CLC number:
On-line Access: 2021-10-12
Received: 2020-12-09
Revision Accepted: 2021-03-11
Crosschecked: 0000-00-00
Cited: 0
Clicked: 3757
Citations: Bibtex RefMan EndNote GB/T7714
Xing DU, Jingjing XIAO, Xufeng FU, Bo XU, Hang HAN, Yin WANG, Xiuying PEI. A proteomic analysis of Bcl-2 regulation of cell cycle arrest: insight into the mechanisms[J]. Journal of Zhejiang University Science B,in press.Frontiers of Information Technology & Electronic Engineering,in press.https://doi.org/10.1631/jzus.B2000802 @article{title="A proteomic analysis of Bcl-2 regulation of cell cycle arrest: insight into the mechanisms", %0 Journal Article TY - JOUR
Bcl-2调控细胞周期阻滞的蛋白质组学分析及其机制研究创新点:基于Bcl-2通过ATP和ROS调控细胞周期的前期发现,本研究首次利用蛋白组学方法系统研究了Bcl-2调控细胞周期的潜在机制。 方法:联合利用蛋白质印迹(western blotting)和蛋白质组学方法研究血清饥饿同步化处理的Bcl-2过表达和对照组细胞株,并结合蛋白组学中差异蛋白的基因本体(Gene Ontology,GO)和Kyoto Encyclopedia of Genes and Genomes(KEGG)分析,进一步明确Bcl-2调控细胞周期的潜在机制。 结论:蛋白组学结果显示,在1.5倍差异下共有169个蛋白发生了上调,120个蛋白发生了下调。通过GO和KEGG分析,这些差异蛋白富集到多个通路,主要集中在呼吸链和核糖体相关信号通路。这些结果表明Bcl-2可能在翻译水平影响核糖体和氧化磷酸化进而调控细胞周期。本研究为进一步靶向Bcl-2调控细胞周期抗癌药物研究了提供重要的理论基础。 关键词组: Darkslateblue:Affiliate; Royal Blue:Author; Turquoise:Article
Reference[1]AdamsCM, Clark-GarveyS, PorcuP, et al., 2019. Targeting the Bcl-2 family in B cell lymphoma. Front Oncol, 8:636. [2]Bonnefoy-BerardN, AouacheriaA, VerscheldeC, et al., 2004. Control of proliferation by Bcl-2 family members. Biochim Biophys Acta-Mol Cell Res, 1644(2-3):159-168. [3]BradyHJ, Gil-GómezG, KirbergJ, et al., 1996. Baxα perturbs T cell development and affects cell cycle entry of T cells. EMBO J, 15(24):6991-7001. [4]ClearyML, SmithSD, SklarJ, 1986. Cloning and structural analysis of cDNAs for bcl-2 and a hybrid bcl-2/immunoglobulin transcript resulting from the t(14;18) translocation. Cell, 47(1):19-28. [5]DelbridgeARD, GrabowS, StrasserA, et al., 2016. Thirty years of BCL-2: translating cell death discoveries into novel cancer therapies. Nat Rev Cancer, 16(2):99-109. [6]del Gaizo MooreV, LetaiA, 2013. BH3 profiling—measuring integrated function of the mitochondrial apoptotic pathway to predict cell fate decisions. Cancer Lett, 332(2):202-205. [7]DuX, FuXF, YaoK, et al., 2017. Bcl-2 delays cell cycle through mitochondrial ATP and ROS. Cell Cycle, 16(7):707-713. [8]FrantziM, LatosinskaA, MischakH, 2019. Proteomics in drug development: the dawn of a New Era? Proteomics Clin Appl, 13(2):e1800087. [9]FuXF, YaoK, DuX, et al., 2016. PGC-1α regulates the cell cycle through ATP and ROS in CH1 cells. J Zhejiang Univ-Sci B (Biomed & Biotechnol), 17(2):136-146. [10]GaoSW, LiuF, 2019. Novel insights into cell cycle regulation of cell fate determination. J Zhejiang Univ-Sci B (Biomed & Biotechnol), 20(6):467-475. [11]GrossA, KatzSG, 2017. Non-apoptotic functions of BCL-2 family proteins. Cell Death Differ, 24(8):1348-1358. [12]HatokJ, RacayP, 2016. Bcl-2 family proteins: master regulators of cell survival. Biomol Concepts, 7(4):259-270. [13]HuSY, ZhuangQQ, QiuY, et al., 2019. Cell models and drug discovery for mitochondrial diseases. J Zhejiang Univ-Sci B (Biomed & Biotechnol), 20(5):449-456. [14]JanumyanYM, SansamCG, ChattopadhyayA, et al., 2003. Bcl-xL/Bcl-2 coordinately regulates apoptosis, cell cycle arrest and cell cycle entry. EMBO J, 22(20):5459-5470. [15]JanumyanYM, CuiQH, YanL, et al., 2008. G0 function of BCL2 and BCL-xL requires BAX, BAK, and p27 phosphorylation by Mirk, revealing a novel role of BAX and BAK in quiescence regulation. J Biol Chem, 283(49):34108-34120. [16]JardimFR, de AlmeidaFJS, LuckachakiMD, et al., 2020. Effects of sulforaphane on brain mitochondria: mechanistic view and future directions. J Zhejiang Univ-Sci B (Biomed & Biotechnol), 21(4):263-279. [17]KaleJ, OsterlundEJ, AndrewsDW, 2018. BCL-2 family proteins: changing partners in the dance towards death. Cell Death Differ, 25(1):65-80. [18]KampenKR, SulimaSO, VerbelenB, et al., 2019. The ribosomal RPL10 R98S mutation drives IRES-dependent BCL-2 translation in T-ALL. Leukemia, 33(2):319-332. [19]KimHJ, MaitiP, BarrientosA, 2017. Mitochondrial ribosomes in cancer. Semin Cancer Biol, 47:67-81. [20]KroemerG, GalluzziL, BrennerC, 2007. Mitochondrial membrane permeabilization in cell death. Physiol Rev, 87(1):99-163. [21]LessardF, Brakier-GingrasL, FerbeyreG, 2019. Ribosomal proteins control tumor suppressor pathways in response to nucleolar stress. Bioessays, 41(3):e1800183. [22]LiFD, WangYC, LiY, et al., 2018. Quantitative analysis of the global proteome in peripheral blood mononuclear cells from patients with new-onset psoriasis. Proteomics, 18(19):e1800003. [23]LinetteGP, LiY, RothK, et al., 1996. Cross talk between cell death and cell cycle progression: BCL-2 regulates NFAT-mediated activation. Proc Natl Acad Sci USA, 93(18):9545-9552. [24]MisraS, SharmaS, AgarwalA, et al., 2010. Cell cycle-dependent regulation of the bi-directional overlapping promoter of human BRCA2/ZAR2 genes in breast cancer cells. Mol Cancer, 9:50. [25]PandeyS, PatilS, BallavN, et al., 2020. Spatial targeting of Bcl-2 on endoplasmic reticulum and mitochondria in cancer cells by lipid nanoparticles. J Mater Chem B, 8(19):4259-4266. [26]PihánP, Carreras-SuredaA, HetzC, 2017. BCL-2 family: integrating stress responses at the ER to control cell demise. Cell Death Differ, 24(9):1478-1487. [27]PopgeorgievN, JabbourL, GilletG, 2018. Subcellular localization and dynamics of the Bcl-2 family of proteins. Front Cell Dev Biol, 6:13. [28]QuinnLM, RichardsonH, 2004. Bcl-2 in cell cycle regulation. Cell Cycle, 3(1):6-8. [29]RobinsonBH, LuoXP, PitkänenS, et al., 1998. Diagnosis of mitochondrial energy metabolism defects in tissue culture. Induction of MnSOD and bcl-2 in mitochondria from patients with complex I (NADH-CoQ reductase) deficiency. Biofactors, 7(3):229-230. [30]SinghR, LetaiA, SarosiekK, 2019. Regulation of apoptosis in health and disease: the balancing act of BCL-2 family proteins. Nat Rev Mol Cell Biol, 20(3):175-193. [31]TaitSWG, GreenDR, 2010. Mitochondria and cell death: outer membrane permeabilization and beyond. Nat Rev Mol Cell Biol, 11(9):621-632. [32]TanakaS, SaitoK, ReedJC, 1993. Structure-function analysis of the Bcl-2 oncoprotein. Addition of a heterologous transmembrane domain to portions of the Bcl-2β protein restores function as a regulator of cell survival. J Biol Chem, 268(15):10920-10926. [33]ThapaM, BommakantiA, ShamsuzzamanM, et al., 2013. Repressed synthesis of ribosomal proteins generates protein-specific cell cycle and morphological phenotypes. Mol Biol Cell, 24(23):3620-3633. [34]TouzeauC, MaciagP, AmiotM, et al., 2018. Targeting Bcl-2 for the treatment of multiple myeloma. Leukemia, 32(9):1899-1907. [35]VairoG, InnesKM, AdamsJM, 1996. Bcl-2 has a cell cycle inhibitory function separable from its enhancement of cell survival. Oncogene, 13(7):1511-1519. [36]VairoG, SoosTJ, UptonTM, et al., 2000. Bcl-2 retards cell cycle entry through p27Kip1, pRB relative p130, and altered E2F regulation. Mol Cell Biol, 20(13):4745-4753. [37]WangCH, WangLK, WuCC, et al., 2019. The ribosomal protein RPLP0 mediates PLAAT4-induced cell cycle arrest and cell apoptosis. Cell Biochem Biophys, 77(3):253-260. [38]WangYQ, LiuYH, WangS, et al., 2020. Hydrogen agronomy: research progress and prospects. J Zhejiang Univ-Sci B (Biomed & Biotechnol), 21(11):841-855. [39]WarrenCFA, Wong-BrownMW, BowdenNA, 2019. BCL-2 family isoforms in apoptosis and cancer. Cell Death Dis, 10(3):177. [40]XieMH, YenY, OwonikokoTK, et al., 2014. Bcl2 induces DNA replication stress by inhibiting ribonucleotide reductase. Cancer Res, 74(1):212-223. [41]XieMH, ParkD, SicaGL, et al., 2020. Bcl2-induced DNA replication stress promotes lung carcinogenesis in response to space radiation. Carcinogenesis, 41(11):1565-1575. [42]XuHD, QinZH, 2019. Beclin 1, Bcl-2 and autophagy. Adv Exp Med Biol, 1206:109-126. [43]ZhouFF, YangY, XingD, 2011. Bcl-2 and Bcl-xL play important roles in the crosstalk between autophagy and apoptosis. FEBS J, 278(3):403-413. Journal of Zhejiang University-SCIENCE, 38 Zheda Road, Hangzhou
310027, China
Tel: +86-571-87952783; E-mail: cjzhang@zju.edu.cn Copyright © 2000 - 2024 Journal of Zhejiang University-SCIENCE |
Open peer comments: Debate/Discuss/Question/Opinion
<1>