 ± 3.30 μmol/L for compound A, 36.48 ± 3.18 and 42.59 ± 4.50 μmol/L for compound B, and 85.86 ± 6.75 and 75.65 ± 2.56 μmol/L for compound C against the Caov-4 and OVCAR-3 cell lines, respectively. Apoptosis evaluation showed that jatrophane derivatives increase both early and late apoptosis (P < 0.01). These compounds also increased ROS generation, ΔΨm, and the activity of caspase 3 and 9 in the treated cells. These results showed that compounds A and B have significant inhibitory effects on OVCAR-3 and Caov-4 proliferation and induction of apoptosis.
      Citation: Biochemistry and Cell Biology
      PubDate: 2017-06-27T07:00:00Z
      DOI: 10.1139/bcb-2017-0034
       
  • Wnt5A regulates the expression of ROR2 tyrosine kinase receptor in ovarian
           cancer cells
    • Authors: Ghamartaj Hossein, Somayeh Arabzadeh, Zahra Salehi-Dulabi, Zeinab Dehghani-Ghobadi, Yassaman Heidarian, Maryam Talebi-Juybari
      Pages: 1 - 7
      Abstract: Biochemistry and Cell Biology, e-First Articles.
      Wnt5A and receptor tyrosine kinase-like orphan receptor 2 (ROR2) proteins both regulate developmental processes, cell movement, and cell polarity. The purpose of this study was to evaluate a possible regulatory role of Wnt5A on ROR2 expression in human ovarian cancer cell lines. Moreover, the expression of Wnt5A and ROR2 mRNA and protein levels were assessed in human epithelial serous ovarian cancer (HSOC) specimens. ROR2 was strongly decreased in cells treated with siRNA against Wnt5A compared with scramble-treated or lipofectamine-treated cells (P < 0.001). There was 34% decreased cell invasion (P < 0.01) in Wnt5A knock-down cells compared with lipofectamine-treated and scramble-treated cells; however, cell invasion remained unchanged upon addition of anti-ROR2 antibody to the culture media of these cells. In contrast, addition of anti-ROR2 antibody to the culture media for lipofectamine-treated and scramble-treated cells led to 32% decreased cell invasion (P < 0.01). Normal ovarian specimens were negative, and variable immunostaining was observed in HSOC for Wnt5A and ROR2 immunostaining. Furthermore, there was a positive correlation between Wnt5A and ROR2 expression in high-grade SOC samples at the mRNA level (P < 0.05; r = 0.38). This is the first report to show the regulatory role of Wnt5A on ROR2 expression in ovarian cancer.
      Citation: Biochemistry and Cell Biology
      PubDate: 2017-05-24T07:00:00Z
      DOI: 10.1139/bcb-2016-0216
       
 
 
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