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细胞衰老在胰腺癌中双重作用的研究进展
作者:梁雅静  徐子惠  徐克群 
单位:南京医科大学附属常州市第二人民医院 肿瘤科, 江苏 常州 213003
关键词:细胞衰老 胰腺癌 衰老相关分泌表型 综述 
分类号:R735.9
出版年·卷·期(页码):2024·43·第二期(267-271)
摘要:

胰腺癌预后差,多种治疗手段均不理想,是死亡率接近发病率的恶性肿瘤。而细胞衰老是可诱导的细胞增殖停滞状态,衰老的细胞仍有高代谢活性,通过分泌过多的衰老相关分泌表型(SASP)参与胰腺癌的发生和发展。在本文中重点阐述胰腺癌中细胞衰老的双重作用,以期为改善胰腺癌治疗效果提供启发。

参考文献:

[1] MCGUIGAN A,KELLY P,TURKINGTON R C,et al.Pancreatic cancer:a review of clinical diagnosis,epidemiology,treatment and outcomes[J].World J Gastroenterol,2018,24(43):4846-4861.
[2] SIEGEL R L,MILLER K D,WAGLE N S,et al.Cancer statistics 2023[J].CA Cancer J Clin,2023,73(1):17-48.
[3] LEE S,SCHMITT C A.The dynamic nature of senescence in cancer[J].Nat Cell Biol,2019,21(1):94-101.
[4] ROBINSON N J,SCHIEMANN W P.Telomerase in cancer:function,regulation,and clinical translation[J].Cancers (Basel),2022,14(3):808.
[5] SALEH T,TYUTYUNYK-MASSEY L,GEWIRTZ D A.Tumor cell escape from therapy-induced senescence as a model of disease recurrence after dormancy[J].Cancer Res,2019,79(6):1044-1046.
[6] ZAINABADI K.A brief history of modern aging research[J].Exp Gerontol,2018,104:35-42.
[7] FAGAGNA F D D,TEO S H,JACKSON S P.Functional links between telomeres and proteins of the DNA-damage response[J].Genes Dev,2004,18(15):1781-1799.
[8] ANTONIETTA C M,ARTURO L V J,SILVIA B.Telomere maintenance by telomerase and by recombination can coexist in human cells[J].Hum Mol Genet,2001,10(18):1945-1952.
[9] PAEZ-RIBES M,GONZáLEZ-GUALDA E,DOHERTY G J,et al.Targeting senescent cells in translational medicine[J].EMBO Mol Med,2019,11(12):e10234.
[10] CAMPISI J.Cancer,aging and cellular senescence[J].Vivo,2000,14(1):183.
[11] BIOL N R M C.Cellular senescence:when bad things happen to good cells[J].Nat Rev Mol Cell Biol,2007,8(9):729-740.
[12] PETROVA N V,VELICHKO A K,RAZIN S V,et al.Small molecule compounds that induce cellular senescence[J].Aging Cell,2016,15(6):999-1017.
[13] ROTTENBERG S,DISLER C,PEREGO P.The rediscovery of platinum-based cancer therapy[J].Nat Rev Cancer,2021,21(1):37-50.
[14] ERKAN M,HAUSMANN S,MICHALSKI C W,et al.The role of stroma in pancreatic cancer:diagnostic and therapeutic implications[J].Nat Rev Gastroenterol Hepatol,2012,9(8):454-467.
[15] BASISTY N,KALE A,JEON O H,et al.A proteomic atlas of senescence-associated secretomes for aging biomarker development[J].PLoS Biol,2020,18(1):e3000599.
[16] BAKER D J,WIJSHAKE T,TCHKONIA T,et al.Clearance of P16Ink4a-positive senescent cells delays ageing-associated disorders[J].Nature,2011,479(7372):232-236.
[17] FREUND A,LABERGE R M,DEMARIA M,et al.Lamin B1 loss is a senescence-associated biomarker[J].Mol Biol Cell,2012,23(11):2066-2075.
[18] ZHANG R,CHEN W,ADAMS P D.Molecular dissection of formation of senescence-associated heterochromatin foci[J].Mol Cell Biol,2007,27(6):2343-2358.
[19] BIRAN A,ZADA L,ABOU KARAM P,et al.Quantitative identification of senescent cells in aging and disease[J].Aging Cell,2017,16(4):661-671.
[20] SUN Y,COPPÉ J P,LAM E W.Cellular senescence:the sought or the unwanted?[J].Trends Mol Med,2018,24(10):871-885
[21] SAINT-GERMAIN E,LOPES-PACIENCIA S,ROWELL M C,et al.The senescence-associated secretory phenotype and its regulation[J].Cytokine,2019,117:15-22.
[22] HARA E,TSURUI H,SHINOZAKI A,et al.Cooperative effect of antisense-Rb and antisense-p53 oligomers on the extension of life span in human diploid fibroblasts,TIG-1[J].Biochem Biophys Res Commun,1991,179(1):528-534.
[23] BEAUSEJOUR C M.Reversal of human cellular senescence:roles of the p53 and p16 pathways[J].EMBO J,2014,22(16):4212-4222.
[24] SERRANO M,LIN A W,MCCURRACH M E,et al.Oncogenic ras provokes premature cell senescence associated with accumulation of p53 and p16INK4a[J].Cell,1997,88(5):593.
[25] KAMIJO T,ZINDY F,ROUSSEL M F,et al.Tumor suppression at the mouse INK4a locus mediated by the alternative reading frame product p19ARF[J].Cell,1997,91(5):649-659.
[26] BARDEESY N,AGUIRRE A J,CHU G C,et al.Both p16(Ink4a) and the p19(Arf)-p53 pathway constrain progression of pancreatic adenocarcinoma in the mouse[J].Proc Natl Acad Sci U S A,2006,103(15):5947-5952.
[27] GUERRA C,COLLADO M,NAVAS C,et al.Pancreatitis-induced inflammation contributes to pancreatic cancer by inhibiting oncogene-induced senescence[J].Cancer Cell,2011,19(6):728-739.
[28] WYLD L,BELLANTUONO I,TCHKONIA T,et al.Senescence and cancer:a review of clinical implications of senescence and senotherapies[J].Cancers,2020,12(8):2134.
[29] RUSCETTI M,MORRIS J P,MEZZADRA R,et al.Senescence-induced vascular remodeling creates therapeutic vulnerabilities in pancreas cancer[J].Cell,2020,181(2):424-441.
[30] CHIBAYA L,MURPHY K C,DEMARCO K D,et al.EZH2 inhibition remodels the inflammatory senescence-associated secretory phenotype to potentiate pancreatic cancer immune surveillance[J].Nat Cancer,2023,4(6):872-892.
[31] LING J,KANG Y,ZHAO R,et al.Kras G12D-induced IKK2/β/NF-κBactivation by IL-1α and p62 feedforward loops is required for development of pancreatic ductal adenocarcinoma[J].Cancer Cell,2012,21(1):105-120.
[32] LAU L,PORCIUNCULA A,YU A,et al.Uncoupling the senescence-associated secretory phenotype from cell cycle exit via interleukin-1 inactivation unveils its protumorigenic role[J].Mol Cell Biol,2019,39(12):e00586-18.
[33] CORCORAN R B,CONTINO G,DESHPANDE V,et al.STAT3 plays a critical role in KRAS-induced pancreatic tumorigenesis[J].Cancer Res,2011,71(14):5020-5029.
[34] MACE T A,SHAKYA R,PITARRESI J R,et al.IL-6 and PD-L1 antibody blockade combination therapy reduces tumour progression in murine models of pancreatic cancer[J].Gut,2016,67(2):320-322.
[35] LI P,ROZICH N,WANG J,et al.Anti-IL-8 antibody activates myeloid cells and potentiates the anti-tumor activity of anti-PD-1 antibody in the humanized pancreatic cancer murine model[J].Cancer Lett,2022,539:215722.
[36] WU M,HAN J,WU H,et al.Proteasome-dependent senescent tumor cells mediate immunosuppression through CCL20 secretion and M2 polarization in pancreatic ductal adenocarcinoma[J].Front Immunol,2023,14:1216376.
[37] GASEK N S,KUCHEL G A,KIRKLAND J L,et al.Strategies for targeting senescent cells in human disease[J].Nat Aging,2021,1(10):870-879.
[38] BAKER D J,CHILDS B G,DURIK M,et al.Naturally occurring p16(Ink4a)-positive cells shorten healthy lifespan[J].Nature,2016,530(7589):184-189.
[39] GONZÁLEZ-GUALDA E,PÁEZ-RIBES M,LOZANO-TORRES B,et al.Galacto-conjugation of Navitoclax as an efficient strategy to increase senolytic specificity and reduce platelet toxicity[J].Aging Cell,2020,19(4):e13142.
[40] ZHU Y,TCHKONIA T,PIRTSKHALAVA T.The Achilles'heel of senescent cells:from transcriptome to senolytic drugs[J].Aging Cell,2015,14(4):644-658.
[41] FUHRMANN-STROISSNIGG H,LING Y Y,ZHAO J,et al.Identification of HSP90 inhibitors as a novel class of senolytics[J].Nat Commun,2017,8(1):422.

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