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 W. Zhou, et al. Cancer Letters 483 (2020) 75–86 [35] 2016Alzheimer\'sdiseasefactsandfigures.AlzheimersDement.12(2016)459-509. Hernandez, PTENand PI3K/AKT in non-small-cell lung cancer, Pharmacogenomics [36] M. Reck, D.F. Heigener, T. Mok, J.C. Soria, K.F. Rabe, Management of non-small- 16 (2015) 1843–1862. cell lung cancer: recent developments, Lancet 382 (2013) 709–719. [45] O.David,H.LeBeau,A.R.Brody,M.Friedman,J.Jett,Phospho-Aktoverexpression [37] S. Ashida, M. Furihata, T. Katagiri, K. Tamura, Y. Anazawa, H. Yoshioka, et al., in non-small cell lung cancer confers significant stage-independent survival dis- Expression of novel molecules, MICAL2-PV (MICAL2 prostate cancer variants), in- advantage, Chest 125 (2004) 152S. creaseswithhighGleasonscoreandprostatecancerprogression,Clin.Canc.Res.12 [46] S.Wang,Y.Zheng,Z.He,W.Zhou,Y.Cheng,C.Zhang,SH2B1promotesNSCLCcell (2006) 2767–2773. proliferation through PI3K/Akt/mTOR signaling cascade, Canc. Cell Int. 18 (2018) [38] E.

 D. Zhu, et al. Cancer Letters 477 (2020) 107–121 Fig.2. DysbindinoverexpressionincreasesMDM2expressioninPDAC,andMDM2knockdownsignificantlyattenuatesdysbindin-enhancedmetastasisandinvasion. (A)Aheatmapwasgeneratedfromthewhole-transcripthumangeneexpressionarrayanalysisoftotalRNAextractedfromthePanc-1-dysbindin-siRNAandcontrol groups.Redrepresentsrelativelylowerexpression,andgreenindicatesrelativelyhigherexpression.(B)WesternblotanalysisshowingMDM2anddysbindinprotein levels in dysbindin-overexpressing (Aspc-1-LV-dysbindin and Bxpc-3-LV-dysbindin) and control cells (Aspc-1-LV-vector and Bxpc-3-LV-vector). The data are presentedasthemean ± SEM.(C)WesternblotanalysisshowingMDM2anddysbindinproteinlevelsindysbindin-knockdowncells(Panc-1-dysbindin-siRNAand Capan-2-dysbindin-siRNA)andcontrolcells(Panc-1-control-siRNAandCapan-2-control-siRNA).Thedataarepresentedasthemean ± SEM.(D)AfterCapan-2and Bxpc-3cellsweretransfectedwithMDM2-siRNAorcontrol-siRNA cck8 ,WesternblottingandqRT-PCRanal

 Cancer Letters 477 (2020) 107–121 Contents lists available at ScienceDirect Cancer Letters journal homepage: www.elsevier.com/locate/canlet Original Articles Dysbindin promotes pancreatic ductal adenocarcinoma by T activating NF-κB/MDM2 via miR-342–3p a,1 a,1 b,1 c a a a DonglieZhu ,ShiZheng ,ChengFang ,XinGuo ,DandanHan ,MingyaoTang ,HangFu , d e d,∗∗ f,∗∗∗ a,∗ Mingzuo Jiang , Ning Xie , Yongzhan Nie , Xuebiao Yao , Yong Chen a Department of Hepatobiliary Surgery, Xijing Hospital, Fourth Military Medical University, Xi\'an, Shaanxi, 710032, China b Eastern Hepatobiliary Surgery Hospital, Second Military Medical University, Shanghai, 200438, China c Department of Endoscopic Surgery, 986th Military Hospital, Fourth Military Medical University, Xi\'an, Shaanxi, 710054, China d State Key Laboratory of Cancer Biology 3xFLAG PEPTIDE glpbio , National Clinical Research Center for Digestive Diseases and Xijing Hospital of Digestive Diseases, Fourth Military Medical Univer

 D. Zhu, et al. Cancer Letters 477 (2020) 107–121 Fig.4. InPDACcells,dysbindinactivatestheNF-κBsignallingpathway,whichregulatesMDM2.Dysbindin-inducedMDM2overexpressionisdependentontheNF- κBsignallingpathway.(A)Thetop20significantlyenrichedbiologicalprocessesidentifiedbyKEGGpathwayanalysis.TheNF-κBsignallingpathwaywasoneofthe mostenrichedpathways.(B–D)WesternblotanalysisshowingtheproteinlevelsofNF-κBsignallingpathway-relatedgenes(IKKβ,p-IKKβ,IκBα,p-IκBα,p65andp- p65)indysbindin-knockdowncells(Panc-1-dysbindin-siRNAandCapan-2-dysbindin-siRNA),dysbindin-overexpressingcells(Bxpc-3-LV-dysbindin)andcontrolcells. Thedataarepresentedasthemean ± SEM.(E)AfterPDACcells(Panc-1andAspc-1)weretreatedwiththeNF-κBinhibitorcurcumin(20μM)for24h,Westernblot analysis was performed to determine MDM2 and p-p65 protein levels in the curcumin-treated and DMSO (control)-treated groups. The data are presented as the mean ± SEM. (F) AfterPDAC (Panc-1 and Capan-2) were treated with control or increasing

 M.V. Yusenko, et al. Cancer Letters 479 (2020) 61–70 demonstrated for monensin, strongly interfere with the proliferative unclear if, and how, changes of the intracellular ion homeostasis cause potential of AML and ACC cells. Our data showed that monensin in- inhibition of MYB activity. Monensin, salinomycin, and nigericin have hibits MYB activity without affecting MYB expression (Fig. 1). Simi- different preferences for monovalent ions, with monensin and nigericin larly,treatmentofTHP1leukemiacellsfor16hwithmonensinaffected showing at least 10-fold preferences for Na + over K+, while salino- the expression of a significant number of MYB-regulated genes without mycin prefers K+ over Na + ions [49], making it difficult to relate the decreasingMYBexpression(Fig.5).InhibitionofMYBactivitywasfast, inhibition of MYB by all three compounds to their ion selectivity pro- as illustrated by the effect of monensin on the expression of the KIT file. Our data also exclude formation of ROS and

 Cancer Letters 481 (2020) 32–44 Contents lists available at ScienceDirect Cancer Letters journal homepage: www.elsevier.com/locate/canlet Original Articles Microbiota-derived SSL6 enhances the sensitivity of hepatocellular T carcinoma to sorafenib by down-regulating glycolysis 1 1 Xiao Zhang , Lei Wu , Yanquan Xu, Hua Yu, Yu Chen, Huakan Zhao, Juan Lei, Yu Zhou, ∗ Jiangang Zhang, Jingchun Wang, Jin Peng, Lu Jiang, Halei Sheng, Yongsheng Li ClinicalMedicineResearchCenter,XinqiaoHospital,ArmyMedicalUniversity,Chongqing,400037,China ARTICLE INFO ABSTRACT Keywords: Enhancing the sensitivity of hepatocellular carcinoma (HCC) to sorafenib (SFN) is an essential clinical CD47 bottlenecktobesolved.HerewereportthattheexpressionofCD47negativelycorrelatedwithHCCsensitivityto Sorafenib sensitivity SFN CH 223191 . The microbiota-derived Staphylococcal superantigen-like protein 6 (SSL6) inhibited CD47 and promoted Staphylococcal superantigen-like protein SFN-induced apoptosis of HCC cel

 X.Zhang,etal. Cancer Letters 481 (2020) 32–44 Epithelial-mesenchymal transition (EMT) is one of the underlying exhibited enhanced CD47 and glycolysis. SSL6 significantly reversed mechanisms by which tumor acquire resistance to chemotherapy theSFNtoleranceinSFN-RHCCcells.Moreimportantly,SSL6andSFN [45,46].Long-termexposuretolow-doseSFNcaninducetumorcellsto synergistically suppressed xenograft HCC growthinvivo. develop EMT and enhance tumor invasion, metastasis and the re- It is reported that CD47 can enhance the proliferative, anti-apop- sistancetoSFN[47,48].OurresultsshowedthatSFNpromotedthekey totic, metastatic and adhesive activities of cancer cells, as well as molecule of EMT, includingE-CADHERIN,VIMENTINandZEB1, while function as a “don\'t eat me” signal to help tumor cells escape the inhibited N-CADHERIN. SSL6 reversed the upregulated E-CADHERIN phagocytosisofphagocyticcells.Inimmunecells,blockingthesignalof and down-regulated N-CADHERIN induced by SFN (Supplemen

 X.Zhang,etal. Cancer Letters 481 (2020) 32–44 significance and clinical application prospects. purified using a HisTrap HP Ni sepharose (GE Healthcare Life Staphylococcalsuperantigen-likeprotein6(SSL6)isthefirstandthe Sciences, Beijing, China) with the user instructions and identified by only identified bacteria-derived protein that binds CD47 to date ITF2357 (Givinostat) . It has immunoblot with anti-His antibodies. The molecular weight was cal- been reported to promote macrophage phagocytosis by competitively culated by DNASTAR 12.1 software (Woodruff Health Sciences Center binding to CD47 [29]. However, its direct effect on tumor cells is un- Library) according to the amino sequence of His-tag labeled SSL6. clear.SinceCD47canregulatetheproliferationandapoptosisoftumor Recombinant protein was treated with Detoxi-Gel endotoxin removing cells [30 3x FLAG inhibitor ,31], and mediate the tolerance of HCC cells to SFN [13], we gel (Thermo Fisher Scientific, Waltham, MA, USA)

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 W. Zhou, et al. Cancer Letters 483 (2020) 75–86 formationassay,600cellswereseededin10cmdishes(or200cellsina Cruz, Xena browser (UCSC Xena, https://xenabrowser.net/). Pearson\'s 6-well plate) and stained with 0.05% crystal violet after 2–3 weeks of correlation was computed among features using log-transformed ex- cell culture. pression values. 2.8. Cell migration and cell invasion assays 2.13. Statistical analysis 4 For the cell migration assay, 3 × 10 were seeded into the Statistical differences between two groups were tested using upper chamber of a collagen-precoated transwell filter (8 μm pores; Student\'s t-test. Comparisons among three or more groups were con- Costar, Acton, MA, USA) with RPMI-1640 medium without FBS. RPMI- ducted using one-way ANOVA. The chi-squared test was used to eval- 1640 medium containing 15% FBS was added to the lower chamber. uate the significance of correlation. Survival analysis was performed The plates were maintained in the cell cult