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1.
PAPER CURRENT
LncRNA THOR promotes human renal cell carcinoma cell growth (2018)
Elsevier
Publication Date: 2018-05-26
Description: Publication date: 27 June 2018 Source: Biochemical and Biophysical Research Communications, Volume 501, Issue 3 Author(s): Xue-ting Ye, Hang Huang, Wei-ping Huang, Wei-lie Hu Background Recent studies have characterized a novel but extremely conserved long non-coding RNA (LncRNA) THOR . THOR directly associates with insulin-like growth factor 2 mRNA-binding protein 1 (IGF2BP1) to promote mRNA stabilization of key pro-cancerous genes. Results Here, we show that THOR is expressed in human renal cell carcinoma (RCC) tissues and established/primary human RCC cells. It was not detected in normal renal tissues nor in HK-2 and primary human renal epithelial cells. THOR silencing (by targeted siRNAs) or CRISPR/Cas9 knockout inhibited RCC cell growth, viability and proliferation in vitro . Reversely, forced over-expression of THOR promoted RCC cell survival and proliferation. IGF2BP1-regulated genes, including IGF2 , GLI1 and Myc , were downregulated by THOR silencing or knockout, but they were upregulated after THOR over-expression. In vivo , THOR -knockout 786-O tumors grew significantly slower than the control tumors in nude mice. Conclusion THOR expression promotes RCC cell growth in vitro and in vivo . THOR could be a novel and important therapeutic target for human RCC.
Print ISSN: 0006-291X
Electronic ISSN: 1090-2104
Topics: Biology , Chemistry and Pharmacology , Physics
Published by Elsevier
2.
PAPER CURRENT
IGF2BP1 over-expression in skin squamous cell carcinoma cells is essential for cell growth (2018)
Elsevier
Publication Date: 2018-05-26
Description: Publication date: 27 June 2018 Source: Biochemical and Biophysical Research Communications, Volume 501, Issue 3 Author(s): Zhengjun Liu, Guangyu Wu, Cai Lin, Hailei Guo, Jianjun Xu, Tianlan Zhao The present study examined expression and potential functions of insulin-like growth factor 2 mRNA-binding protein 1 (IGF2BP1) in human skin squamous cell carcinoma (SCC). We show that IGF2BP1 mRNA and protein expression levels were upregulated in established (A431 line) and primary human skin SCC cells. Its expression was also increased in human skin SCC tissues, as compared to the normal skin tissues. In skin SCC cells, IGF2BP1 silencing or CRISPR/Cas9 knockout decreased levels of IGF2BP1-stablized mRNAs, including IGF2 , CD44 , Gli1 and Myc . Furthermore, skin SCC cell survival and proliferation were inhibited by IGF2BP1 silencing/knockout. Conversely, forced over-expression of IGF2BP1 further promoted A431 cell survival and proliferation. Furthermore, siRNA-mediated knockdown of IGF2BP1-bound long non-coding RNA THOR (“ Lnc-THOR ”) similarly depleted IGF2BP1-dependent mRNAs, causing inhibition on A431 cell survival and proliferation. In vivo , IGF2BP1 silencing or knockout inhibited A431 tumor xenograft growth in mice. Together, we conclude that IGF2BP1 over-expression in skin SCC cells is essential for cell growth.
Print ISSN: 0006-291X
Electronic ISSN: 1090-2104
Topics: Biology , Chemistry and Pharmacology , Physics
Published by Elsevier
3.
PAPER CURRENT
Inhibition of pancreatic cancer Panc1 cell migration by omeprazole is dependent on aryl hydrocarbon receptor activation of JNK (2018)
Elsevier
Publication Date: 2018-05-26
Description: Publication date: 27 June 2018 Source: Biochemical and Biophysical Research Communications, Volume 501, Issue 3 Author(s): Un-Ho Jin, Keshav Karki, Sang-Bae Kim, Stephen Safe Several aryl hydrocarbon receptor (AhR)-active pharmaceuticals were screened as inhibitors of pancreatic cancer cell invasion and identified two compounds, omeprazole, that inhibited invasion. Inhibition of highly invasive Panc1 cell invasion by omeprazole involves an AhR-dependent non-genomic pathway, and omeprazole-mediated inhibition of Panc1 cell invasion was dependent on Jun-N-terminal kinase (JNK) and mitogen-activated kinase kinase 7 (MKK7). The failure of omeprazole to induce nuclear translocation of the AhR was not due to overexpression of cytosolic AhR partner proteins Hsp90 or XAP2, and results of DNA sequencing show that the AhR expressed in Panc1 cells was not mutated. Results of RNAseq studies indicate that omeprazole induced an AhR-dependent downregulation of several pro-invasion factors including activated leukocyte cell adhesion molecule (ALCAM), long chain fatty acid CoA-synthase (CSL4), stathmin 3 (STMN3) and neuropillin 2 (NRP2), and the specific functions of these genes are currently being investigated. Graphical abstract
Print ISSN: 0006-291X
Electronic ISSN: 1090-2104
Topics: Biology , Chemistry and Pharmacology , Physics
Published by Elsevier
4.
PAPER CURRENT
Structure-based protein engineering of bacterial β-xylosidase to increase the production yield of xylobiose from xylose (2018)
Elsevier
Publication Date: 2018-05-26
Description: Publication date: 27 June 2018 Source: Biochemical and Biophysical Research Communications, Volume 501, Issue 3 Author(s): Seokho Hong, Myungok Kyung, Inseong Jo, Yong-Ro Kim, Nam-Chul Ha Xylobiose consists of two molecules of xylose and has been highly recognized as a food supplement because it possesses high prebiotic functions. β-xylosidase exhibits enzymatic activity to hydrolyze xylobiose, and the enzyme can also catalyze the reverse reaction in the presence of high concentrations of xylose. Previously, β-xylosidase from Bacillus pumilus IPO (BpXynB), belonging to GH family 43, was employed to produce xylobiose from xylose. To improve the enzymatic efficiency, this study determined the high-resolution structure of BpXynB in a complex with xylobiose and engineered BpXynB based on the structures. The structure of BpXynB deciphered the residues involved in the recognition of the xylobiose. A site-directed mutation at the residue for xylobiose recognition increased the yield of xylobiose by 20% compared to a similar activity of the wild type enzyme. The complex structure of the mutant enzyme and xylobiose provided the structural basis for a higher yield of the engineered protein. This engineered enzyme would enable a higher economic production of xylobiose, and a similar engineering strategy could be applied within the same family of enzymes.
Print ISSN: 0006-291X
Electronic ISSN: 1090-2104
Topics: Biology , Chemistry and Pharmacology , Physics
Published by Elsevier
5.
PAPER CURRENT
PGC1α is required for the induction of contact inhibition by suppressing ROS (2018)
Elsevier
Publication Date: 2018-05-26
Description: Publication date: 27 June 2018 Source: Biochemical and Biophysical Research Communications, Volume 501, Issue 3 Author(s): Seungyeon Yang, Sunsook Hwang, Jiho Jang, Minjoong Kim, Jihye Gwak, Seung Min Jeong Contact inhibition (CI) is an important tumor-suppressive mechanism that arrests cell cycle when cells reach high density. Indeed, CI is aberrantly absent in cancer cells and the dysregulation of this can contribute to tumorigenesis. Previously, it has been shown that reactive oxygen species (ROS) levels are repressed at high cell density, which is required for CI, but no molecular mechanism of this ROS regulation has been reported. Here, we show that PGC1α regulates cell density-dependent CI. PGC1α is markedly induced in response to high cell density and suppresses ROS production. Although cellular ROS levels are progressively decreased with increasing cell density, knockdown of PGC1α results in a defect of density-dependent ROS suppression. Importantly, PGC1α knockdown cells become less sensitive to high cell density and exhibit loss of CI. Mechanistically, PGC1α represses ROS production by inducing mitochondrial SIRT3, and thus SIRT3 overexpression rescues the defects of CI by PGC1α knockdown. These results demonstrate that mitochondrial ROS production is a crucial regulator of cell proliferation and identify a new role of PGC1α in CI.
Print ISSN: 0006-291X
Electronic ISSN: 1090-2104
Topics: Biology , Chemistry and Pharmacology , Physics
Published by Elsevier
6.
PAPER CURRENT
Reduced adiposity by compensatory WAT browning upon iBAT removal in mice (2018)
Elsevier
Publication Date: 2018-05-26
Description: Publication date: 27 June 2018 Source: Biochemical and Biophysical Research Communications, Volume 501, Issue 3 Author(s): Zhengyu Piao, Baiqiang Zhai, Xiaoxiao Jiang, Meng Dong, Changguo Yan, Jun Lin, Wanzhu Jin The strong effects of classic brown adipose tissue (BAT) and recruited beige adipocytes in treatment of obesity and metabolic syndrome have been attracting increasing research interest. Cold treatment is an effective, convenient approach to stimulate BAT activity and induce white adipose tissue (WAT) browning. Here, we utilized prolonged cold exposure (from 2 h to 2 weeks in a 4° cold chamber) to elucidate dynamic changes in BAT and in WAT browning during acute and chronic cold exposure in mice. BAT mass decreased quickly, with reduced lipid droplet sizes within 8 h of cold exposure owing to the utilization of BAT pre-storage triglycerides, and subsequently increased during prolonged cold exposure. These dynamic morphological changes in BAT were confirmed by gene expression changes in ADRB3 and PGC1α, while UCP1 and ELOVL3 expression was continuously up-regulated throughout the entire cold exposure period. Additionally, cold treatment increased BAT secretion of FGF21, which has been reported to activate beige adipocyte formation. Thus, to illustrate potential crosstalk between secreted BAT proteins (so-called BATokines) and beige adipogenesis during cold stress, we performed an interscapular BAT (iBAT) removal experiment in mice. Surprisingly, loss of classic iBAT enhanced WAT browning due to compensatorily increased sympathetic WAT input. Unexpectedly, we observed significantly reduced adiposity in the iBAT removal group compared with the control group. These results further suggest that WAT browning plays an important role in whole-body energy metabolism during cold acclimation, even without iBAT. Furthermore, our data imply that enhanced WAT browning may be an efficient therapeutic tool to combat obesity and related syndromes.
Print ISSN: 0006-291X
Electronic ISSN: 1090-2104
Topics: Biology , Chemistry and Pharmacology , Physics
Published by Elsevier
7.
PAPER CURRENT
Retraction notice to "Overlapping signal sequences control nuclear localization and endoplasmic reticulum retention of GRP58" [Biochemical and Biophysical Research Communications 377 (2) (2008) 407–412] (2018)
Elsevier
Publication Date: 2018-05-26
Description: Publication date: 27 June 2018 Source: Biochemical and Biophysical Research Communications, Volume 501, Issue 3 Author(s): Anbu Karani Adikesavan, Emmanual Unni, Anil K. Jaiswal This article has been retracted: please see Elsevier Policy on Article Withdrawal ( https://www.elsevier.com/about/our-business/policies/article-withdrawal ). The University of Maryland, Baltimore conducted an internal investigation which found that the article was compromised and a preponderance of evidence supports retraction of the publication in order to correct the scientific record and ensure its integrity. The Editor-in-Chief has decided to retract this article. This article has been found to contain manipulated and enhanced figures, namely figures 1D and 1E, 4A and 4B.
Print ISSN: 0006-291X
Electronic ISSN: 1090-2104
Topics: Biology , Chemistry and Pharmacology , Physics
Published by Elsevier
8.
PAPER CURRENT
On the S-layer of Thermus thermophilus and the assembling of its main protein SlpA (2018)
Elsevier
Publication Date: 2018-05-26
Description: Publication date: Available online 25 May 2018 Source: Biochimica et Biophysica Acta (BBA) - Biomembranes Author(s): Domenica Farci, Stefano Francesco Farci, Francesca Esposito, Enzo Tramontano, Joanna Kirkpatrick, Dario Piano We have isolated and analysed the cell envelope of the thermophilic bacterium Thermus thermophilus HB8. Isolated cell walls, characterized by the dominance of the S-layer protein SlpA, are found to be constituted by several protein complexes of high molecular weights. Further isolation steps, starting from the cell wall samples, led to the selective release of the S-layer protein SlpA in solution as confirmed by mass spectrometry. Blue Native gel electrophoresis on these samples showed that SlpA is organized into a specific hierarchical order of oligomeric states that are consistent with the complexes at high molecular weight identified on the total cell wall fraction. The analysis showed that SlpA bases this peculiar organization on monomers and exceptionally stable dimers, leading to the formation of tetramers, heptamers, and decamers. Furthermore, the two elementary units of SlpA, monomers and dimers, are regulated by the presence of calcium not only for the assembling of monomers into dimers, but also for the splitting of dimers into monomers. Finally, the SlpA protein was found to be subjected to specific proteolysis leading to characteristic degradation products. Findings are discussed in terms of S-layer assembling properties as bases for understanding its structure, turn-over and organization. Graphical abstract
Print ISSN: 0005-2736
Electronic ISSN: 1879-2642
Topics: Biology , Chemistry and Pharmacology , Medicine , Physics
Published by Elsevier
9.
PAPER CURRENT
Neuroglobin mediates neuroprotection of hypoxic postconditioning against transient global cerebral ischemia in rats through preserving the activity of Na + /K + ATPases (2018)
Nature Publishing Group (NPG)
Publication Date: 2018-05-26
Description: Neuroglobin mediates neuroprotection of hypoxic postconditioning against transient global cerebral ischemia in rats through preserving the activity of Na + /K + ATPases Neuroglobin mediates neuroprotection of hypoxic postconditioning against transient global cerebral ischemia in rats through preserving the activity of Na<sup>+</sup>/K<sup>+</sup> ATPases, Published online: 25 May 2018; doi:10.1038/s41419-018-0656-0 Neuroglobin mediates neuroprotection of hypoxic postconditioning against transient global cerebral ischemia in rats through preserving the activity of Na + /K + ATPases
Electronic ISSN: 2041-4889
Topics: Biology , Medicine
10.
PAPER CURRENT
Aerobic Glycolysis Controls Myeloid-Derived Suppressor Cells and Tumor Immunity via a Specific CEBPB Isoform in Triple-Negative Breast Cancer (2018)
Elsevier
Publication Date: 2018-05-26
Description: Publication date: Available online 24 May 2018 Source: Cell Metabolism Author(s): Wei Li, Takashi Tanikawa, Ilona Kryczek, Houjun Xia, Gaopeng Li, Ke Wu, Shuang Wei, Lili Zhao, Linda Vatan, Bo Wen, Pan Shu, Duxin Sun, Celina Kleer, Max Wicha, Michael Sabel, Kaixiong Tao, Guobin Wang, Weiping Zou Myeloid-derived suppressor cells (MDSCs) inhibit anti-tumor immunity. Aerobic glycolysis is a hallmark of cancer. However, the link between MDSCs and glycolysis is unknown in patients with triple-negative breast cancer (TNBC). Here, we detect abundant glycolytic activities in human TNBC. In two TNBC mouse models, 4T1 and Py8119, glycolysis restriction inhibits tumor granulocyte colony-stimulating factor (G-CSF) and granulocyte macrophage colony-stimulating factor (GM-CSF) expression and reduces MDSCs. These are accompanied with enhanced T cell immunity, reduced tumor growth and metastasis, and prolonged mouse survival. Mechanistically, glycolysis restriction represses the expression of a specific CCAAT/enhancer-binding protein beta (CEBPB) isoform, liver-enriched activator protein (LAP), via the AMP-activated protein kinase (AMPK)-ULK1 and autophagy pathways, whereas LAP controls G-CSF and GM-CSF expression to support MDSC development. Glycolytic signatures that include lactate dehydrogenase A correlate with high MDSCs and low T cells, and are associated with poor human TNBC outcome. Collectively, tumor glycolysis orchestrates a molecular network of the AMPK-ULK1, autophagy, and CEBPB pathways to affect MDSCs and maintain tumor immunosuppression. Graphical abstract Teaser Tumor-derived myeloid-derived suppressor cells (MDSCs) are critical tumor immunosuppression components. Li et al. show that the high glycolytic rate in triple-negative breast cancer cells is associated with MDSC promotion through an AMPK-ULK1 and autophagy pathway. Glycolysis restriction inhibits tumor G-CSF and GM-CSF and consequently MDSC development.
Print ISSN: 1550-4131
Electronic ISSN: 1932-7420
Topics: Biology , Medicine
Published by Elsevier on behalf of Cell Press.