NRF2 activation by cysteine as a survival mechanism for triple-negative breast cancer cells.


Journal

Oncogene
ISSN: 1476-5594
Titre abrégé: Oncogene
Pays: England
ID NLM: 8711562

Informations de publication

Date de publication:
10 Apr 2024
Historique:
received: 10 01 2024
accepted: 02 04 2024
revised: 28 03 2024
medline: 11 4 2024
pubmed: 11 4 2024
entrez: 10 4 2024
Statut: aheadofprint

Résumé

Triple-negative breast cancer (TNBC) is a very aggressive and heterogeneous group of tumors. In order to develop effective therapeutic strategies, it is therefore essential to identify the subtype-specific molecular mechanisms underlying disease progression and resistance to chemotherapy. TNBC cells are highly dependent on exogenous cystine, provided by overexpression of the cystine/glutamate antiporter SLC7A11/xCT, to fuel glutathione synthesis and promote an oxidative stress response consistent with their high metabolic demands. Here we show that TNBC cells of the mesenchymal stem-like subtype (MSL) utilize forced cystine uptake to induce activation of the transcription factor NRF2 and promote a glutathione-independent mechanism to defend against oxidative stress. Mechanistically, we demonstrate that NRF2 activation is mediated by direct cysteinylation of the inhibitor KEAP1. Furthermore, we show that cystine-mediated NRF2 activation induces the expression of important genes involved in oxidative stress response, but also in epithelial-to-mesenchymal transition and stem-like phenotype. Remarkably, in survival analysis, four upregulated genes (OSGIN1, RGS17, SRXN1, AKR1B10) are negative prognostic markers for TNBC. Finally, expression of exogenous OSGIN1, similarly to expression of exogenous NRF2, can prevent cystine depletion-dependent death of MSL TNBC cells. The results suggest that the cystine/NRF2/OSGIN1 axis is a potential target for effective treatment of MSL TNBCs.

Identifiants

pubmed: 38600165
doi: 10.1038/s41388-024-03025-0
pii: 10.1038/s41388-024-03025-0
doi:

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Informations de copyright

© 2024. The Author(s).

Références

Ahmad A. Breast cancer statistics: recent trends. Adv Exp Med Biol. 2019;1152:1–7.
pubmed: 31456176 doi: 10.1007/978-3-030-20301-6_1
Foulkes WD, Smith IE, Reis-Filho JS. Triple-negative breast cancer. N Engl J Med. 2010;363:1938–48.
pubmed: 21067385 doi: 10.1056/NEJMra1001389
Marra A, Trapani D, Viale G, Criscitiello C, Curigliano G. Practical classification of triple-negative breast cancer: intratumoral heterogeneity, mechanisms of drug resistance, and novel therapies. NPJ Breast Cancer. 2020;6:54–2.
pubmed: 33088912 pmcid: 7568552 doi: 10.1038/s41523-020-00197-2
Lehmann BD, Bauer JA, Chen X, Sanders ME, Chakravarthy AB, Shyr Y, et al. Identification of human triple-negative breast cancer subtypes and preclinical models for selection of targeted therapies. J Clin Investig. 2011;121:2750–67.
pubmed: 21633166 pmcid: 3127435 doi: 10.1172/JCI45014
Herschkowitz JI, Simin K, Weigman VJ, Mikaelian I, Usary J, Hu Z, et al. Identification of conserved gene expression features between murine mammary carcinoma models and human breast tumors. Genome Biol. 2007;8:R76–r76.
pubmed: 17493263 pmcid: 1929138 doi: 10.1186/gb-2007-8-5-r76
Prat A, Parker JS, Karginova O, Fan C, Livasy C, Herschkowitz JI, et al. Phenotypic and molecular characterization of the claudin-low intrinsic subtype of breast cancer. Breast Cancer Res. 2010;12:R68.
pubmed: 20813035 pmcid: 3096954 doi: 10.1186/bcr2635
Wahdan-Alaswad R, Harrell JC, Fan Z, Edgerton SM, Liu B, Thor AD. Metformin attenuates transforming growth factor beta (TGF-beta) mediated oncogenesis in mesenchymal stem-like/claudin-low triple negative breast cancer. Cell Cycle. 2016;15:1046–59.
pubmed: 26919310 pmcid: 4889288 doi: 10.1080/15384101.2016.1152432
Le Du F, Eckhardt BL, Lim B, Litton JK, Moulder S, Meric-Bernstam F, et al. Is the future of personalized therapy in triple-negative breast cancer based on molecular subtype? Oncotarget. 2015;6:12890–908.
pubmed: 25973541 pmcid: 4536987 doi: 10.18632/oncotarget.3849
Panieri E, Santoro MM. ROS homeostasis and metabolism: a dangerous liason in cancer cells. Cell Death Dis. 2016;7:e2253.
pubmed: 27277675 pmcid: 5143371 doi: 10.1038/cddis.2016.105
McMahon M, Itoh K, Yamamoto M, Hayes JD. Keap1-dependent proteasomal degradation of transcription factor Nrf2 contributes to the negative regulation of antioxidant response element-driven gene expression. J Biol Chem. 2003;278:21592–21600.
pubmed: 12682069 doi: 10.1074/jbc.M300931200
Yamamoto M, Kensler TW, Motohashi H. The KEAP1-NRF2 system: a thiol-based sensor-effector apparatus for maintaining redox homeostasis. Physiol Rev. 2018;98:1169–203.
pubmed: 29717933 pmcid: 9762786 doi: 10.1152/physrev.00023.2017
Almeida M, Soares M, Ramalhinho AC, Moutinho JF, Breitenfeld L, Pereira L. The prognostic value of NRF2 in breast cancer patients: a systematic review with meta-analysis. Breast Cancer Res Treat. 2020;179:523–32.
pubmed: 31745730 doi: 10.1007/s10549-019-05494-4
De Blasio A, Di Fiore R, Pratelli G, Drago-Ferrante R, Saliba C, Baldacchino S, et al. A loop involving NRF2, miR-29b-1-5p and AKT, regulates cell fate of MDA-MB-231 triple-negative breast cancer cells. J Cell Physiol. 2020;235:629–37.
pubmed: 31313842 doi: 10.1002/jcp.29062
Qin S, He X, Lin H, Schulte BA, Zhao M, Tew KD, et al. Nrf2 inhibition sensitizes breast cancer stem cells to ionizing radiation via suppressing DNA repair. Free Radic Biol Med. 2021;169:238–47.
pubmed: 33892113 pmcid: 8138866 doi: 10.1016/j.freeradbiomed.2021.04.006
Lee YS, Kang J, Jung ES, Lee A. High expression of NRF2 and low expression of KEAP1 predict worse survival in patients with operable triple-negative breast cancer. J Breast Cancer. 2023;26:461–78.
pubmed: 37926068 pmcid: 10625868 doi: 10.4048/jbc.2023.26.e42
Harris IS, Treloar AE, Inoue S, Sasaki M, Gorrini C, Lee KC, et al. Glutathione and thioredoxin antioxidant pathways synergize to drive cancer initiation and progression. Cancer Cell. 2015;27:211–22.
pubmed: 25620030 doi: 10.1016/j.ccell.2014.11.019
Zou M, Hu X, Xu B, Tong T, Jing Y, Xi L, et al. Glutathione S-transferase isozyme alpha 1 is predominantly involved in the cisplatin resistance of common types of solid cancer. Oncol Rep. 2019;41:989–98.
pubmed: 30431119
Niu B, Liao K, Zhou Y, Wen T, Quan G, Pan X, et al. Application of glutathione depletion in cancer therapy: Enhanced ROS-based therapy, ferroptosis, and chemotherapy. Biomaterials. 2021;277:121110.
pubmed: 34482088 doi: 10.1016/j.biomaterials.2021.121110
Mandal PK, Seiler A, Perisic T, Kolle P, Banjac Canak A, Forster H, et al. System x(c)- and thioredoxin reductase 1 cooperatively rescue glutathione deficiency. J Biol Chem. 2010;285:22244–53.
pubmed: 20463017 pmcid: 2903358 doi: 10.1074/jbc.M110.121327
Timmerman LA, Holton T, Yuneva M, Louie RJ, Padro M, Daemen A, et al. Glutamine sensitivity analysis identifies the xCT antiporter as a common triple-negative breast tumor therapeutic target. Cancer Cell. 2013;24:450–65.
pubmed: 24094812 pmcid: 3931310 doi: 10.1016/j.ccr.2013.08.020
Dai X, Cheng H, Bai Z, Li J. Breast cancer cell line classification and its relevance with breast tumor subtyping. J Cancer. 2017;8:3131–41.
pubmed: 29158785 pmcid: 5665029 doi: 10.7150/jca.18457
Jaramillo MC, Zhang DD. The emerging role of the Nrf2-Keap1 signaling pathway in cancer. Genes Dev. 2013;27:2179–91.
pubmed: 24142871 pmcid: 3814639 doi: 10.1101/gad.225680.113
Dixon SJ, Lemberg KM, Lamprecht MR, Skouta R, Zaitsev EM, Gleason CE, et al. Ferroptosis: an iron-dependent form of nonapoptotic cell death. Cell. 2012;149:1060–72.
pubmed: 22632970 pmcid: 3367386 doi: 10.1016/j.cell.2012.03.042
Tosi GM, Giustarini D, Franci L, Minetti A, Imperatore F, Caldi E, et al. Superior properties of N-acetylcysteine ethyl ester over N-acetyl cysteine to prevent retinal pigment epithelial cells oxidative damage. Int J Mol Sci. 2021;22:600. https://doi.org/10.3390/ijms22020600 .
doi: 10.3390/ijms22020600 pubmed: 33435325 pmcid: 7827200
Suzuki T, Muramatsu A, Saito R, Iso T, Shibata T, Kuwata K, et al. Molecular mechanism of cellular oxidative stress sensing by Keap1. Cell Rep. 2019;28:746–758.e4.
pubmed: 31315052 doi: 10.1016/j.celrep.2019.06.047
Xie L, Gu Y, Wen M, Zhao S, Wang W, Ma Y, et al. Hydrogen sulfide induces keap1 S-sulfhydration and suppresses diabetes-accelerated atherosclerosis via Nrf2 activation. Diabetes. 2016;65:3171–84.
pubmed: 27335232 pmcid: 8928786 doi: 10.2337/db16-0020
Gyorffy B. Survival analysis across the entire transcriptome identifies biomarkers with the highest prognostic power in breast cancer. Comput Struct Biotechnol J. 2021;19:4101–9.
pubmed: 34527184 pmcid: 8339292 doi: 10.1016/j.csbj.2021.07.014
Curtis C, Shah SP, Chin S, Turashvili G, Rueda OM, Dunning MJ, et al. The genomic and transcriptomic architecture of 2,000 breast tumours reveals novel subgroups. Nature. 2012;486:346–52.
pubmed: 22522925 pmcid: 3440846 doi: 10.1038/nature10983
Beatty A, Fink LS, Singh T, Strigun A, Peter E, Ferrer CM, et al. Metabolite profiling reveals the glutathione biosynthetic pathway as a therapeutic target in triple-negative breast cancer. Mol Cancer Ther. 2018;17:264–75.
pubmed: 29021292 doi: 10.1158/1535-7163.MCT-17-0407
Chen L, Liu C, Zhu S, Ge J, Chen Y, Ma D, et al. Multiomics of HER2-low triple-negative breast cancer identifies a receptor tyrosine kinase-relevant subgroup with therapeutic prospects. JCI Insight. 2023;8:e172366. https://doi.org/10.1172/jci.insight.172366 .
doi: 10.1172/jci.insight.172366 pubmed: 37991016 pmcid: 10721318
Suzuki T, Takahashi J, Yamamoto M. Molecular basis of the KEAP1-NRF2 signaling pathway. Mol Cells. 2023;46:133–41.
pubmed: 36994473 pmcid: 10070164 doi: 10.14348/molcells.2023.0028
Wei W, Li Y, Wang C, Gao S, Zhao Y, Yang Z, et al. Diterpenoid Vinigrol specifically activates ATF4/DDIT3-mediated PERK arm of unfolded protein response to drive non-apoptotic death of breast cancer cells. Pharm Res. 2022;182:106285.
doi: 10.1016/j.phrs.2022.106285
Lee K, Hong H, Lim J, Ko K, Lee M, Chi S. XAF1 drives apoptotic switch of endoplasmic reticulum stress response through destabilization of GRP78 and CHIP. Cell Death Dis. 2022;13:655–0.
pubmed: 35902580 pmcid: 9334361 doi: 10.1038/s41419-022-05112-0
Keil E, Hocker R, Schuster M, Essmann F, Ueffing N, Hoffman B, et al. Phosphorylation of Atg5 by the Gadd45beta-MEKK4-p38 pathway inhibits autophagy. Cell Death Differ. 2013;20:321–32.
pubmed: 23059785 doi: 10.1038/cdd.2012.129
Fan T, Wang X, Zhang S, Deng P, Jiang Y, Liang Y, et al. NUPR1 promotes the proliferation and metastasis of oral squamous cell carcinoma cells by activating TFE3-dependent autophagy. Signal Transduct Target Ther. 2022;7:130.
pubmed: 35462576 pmcid: 9035452 doi: 10.1038/s41392-022-00939-7
Yuxiong W, Faping L, Bin L, Yanghe Z, Yao L, Yunkuo L, et al. Regulatory mechanisms of the cAMP-responsive element binding protein 3 (CREB3) family in cancers. Biomed Pharmacother. 2023;166:115335.
pubmed: 37595431 doi: 10.1016/j.biopha.2023.115335
Zhou J, Liu H, Zhang T, Wang Z, Zhang J, Lu Y, et al. MORN4 protects cardiomyocytes against ischemic injury via MFN2-mediated mitochondrial dynamics and mitophagy. Free Radic Biol Med. 2023;196:156–70.
pubmed: 36682578 doi: 10.1016/j.freeradbiomed.2023.01.016
Scarpulla RC. Transcriptional paradigms in mammalian mitochondrial biogenesis and function. Physiol Rev. 2008;88:611–38.
pubmed: 18391175 doi: 10.1152/physrev.00025.2007
Dinkova-Kostova AT, Abramov AY. The emerging role of Nrf2 in mitochondrial function. Free Radic Biol Med. 2015;88:179–88.
pubmed: 25975984 pmcid: 4726722 doi: 10.1016/j.freeradbiomed.2015.04.036
Cullinan SB, Diehl JA. Coordination of ER and oxidative stress signaling: the PERK/Nrf2 signaling pathway. Int J Biochem Cell Biol. 2006;38:317–32.
pubmed: 16290097 doi: 10.1016/j.biocel.2005.09.018
Li R, Chen W, Yanes R, Lee S, Berliner JA. OKL38 is an oxidative stress response gene stimulated by oxidized phospholipids. J Lipid Res. 2007;48:709–15.
pubmed: 17192422 doi: 10.1194/jlr.M600501-JLR200
Erickson AM, Nevarea Z, Gipp JJ, Mulcahy RT. Identification of a variant antioxidant response element in the promoter of the human glutamate-cysteine ligase modifier subunit gene. Revision of the ARE consensus sequence. J Biol Chem. 2002;277:30730–7.
pubmed: 12070177 doi: 10.1074/jbc.M205225200
Sakurai A, Nishimoto M, Himeno S, Imura N, Tsujimoto M, Kunimoto M, et al. Transcriptional regulation of thioredoxin reductase 1 expression by cadmium in vascular endothelial cells: role of NF-E2-related factor-2. J Cell Physiol. 2005;203:529–37.
pubmed: 15521073 doi: 10.1002/jcp.20246
Soriano FX, Baxter P, Murray LM, Sporn MB, Gillingwater TH, Hardingham GE. Transcriptional regulation of the AP-1 and Nrf2 target gene sulfiredoxin. Mol Cells. 2009;27:279–82.
pubmed: 19326073 doi: 10.1007/s10059-009-0050-y
Nishinaka T, Miura T, Okumura M, Nakao F, Nakamura H, Terada T. Regulation of aldo-keto reductase AKR1B10 gene expression: involvement of transcription factor Nrf2. Chem Biol Interact. 2011;191:185–91.
pubmed: 21277289 doi: 10.1016/j.cbi.2011.01.026
Park H, Azzara D, Cohen ED, Boomhower SR, Diwadkar AR, Himes BE, et al. Identification of novel NRF2-dependent genes as regulators of lead and arsenic toxicity in neural progenitor cells. J Hazard Mater. 2024;463:132906.
pubmed: 37939567 doi: 10.1016/j.jhazmat.2023.132906
Hayes JD, Dinkova-Kostova AT, Tew KD. Oxidative stress in cancer. Cancer Cell. 2020;38:167–97.
pubmed: 32649885 pmcid: 7439808 doi: 10.1016/j.ccell.2020.06.001
Huang C, Cao Z, Ma J, Shen Y, Bu Y, Khoshaba R, et al. AKR1B10 activates diacylglycerol (DAG) second messenger in breast cancer cells. Mol Carcinog. 2018;57:1300–10.
pubmed: 29846015 pmcid: 6800193 doi: 10.1002/mc.22844
Huang C, Verhulst S, Shen Y, Bu Y, Cao Y, He Y, et al. AKR1B10 promotes breast cancer metastasis through integrin alpha5/delta-catenin mediated FAK/Src/Rac1 signaling pathway. Oncotarget. 2016;7:43779–91.
pubmed: 27248472 pmcid: 5190059 doi: 10.18632/oncotarget.9672
Li Y, Li L, Lin J, Hu X, Li B, Xue A, et al. Deregulation of RGS17 expression promotes breast cancer progression. J Cancer. 2015;6:767–75.
pubmed: 26185539 pmcid: 4504113 doi: 10.7150/jca.11833
Samanta S, Sun H, Goel HL, Pursell B, Chang C, Khan A, et al. IMP3 promotes stem-like properties in triple-negative breast cancer by regulating SLUG. Oncogene. 2016;35:1111–21.
pubmed: 25982283 doi: 10.1038/onc.2015.164
Jiang T, He X, Zhao Z, Zhang X, Wang T, Jia L. RNA m6A reader IGF2BP3 promotes metastasis of triple-negative breast cancer via SLIT2 repression. FASEB J. 2022;36:e22618.
pubmed: 36250924 doi: 10.1096/fj.202200751RR
Su P, Hu J, Zhang H, Li W, Jia M, Zhang X, et al. IMP3 expression is associated with epithelial-mesenchymal transition in breast cancer. Int J Clin Exp Pathol. 2014;7:3008–17.
pubmed: 25031719 pmcid: 4097240
Zhang X, Shi L, Sun H, Wang Z, Xu F, Wei J, et al. IGF2BP3 mediates the mRNA degradation of NF1 to promote triple-negative breast cancer progression via an m6A-dependent manner. Clin Transl Med. 2023;13:e1427.
pubmed: 37743642 pmcid: 10518495 doi: 10.1002/ctm2.1427
Wong RC, Pollan S, Fong H, Ibrahim A, Smith EL, Ho M, et al. A novel role for an RNA polymerase III subunit POLR3G in regulating pluripotency in human embryonic stem cells. Stem Cells. 2011;29:1517–27.
pubmed: 21898682 doi: 10.1002/stem.714
Lautre W, Richard E, Feugeas J, Dumay-Odelot H, Teichmann M. The POLR3G subunit of human RNA polymerase III regulates tumorigenesis and metastasis in triple-negative breast cancer. Cancers. 2022;14:5732. https://doi.org/10.3390/cancers14235732 .
doi: 10.3390/cancers14235732 pubmed: 36497214 pmcid: 9735567
Hallis SP, Kim JM, Kwak M. Emerging role of NRF2 signaling in cancer stem cell phenotype. Mol Cells. 2023;46:153–64.
pubmed: 36994474 pmcid: 10070166 doi: 10.14348/molcells.2023.2196
Tsai C, Shen Y, Chen H, Liu K, Chang J, Chen P, et al. Docosahexaenoic acid increases the expression of oxidative stress-induced growth inhibitor 1 through the PI3K/Akt/Nrf2 signaling pathway in breast cancer cells. Food Chem Toxicol. 2017;108:276–88.
pubmed: 28807874 doi: 10.1016/j.fct.2017.08.010
Huynh H, Ng CY, Ong CK, Lim KB, Chan TW. Cloning and characterization of a novel pregnancy-induced growth inhibitor in mammary gland. Endocrinology. 2001;142:3607–15.
pubmed: 11459809 doi: 10.1210/endo.142.8.8297
Wang G, Zhou H, Strulovici-Barel Y, Al-Hijji M, Ou X, Salit J, et al. Role of OSGIN1 in mediating smoking-induced autophagy in the human airway epithelium. Autophagy. 2017;13:1205–20.
pubmed: 28548877 pmcid: 5529077 doi: 10.1080/15548627.2017.1301327
Brennan MS, Matos MF, Richter KE, Li B, Scannevin RH. The NRF2 transcriptional target, OSGIN1, contributes to monomethyl fumarate-mediated cytoprotection in human astrocytes. Sci Rep. 2017;7:42054.
pubmed: 28181536 pmcid: 5299414 doi: 10.1038/srep42054
Giustarini D, Galvagni F, Dalle Donne I, Milzani A, Severi FM, Santucci A, et al. N-acetylcysteine ethyl ester as GSH enhancer in human primary endothelial cells: A comparative study with other drugs. Free Radic Biol Med. 2018;126:202–9.
pubmed: 30114478 doi: 10.1016/j.freeradbiomed.2018.08.013
Chen X, Li J, Gray WH, Lehmann BD, Bauer JA, Shyr Y, et al. TNBCtype: A Subtyping Tool for Triple-Negative Breast Cancer. Cancer Inf. 2012;11:147–56.
Anselmi F, Orlandini M, Rocchigiani M, De Clemente C, Salameh A, Lentucci C, et al. c-ABL modulates MAP kinases activation downstream of VEGFR-2 signaling by direct phosphorylation of the adaptor proteins GRB2 and NCK1. Angiogenesis. 2012;15:187–97.
pubmed: 22327338 doi: 10.1007/s10456-012-9252-6
Elia I, Realini G, Di Mauro V, Borghi S, Bottoni L, Tornambe S, et al. SNAI1 is upregulated during muscle regeneration and represses FGF21 and ATF3 expression by directly binding their promoters. FASEB J. 2022;36:e22401.
pubmed: 35726676 doi: 10.1096/fj.202200215R

Auteurs

Laura Bottoni (L)

Department of Biotechnology, Chemistry and Pharmacy, University of Siena, 53100, Siena, Italy.

Alberto Minetti (A)

Department of Biotechnology, Chemistry and Pharmacy, University of Siena, 53100, Siena, Italy.
Leibniz Institute on Aging - Fritz Lipmann Institute (FLI), Jena, Germany.

Giulia Realini (G)

Department of Biotechnology, Chemistry and Pharmacy, University of Siena, 53100, Siena, Italy.

Elena Pio (E)

Department of Biotechnology, Chemistry and Pharmacy, University of Siena, 53100, Siena, Italy.

Daniela Giustarini (D)

Department of Biotechnology, Chemistry and Pharmacy, University of Siena, 53100, Siena, Italy.
Center for Colloid and Surface Science (CSGI), University of Florence, Sesto Fiorentino, 50019, Florence, Italy.

Ranieri Rossi (R)

Department of Biotechnology, Chemistry and Pharmacy, University of Siena, 53100, Siena, Italy.
Center for Colloid and Surface Science (CSGI), University of Florence, Sesto Fiorentino, 50019, Florence, Italy.

Chiara Rocchio (C)

Department of Biotechnology, Chemistry and Pharmacy, University of Siena, 53100, Siena, Italy.

Lorenzo Franci (L)

Istituto di Fisiologia Clinica (IFC), Consiglio Nazionale delle Ricerche (CNR) and Core Research Laboratory, Istituto per lo Studio, la Prevenzione e la Rete Oncologica (ISPRO), 53100, Siena, Italy.

Laura Salvini (L)

Toscana Life Sciences Foundation, Siena, Italy.

Orazio Catona (O)

Institute of Informatics and Telematics (IIT), CNR, Pisa, Italy.

Romina D'Aurizio (R)

Institute of Informatics and Telematics (IIT), CNR, Pisa, Italy.

Mahdi Rasa (M)

Leibniz Institute on Aging - Fritz Lipmann Institute (FLI), Jena, Germany.
Institute of Immunology, University Medical Center Schleswig-Holstein, Kiel, Germany.

Emanuele Giurisato (E)

Department of Biotechnology, Chemistry and Pharmacy, University of Siena, 53100, Siena, Italy.

Francesco Neri (F)

Leibniz Institute on Aging - Fritz Lipmann Institute (FLI), Jena, Germany.
Department of Life Sciences and Systems Biology, University of Torino, Torino, Italy.
Molecular Biotechnology Center, University of Turin, Torino, Italy.

Maurizio Orlandini (M)

Department of Biotechnology, Chemistry and Pharmacy, University of Siena, 53100, Siena, Italy.

Mario Chiariello (M)

Istituto di Fisiologia Clinica (IFC), Consiglio Nazionale delle Ricerche (CNR) and Core Research Laboratory, Istituto per lo Studio, la Prevenzione e la Rete Oncologica (ISPRO), 53100, Siena, Italy.

Federico Galvagni (F)

Department of Biotechnology, Chemistry and Pharmacy, University of Siena, 53100, Siena, Italy. federico.galvagni@unisi.it.

Classifications MeSH