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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-PCR...

 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 increas...

 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...

 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...

 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...