cck8 chemicals

 D. Zhu, et al. Cancer Letters 477 (2020) 107–121 Fig. 3. MDM2 is upregulated in PDAC tissues and correlates with clinicopathological characteristics, and dysbindin expression is positively correlated withMDM2expressioninPDACtissues.(A)WesternblotanalysisshowingMDM2proteinlevelsinPDACtissues(n=8)andpairedadjacentnoncanceroustissues. Thedataarepresentedasthemean ± SEM.(B)qRT-PCRanalysisshowingMDM2mRNAlevelsinPDACtissues(n=8)andpairedadjacentnoncanceroustissues. Thedataarepresentedasthemean ± SEM.(C)MDM2expressionwasdetectedonatissuemicroarraycontaining63PDACspecimensand57adjacentnoncancerous tissues.RepresentativeIHCstainingprofilesofMDM2indifferentgroupsareshown.ANT,adjacentnoncanceroustissue;T,tumourtissue.Scalebars:top,200μm; bottom,50μm.(D)MDM2expressionlevelsin63PDACtissuesand57adjacentnoncanceroustissueswereanalysedbyPearson\'schi-squaretest.(E)Analysisofthe IHC scores for MDM2 in PDAC tissues and adjacent noncancerous tissues.    ANT, adjacent noncancerous tissue;

 M.V. Yusenko, et al. Cancer Letters 479 (2020) 61–70 Fig. 2. Influence of monensin on viability and MYB expression of human AML cell lines. A. Cells were cultured for 48 h in the presence of the indicated concentrations of monensin, followed by an MTS assay. Data is presented as percentage of remaining viable relative to cells cultured without monensin. B. Different AML cell lines and HEKMYBLuc cells were treated for 24 or 48 h with the indicated concentrations of monensin. Total cell extracts were then analyzed by western blotting for MYB and β-actin expression. C. Northern blot analysis of MYB mRNA expression in NB4 cells treated for 2 days with 0.3 or 1 μM monensin. Ribosomal protein S17 mRNA was used as a loading control. The numbers refer to the amounts of MYB mRNA relative to untreated NB4 cells. D. NB4 cells were treatedfor12hwithdifferentamountsofmonensinintheabsenceorpresence of10μMMG132. Totalcellextracts werethenanalyzed bywesternblottingforMYB and β-actin express

 W. Zhou, et al. Cancer Letters 483 (2020) 75–86 the possibility that myosin-9 promotes cancer metastasis through [5] S.M. Kolk, R.J. Pasterkamp, MICALflavoprotein monooxygenases: structure, func- tion and role in semaphorin signaling, Adv. Exp. Med. Biol. 600 (2007) 38–51. MICAL2 in LUADs. First, the redox-regulation of myosin-9 results in [6] Y. Cai, J. Lu, F. Tang, Overexpression of MICAL2, a novel tumor-promoting factor, microfilamentremodelingandalteredcellularmotility[50].Giventhat accelerates tumor progression through regulating cell proliferation and EMT, J. MICAL2isaredoxenzyme[9,51]andthatmyosin-9wasshowntobind Canc. 9 (2018) 521–527. [7] J. Fischer, T. Weide, A. Barnekow, The MICAL proteins and rab1: a possible link to MICAL2 (Fig. 4), further study could focus on whether MICAL2 can the cytoskeleton? Biochem Temozolomide . Biophys. Res. Commun Hexa His tag peptide . 328 (2005) 415–423. redox myosin-9 regulating microfilament depolymerization. Secondly, [8] B.C.Le

 Cancer Letters 481 (2020) 15–23 Contents lists available at ScienceDirect Cancer Letters journal homepage: www.elsevier.com/locate/canlet Prodigiosin impairs autophagosome-lysosome fusion that sensitizes T colorectal cancer to 5-fluorouracil-induced cell death a,b,1 a,b,1 a,b a,b a,b a,b Chong Zhao , ShaoZhuang Qiu , Jie He , Yao Peng , Haoming Xu , Zhiqiang Feng , a,b a,b a,b a,b,∗ Hongli Huang , Yanlei Du , Yongjian Zhou , Yuqiang Nie a Department of Gastroenterology, Guangzhou Digestive Disease Center, Guangzhou First People\'s Hospital, Guangzhou Medical University, Guangzhou, 510180, China b Department of Gastroenterology, Guangzhou First People\'s Hospital, School of Medical, South China University of Technology, Guangzhou, 510180, China ARTICLE INFO ABSTRACT Keywords: Chemotherapy failure is a major cause of recurrence and poor prognosis in colorectal cancer (CRC) patients. Prodigiosin Inhibition of autophagy is a promising strategy to augment the cytotoxicit

 M.V. Yusenko, et al. Cancer Letters 479 (2020) 61–70 Münster for performing next-generation-sequencing and preliminary [25] V. Walf-Vorderwülbecke, K. Pearce, T. Brooks, M. Hubank, M.M. van den Heuvel- Eibrink, C.M. Zwaan, et al., Targeting acute myeloid leukemia by drug-induced c- data analysis. MYB degradation, Leukemia 32 (2018) 882–889. [26] K. Ramaswamy, L. Forbes, G. Minuesa, T. Gindin, F. Brown, M.G. Kharas, et al., Appendix A. Supplementary data Peptidomimetic blockade of MYB in acute myeloid leukemia, Nat. Commun. 9 (2018) 110. [27] J. Mandelbaum, I.A. Shestopalov, R.E. Henderson, N.G. Chau, B. Knoechel, Supplementary data to this article can be found online at https:// M.J. Wick,etal.,Zebrafishblastomerescreen identifiesretinoicacid suppression of doi.org/10.1016/j.canlet.2020.01.039. MYB in adenoid cystic carcinoma, J. Exp. Med. 215 (2018) 2673–2685. [28] Ø. Dahle, T.Ø. Andersen, O. Nordgård, V. Matre, G. Del Sal, O.S. Gabrielsen, Transactivation properties of c-M

 X.Zhang,etal. Cancer Letters 481 (2020) 32–44 cell extract. Secondly, our data indicated that SSL6 regulates metabo- [8] P.E. Hughes, S. Caenepeel, L.C. Wu, Targeted therapy and checkpoint im- munotherapycombinationsforthetreatmentofcancer,TrendsImmunol.37(2016) lism in HCC cells. Thirdly, SSL6 sensitizes HCC to SFN by down- 462–476. regulating glycolysis. Nonetheless, some limits remain exist in this [9] M.E.W. Logtenberg, J.H.M. Jansen, M. Raaben, M. Toebes, K. Franke, study. For instant, the effects of other metabolism such as lipid meta- A.M. Brandsma, H.L. Matlung, A. Fauster, Glutaminyl cyclase is an enzymatic modifier of the CD47- SIRPalpha axis and a target for cancer immunotherapy, bolism on the SFN sensitivity also should be investigated, which may Mainten. Immune Bal. Eff. Targeted Ther. 25 (2019) 612–619. also provide new effective intervention targets. Whether SSL6 could [10] S. Kaur, S.P. Singh, A.G. Elkahloun, W. Wu, M.S. Abu-Asab, D.D. Roberts, CD47- modul

 Cancer Letters 483 (2020) 75–86 Contents lists available at ScienceDirect Cancer Letters journal homepage: www.elsevier.com/locate/canlet MICAL2 is a novel nucleocytoplasmic shuttling protein promoting cancer T invasion and growth of lung adenocarcinoma a a a a a a a WolongZhou ,YuanqiLiu ,YangGao ,YuandaCheng ,RuiminChang ,XizheLi ,YanwuZhou , b c a,d,∗∗ a,d,e,∗ Shaoqiang Wang , Lubiao Liang , Chaojun Duan , Chunfang Zhang a Department of Thoracic Surgery, Xiangya Hospital, Central South University, Changsha, 410008, PR China b Department of Thoracic Surgery, Affiliated Hospital of Jining Medical College, Jining Medical College, Jining, 272000, PR China c Department of Thoracic Surgery, Affiliated Hospital of Zunyi Medical University, Zunyi Medical University, Zunyi, 563000, PR China d National Clinical Research Center for Geriatric Disorders, Xiangya Hospital, Central South University, Changsha, 410008, PR China e Hunan Engineering Research Center for Pulmonary Nodules Preci

 C. Zhao, et al. Cancer Letters 481 (2020) 15–23 Y. Ohsumi, T. Tokuhisa, N. Mizushima, The role of autophagy during the early of autophagosome-lysosome fusion in human cancer cells, Autophagy 8 (2012) neonatal starvation period, Nature 432 (2004) 1032–1036. 338–349 Diphenylterazine (DTZ) . [11] S.H. Noh, S.R. Park, H.K. Yang, H.C. Chung, I.J. Chung, S.W. Kim, H.H. Kim, [30] J. Li, N. Hou, A. Faried, S. Tsutsumi, T. Takeuchi, H. Kuwano, Inhibition of au- J.H. Choi, H.K. Kim, W. Yu, J.I. Lee, D.B. Shin, J. Ji, J.S. Chen, Y. Lim, S. Ha, tophagy by 3-MA enhances the effect of 5-FU-induced apoptosis in colon cancer Y.J. Bang, C.t. investigators, Adjuvant capecitabine plus oxaliplatin for gastric cells, Ann. Surg Oncol. 16 (2009) 761–771. cancer after D2 gastrectomy (CLASSIC): 5-year follow-up of an open-label, rando- [31] K.N. Dalby, I. Tekedereli, G. Lopez-Berestein, B. Ozpolat, Targeting the prodeath mised phase 3 trial, Lancet Oncol. 15 (2014) 1389–1396. and prosurvival funct

 r> C. Zhao, et al. Cancer Letters 481 (2020) 15–23 Fig. 5. The combination of Prodigiosin and 5-Fu inhibits the growth of HCT116 xenografts in nude mice. Nude mice bearing HCT116 xenograft tumors were treated with vehicle, prodigiosin alone (1 mg/kg), 5-Fu alone (30 mg/ kg), or a combination of prodigiosin and 5-Fu twice weekly through i.p. injection for 21 days after inocula- tion with cultured tumor cells. (A) Tumor images and tumor weights are shown.Onday21afterinoculation,the mice were sacrificed, and the tumor tissues were imaged, weighed, and de- tailed. Mean ± SD (n = 5); **, P < 0.01 versus control, prodigiosin or 5-Fu alone. (B) Tumor volume was recorded every three days after treat- ment. Mean ± SD (n = 5); **, P < 0.01 versus control, prodigiosin or 5-Fu alone.  (C) Body weight was recorded every three days during the 21 day of exposure. No sig- nificant differences were detected be- tween the vehicle and other groups: prodigiosin alone CORM-3 , 5-Fu alone

  X.Zhang,etal. Cancer Letters 481 (2020) 32–44 Fig. 5. SSL6 suppresses glycolysisvia blocking CD47/PI3K/Akt/HIF-1 signaling pathway. (A) After 72 h of SSL6 treatment (10 μg/mL), protein levels of PI3K/Akt/ HIF-1 pathway and key enzymes involved in glycolysis in Huh-7 were determined. (B) After 72 h of SSL6 treatment (10 μg/mL), protein levels of PLCγ and phosphorylated-PLCγ were assessed. (C) Huh-7 cells were treated with SFN (5 μM) and/or SSL6 (10 μg/mL) for 72 h, the expression of PKA, AMPK and phos- phorylated-AMPK were examined.  (D,E) After knockdown of CD47, protein levels of PI3K/Akt/HIF-1 pathway and key enzymes in glycolysis in Huh-7 (D) and MHCC97H (E) cells. (F) Flow cytometry detection of cell death after Huh-7 cells were pre-treated with LY294002 (20 μM) or 2-DG (2.5 mM) for 12 h, SFN (5 μM) and/orSSL6(10μg/mL)wereadministratedfor72h.(G,H)Huh-7cellswerepre-treatedwithLY294002(20μM),theintracellularlactatelevels(G)andthemRNA expression of CD47,HIF1A and key enzy