Skip to main content

Thank you for visiting nature.com. You are using a browser version with limited support for CSS. To obtain the best experience, we recommend you use a more up to date browser (or turn off compatibility mode in Internet Explorer). In the meantime, to ensure continued support, we are displaying the site without styles and JavaScript.

  • Article
  • Published:

High expression of PPP1CC promotes NHEJ-mediated DNA repair leading to radioresistance and poor prognosis in nasopharyngeal carcinoma

Cell Death & Differentiation (2024)Cite this article

Subjects

Abstract

Protein phosphatase 1 catalytic subunit gamma (PPP1CC) promotes DNA repair and tumor development and progression, however, its underlying mechanisms remain unclear. This study investigated the molecular mechanism of PPP1CC’s involvement in DNA repair and the potential clinical implications. High expression of PPP1CC was significantly correlated with radioresistance and poor prognosis in human nasopharyngeal carcinoma (NPC) patients. The mechanistic study revealed that PPP1CC bound to Ku70/Ku80 heterodimers and activated DNA-PKcs by promoting DNA-PK holoenzyme formation, which enhanced nonhomologous end junction (NHEJ) -mediated DNA repair and led to radioresistance. Importantly, BRCA1-BRCA2-containing complex subunit 3 (BRCC3) interacted with PPP1CC to enhance its stability by removing the K48-linked polyubiquitin chain at Lys234 to prevent PPP1CC degradation. Therefore, BRCC3 helped the overexpressed PPP1CC to maintain its high protein level, thereby sustaining the elevation of DNA repair capacity and radioresistance. Our study identified the molecular mechanism by which PPP1CC promotes NHEJ-mediated DNA repair and radioresistance, suggesting that the BRCC3-PPP1CC-Ku70 axis is a potential therapeutic target to improve the efficacy of radiotherapy.

This is a preview of subscription content, access via your institution

Access options

Buy this article

  • Purchase on Springer Link
  • Instant access to full article PDF
Buy now

Prices may be subject to local taxes which are calculated during checkout

Fig. 1: High PPP1CC expression is correlated with poor prognosis and tumor recurrence.
Fig. 2: PPP1CC enhances radioresistance by promoting nonhomologous end joining (NHEJ)-mediated double-strand break (DSB) repair.
Fig. 3: PPP1CC protein expression is stabilized by BRCC3-mediated deubiquitination.
Fig. 4: PPP1CC recruits Ku70 and enhances DNA-PKcs phosphorylation by promoting DNA-PK holoenzyme formation.
Fig. 5: PPP1CC overexpression reverses the radiosensitization of BRCC3 knockdown in vitro and in vivo.
Fig. 6: PPP1CC overexpression reverses the radiosensitizing effect of knockdown BRCC3 by enhancing NHEJ-mediated DNA repair.
Fig. 7: High expression of the BRCC3-PPP1CC-Ku70 pathway protein is linked to locoregional recurrence of NPC.
Fig. 8: Proposed working model of PPP1CC.

Similar content being viewed by others

Data availability

The data used in this study for protein expression are available in the Clinical Proteome Tumor Analysis Consortium (CPTAC; https://hupo.org/Clinical-Proteome-Tumor-Analysis-Consortium-(CPTAC)). The microarray data used in this study are available in the Gene Expression Omnibus (GEO; http://www.ncbi.nlm.nih.gov/geo/) under accession codes GSE12452 and GSE61218. The data used in this study for gene expression profiling interactive analysis (GEPIA; http://gepia.cancer-pku.cn/index.html) are available in The Cancer Genome Atlas (TCGA; https://tcga-data.nci.nih.gov/). The datasets supporting the conclusions of this article are included within the article and its supplementary information files. All original western blots are provided as supplementary material. Data that support the findings of this study are available from the corresponding author upon reasonable request.

References

  1. Kockler ZW, Osia B, Lee R, Musmaker K, Malkova A. Repair of DNA breaks by break-induced replication. Annu Rev Biochem. 2021;90:165–91.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  2. Groelly FJ, Fawkes M, Dagg RA, Blackford AN, Tarsounas M. Targeting DNA damage response pathways in cancer. Nat Rev Cancer. 2023;23:78–94.

    Article  CAS  PubMed  Google Scholar 

  3. Awwad SW, Serrano-Benitez A, Thomas JC, Gupta V, Jackson SP. Revolutionizing DNA repair research and cancer therapy with CRISPR-Cas screens. Nat Rev Mol Cell Biol. 2023;24:477–94.

    Article  CAS  PubMed  Google Scholar 

  4. Pilie PG, Tang C, Mills GB, Yap TA. State-of-the-art strategies for targeting the DNA damage response in cancer. Nat Rev Clin Oncol. 2019;16:81–104.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  5. Xu Y, et al. The Largest Chinese Cohort Study indicates homologous recombination pathway gene mutations as another major genetic risk factor for colorectal cancer with heterogeneous clinical phenotypes. Research. 2023;6:0249.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  6. Murmann-Konda T, Soni A, Stuschke M, Iliakis G. Analysis of chromatid-break-repair detects a homologous recombination to non-homologous end-joining switch with increasing load of DNA double-strand breaks. Mutat Res Gen Toxicol Environ Mutagen. 2021;867:503372.

    Article  CAS  Google Scholar 

  7. Frank KM, et al. Late embryonic lethality and impaired V(D)J recombination in mice lacking DNA ligase IV. Nature. 1998;396:173–7.

    Article  CAS  PubMed  Google Scholar 

  8. Gao Y, et al. A critical role for DNA end-joining proteins in both lymphogenesis and neurogenesis. Cell. 1998;95:891–902.

    Article  CAS  PubMed  Google Scholar 

  9. Woodbine L, Gennery AR, Jeggo PA. Reprint of “The clinical impact of deficiency in DNA non-homologous end-joining. DNA Repair. 2014;17:9–20.

    Article  CAS  PubMed  Google Scholar 

  10. Stephens PJ, et al. Massive genomic rearrangement acquired in a single catastrophic event during cancer development. Cell. 2011;144:27–40.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  11. Ghezraoui H, et al. Chromosomal translocations in human cells are generated by canonical nonhomologous end-joining. Mol Cell. 2014;55:829–42.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  12. Peycheva M, et al. DNA replication timing directly regulates the frequency of oncogenic chromosomal translocations. Science. 2022;377:1277.

    Article  Google Scholar 

  13. Sishc BJ, Davis AJ. The role of the core non-homologous end joining factors in carcinogenesis and cancer. Cancers. 2017;9:1–30.

  14. Stavridi AK, Appleby R, Liang SK, Blundell TL, Chaplin AK. Druggable binding sites in the multicomponent assemblies that characterise DNA double-strand-break repair through non-homologous end joining. Essays Biochem. 2020;64:791–806.

    Article  CAS  Google Scholar 

  15. Chen YK, et al. LRRC31 inhibits DNA repair and sensitizes breast cancer brain metastasis to radiation therapy. Nature Cell Biology. 2020;22:1276.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  16. Chen Y, et al. USP44 regulates irradiation-induced DNA double-strand break repair and suppresses tumorigenesis in nasopharyngeal carcinoma. Nature Communications. 2022;13:501.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  17. Liao JB, et al. Methyltransferase 1 is required for nonhomologous end-joining repair and renders hepatocellular carcinoma resistant to radiotherapy. Hepatology. 2023;77:1896–1910.

  18. Wang XC, et al. Genome-wide RNAi screening identifies RFC4 as a factor that mediates radioresistance in colorectal cancer by facilitating nonhomologous end joining repair. Clin Cancer Res. 2019;25:4567–79.

    Article  CAS  PubMed  Google Scholar 

  19. Zhou W, et al. GTP signaling links metabolism, DNA repair, and responses to genotoxic stress. bioRxiv. 2024;14:158–76.

  20. Réthi-Nagy Z, Abrahám E, Sinka R, Juhász S, Lipinszki Z. Protein phosphatase 4 is required for centrobin function in DNA damage repair. Cells-Basel. 2023;12:2219.

    Article  Google Scholar 

  21. Lee DH, et al. A PP4 phosphatase complex dephosphorylates RPA2 to facilitate DNA repair via homologous recombination. Nat Struct Mol Biol. 2010;17:365–U138.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  22. Ambjorn SM, et al. A complex of BRCA2 and PP2A-B56 is required for DNA repair by homologous recombination. Nat Commun. 2021;12:5748.

    Article  PubMed  PubMed Central  Google Scholar 

  23. Xie WJ, et al. Comprehensive analysis of PPPCs family reveals the clinical significance of PPP1CA and PPP4C in breast cancer. Bioengineered. 2022;13:190–205.

    Article  CAS  PubMed  Google Scholar 

  24. Liu JP, et al. Protein phosphatase PP4 is involved in NHEJ-mediated repair of DNA double-strand breaks. Cell Cycle. 2012;11:2643–9.

    Article  CAS  PubMed  Google Scholar 

  25. Douglas P, et al. Protein phosphatase 6 interacts with the DNA-dependent protein kinase catalytic subunit and dephosphorylates gamma-H2AX. Mol Cell Biol. 2010;30:1368–81.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  26. Yu YM, Pace SM, Allen SR, Deng CX, Hsu LC. A PP1-binding motif present in BRCA1 plays a role in its DNA repair function. Int J Biol Sci. 2008;4:352–61.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  27. Hsu LC. Identification and functional characterization of a PP1-binding site in BRCA1. Biochem Biophys Res Commun. 2007;360:507–12.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  28. Liu Y, Virshup DM, White RL, Hsu LC. Regulation of BRCA1 phosphorylation by interaction with protein phosphatase 1α. Cancer Res. 2002;62:6357–61.

    CAS  PubMed  Google Scholar 

  29. Scully R, et al. Association of BRCA1 with Rad51 in mitotic and meiotic cells. Cell. 1997;88:265–75.

    Article  CAS  PubMed  Google Scholar 

  30. Scully R, et al. Dynamic changes of BRCA1 subnuclear location and phosphorylation state are initiated by DNA damage. Cell. 1997;90:425–435.

    Article  CAS  PubMed  Google Scholar 

  31. Zhong Q, et al. Association of BRCA1 with the hRad50-hMre11-p95 complex and the DNA damage response. Science. 1999;285:747–50.

    Article  CAS  PubMed  Google Scholar 

  32. Deng CX, Wang RH. Roles of BRCA1 in DNA damage repair: a link between development and cancer. Hum Mol Genet. 2003;12:R113–23.

    Article  CAS  PubMed  Google Scholar 

  33. Hartman AR, Ford JM. BRCA1 induces DNA damage recognition factors and enhances nucleotide excision repair. Nat Genet. 2002;32:180–4.

    Article  CAS  PubMed  Google Scholar 

  34. Zhu SL, Fisher LA, Bessho T, Peng AM. Protein phosphatase 1 and phosphatase 1 nuclear targeting subunit-dependent regulation of DNA-dependent protein kinase and non-homologous end joining. Nucleic Acids Res. 2017;45:10583–94.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  35. Tu ZW, et al. BRCC3 acts as a prognostic marker in nasopharyngeal carcinoma patients treated with radiotherapy and mediates radiation resistance in vitro. Radiat Oncol. 2015;10:123.

    Article  PubMed  PubMed Central  Google Scholar 

  36. Lee AWM, Ma BBY, Ng WT, Chan ATC. Management of nasopharyngeal carcinoma: current practice and future perspective. J Clin Oncol. 2015;33:3356.

    Article  PubMed  Google Scholar 

  37. Wong KCW, et al. Nasopharyngeal carcinoma: an evolving paradigm. Nat Rev Clin Oncol. 2021;18:679–95.

    Article  CAS  PubMed  Google Scholar 

  38. Qiao H, et al. Association of intratumoral microbiota with prognosis in patients with nasopharyngeal carcinoma from 2 hospitals in China. JAMA Oncol. 2022;8:1301–9.

    Article  PubMed  PubMed Central  Google Scholar 

  39. Zhang PP, et al. Protein C receptor maintains cancer stem cell properties via activating lipid synthesis in nasopharyngeal carcinoma. Signal Transduct Targeted Ther. 2022;7:46.

    Article  CAS  Google Scholar 

  40. Li JY, et al. TRIM21 inhibits irradiation-induced mitochondrial DNA release and impairs antitumour immunity in nasopharyngeal carcinoma tumour models. Nat Commun. 2023;14:865.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  41. Jackson L, et al. Influence of family history on penetrance of hereditary cancers in a population setting. Eclinicalmedicine. 2023;64:102159.

    Article  PubMed  PubMed Central  Google Scholar 

  42. Ayoub N, Jeyasekharan AD, Bernal JA, Venkitaraman AR. HP1-beta mobilization promotes chromatin changes that initiate the DNA damage response. Nature. 2008;453:682–6.

    Article  CAS  PubMed  Google Scholar 

  43. Patil A, Nakai K, Nakamura H. HitPredict: a database of quality assessed protein-protein interactions in nine species. Nucleic Acids Res. 2011;39:D744–9.

    Article  CAS  PubMed  Google Scholar 

  44. Yu YL, Yu J, Ge SF, Su Y, Fan XQ. Novel insight into metabolic reprogrammming in cancer radioresistance: a promising therapeutic target in radiotherapy. Int J Biol Sci. 2023;19:811–28.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  45. Jiang K, et al. STC2 activates PRMT5 to induce radioresistance through DNA damage repair and ferroptosis pathways in esophageal squamous cell carcinoma. Redox Biol. 2023;60:102626.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  46. Price JM, Prabhakaran A, West CML. Predicting tumour radiosensitivity to deliver precision radiotherapy. Nat Rev Clin Oncol. 2023;20:83–98.

    Article  CAS  PubMed  Google Scholar 

  47. Wu Y, Song Y, Wang R, Wang T. Molecular mechanisms of tumor resistance to radiotherapy. Mol Cancer. 2023;22:96.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  48. Chen QP, et al. SOCS2-enhanced ubiquitination of SLC7A11 promotes ferroptosis and radiosensitization in hepatocellular carcinoma. Cell Death Differ. 2023;30:137–51.

    Article  CAS  PubMed  Google Scholar 

  49. Jie XH, et al. USP9X-mediated KDM4C deubiquitination promotes lung cancer radioresistance by epigenetically inducing TGF-beta 2 transcription. Cell Death Differ. 2021;28:2095–111.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  50. Zetrini AE, et al. Remodeling tumor immune microenvironment by using polymer-lipid-manganese dioxide nanoparticles with radiation therapy to boost immune response of castration-resistant prostate cancer. Research. 2023;6:0247.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  51. Nambiar DK, Mishra D, Singh RP. Targeting DNA repair for cancer treatment: lessons from PARP inhibitor trials. Oncol Res. 2023;31:405–21.

    Article  PubMed  PubMed Central  Google Scholar 

  52. Wan CH, Wu MM, Zhang SS, Chen YY, Lu CH. alpha 7nAChR-mediated recruitment of PP1 gamma promotes TRAF6/NF-kappa B cascade to facilitate the progression of hepatocellular carcinoma. Mol Carcinogen. 2018;57:1626–39.

    Article  CAS  Google Scholar 

  53. Li CS, et al. Overexpression of protein phosphatase 1 gamma (PP1 gamma) is associated with enhanced cell proliferation and poor prognosis in hepatocellular carcinoma. Digest Dis Sci. 2017;62:133–42.

    Article  CAS  PubMed  Google Scholar 

  54. Sogawa K, et al. Enhanced expression of PP1 gamma 1, a catalytic subunit isoform of protein phosphatase type 1, in invasive ductal carcinoma of the breast. Cancer Lett. 1997;112:263–8.

    Article  CAS  PubMed  Google Scholar 

  55. Sogawa K, et al. Enhanced expression of catalytic subunit isoform PP1 gamma 1 of protein phosphatase type 1 associated with malignancy of osteogenic tumor. Cancer Lett. 1995;89:1–6.

    CAS  PubMed  Google Scholar 

  56. Kou Y, Zhang S, Chen X, Hu S. Gene expression profile analysis of colorectal cancer to investigate potential mechanisms using bioinformatics. Onco Targets Ther. 2015;8:745–52.

    PubMed  PubMed Central  Google Scholar 

  57. Malone D, Lardelli RM, Li MQ, David M. Dephosphorylation activates the interferon-stimulated Schlafen family member 11 in the DNA damage response. J Biol Chem. 2019;294:14674–85.

    Article  PubMed  PubMed Central  Google Scholar 

  58. Dobbs TA, Tainer JA, Lees-Miller SP. A structural model for regulation of NHEJ by DNA-PKcs autophosphorylation. DNA Repair. 2010;9:1307–14.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  59. Hammel M, et al. Ku and DNA-dependent protein kinase dynamic conformations and assembly regulate DNA binding and the initial non-homologous end joining complex. J Biol Chem. 2010;285:1414–23.

    Article  PubMed  Google Scholar 

  60. Dong YS, et al. Regulation of BRCC, a holoenzyme complex containing BRCA1 and BRCA2, by a signalosome-like subunit and its role in DNA repair. Mol Cell. 2003;12:1087–1099.

    Article  CAS  PubMed  Google Scholar 

  61. Chen XW, Arciero CA, Wang CR, Broccoli D, Godwin AK. BRCC36 is essential for ionizing radiation-induced BRCA1 phosphorylation and nuclear foci formation. Cancer Res. 2006;66:5039–46.

    Article  CAS  PubMed  Google Scholar 

  62. Tao H, et al. BRCC3 promotes tumorigenesis of bladder cancer by activating the NF-kappaB signaling pathway through targeting TRAF2. Front Cell Dev Biol. 2021;9:720349.

    Article  PubMed  PubMed Central  Google Scholar 

  63. Hu Y, Zhang Y, Ding M, Xu R. Long noncoding RNA TMPO-AS1/miR-126-5p/BRCC3 axis accelerates gastric cancer progression and angiogenesis via activating PI3K/Akt/mTOR pathway. J Gastroenterol Hepatol. 2021;36:1877–88.

    Article  CAS  PubMed  Google Scholar 

  64. Zhao Y, et al. Hypermethylation of UCHL1 promotes metastasis of nasopharyngeal carcinoma by suppressing degradation of cortactin (CTTN). Cells. 2020;9:559.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  65. Zhao Y, et al. USP2a supports metastasis by tuning TGF-beta signaling. Cell Rep. 2018;22:2442–54.

    Article  CAS  PubMed  Google Scholar 

  66. Liu N, et al. Reduced expression of Dicer11 is associated with poor prognosis in patients with nasopharyngeal carcinoma. Med Oncol. 2013;30:360.

    Article  CAS  PubMed  Google Scholar 

Download references

Acknowledgements

The authors thank Prof. M. Zeng, Prof. and Prof. H. Mai (Sun Yat-sen University Cancer Center, China) for human NPC cells, plasmids and technical advice. Professor Liu Ranyi (Sun Yat-sen University Cancer Center, China) kindly contributed reporter constructs for HR, NHEJ, and the I-SceI expression plasmid pCMV-NLS-I-SceI. This work was sponsored by the National Natural Science Foundation of China (81872464), Science and Technology Program of Guangdong Province, China (2021A0505110010), and National High-tech R&D Program of China (863 Program) (2006AA02Z4B4).

Funding

This work was sponsored by the National Natural Science Foundation of China (81872464), Science and Technology Program of Guangdong Province, China (2021A0505110010 and 010192200059), and National High-tech R&D Program of China (863 Program) (2006AA02Z4B4).

Author information

Author notes

  1. These authors contributed equally: Ping Feng, Ying Wang.

Authors and Affiliations

  1. State Key Laboratory of Oncology in South China; Guangdong Key Laboratory of Nasopharyngeal Carcinoma Diagnosis and Therapy; Guangdong Provincial Clinical Research Center for Cancer, Sun Yat-sen University Cancer Center, Guangzhou, 510060, China

    Ping Feng, Ying Wang, Na Liu, Yujun Hu, Zilu Huang, Ya Liu, Shuohan Zheng, Tongchao Jiang, Xiang Xiao, Peng Huang & Yunfei Xia

  2. Department of Radiation Oncology, Sun Yat-sen University Cancer Center, Guangzhou, 510060, China

    Ping Feng, Ying Wang, Na Liu, Yujun Hu, Zilu Huang, Ya Liu, Shuohan Zheng, Tongchao Jiang, Xiang Xiao & Yunfei Xia

  3. The Second Affiliated Hospital, Hengyang Medical School, University of South China, Hengyang, 421001, Hunan, China

    Yanming Chen

  4. Department of Clinical Oncology, University of Hong Kong, Hong Kong (SAR), China

    Wei Dai

  5. University of Hong Kong-Shenzhen Hospital, Shenzhen, China

    Wei Dai

  6. Metabolic Innovation Center, Sun Yat-sen University, Guangzhou, 510060, China

    Peng Huang

Authors
  1. Ping Feng
    View author publications

    You can also search for this author in PubMed Google Scholar

  2. Ying Wang
    View author publications

    You can also search for this author in PubMed Google Scholar

  3. Na Liu
    View author publications

    You can also search for this author in PubMed Google Scholar

  4. Yanming Chen
    View author publications

    You can also search for this author in PubMed Google Scholar

  5. Yujun Hu
    View author publications

    You can also search for this author in PubMed Google Scholar

  6. Zilu Huang
    View author publications

    You can also search for this author in PubMed Google Scholar

  7. Ya Liu
    View author publications

    You can also search for this author in PubMed Google Scholar

  8. Shuohan Zheng
    View author publications

    You can also search for this author in PubMed Google Scholar

  9. Tongchao Jiang
    View author publications

    You can also search for this author in PubMed Google Scholar

  10. Xiang Xiao
    View author publications

    You can also search for this author in PubMed Google Scholar

  11. Wei Dai
    View author publications

    You can also search for this author in PubMed Google Scholar

  12. Peng Huang
    View author publications

    You can also search for this author in PubMed Google Scholar

  13. Yunfei Xia
    View author publications

    You can also search for this author in PubMed Google Scholar

Contributions

PF, YFX, and YW designed, carried out and analyzed most of the experiments. NL checked the Figures, controlled the experiment steps, and was involved in discussions of the data. YMC provided helped with pathological analysis. YJH, SHZ, and YL helped organize and analyze clinical information and follow-up data. XX, ZLH, and TCJ contributed to several experiments. WD touched up the manuscript. PF wrote the manuscript with input from all other authors. PH and YFX conceived the study, provided scientific directions, and established collaborations. All authors read and approved the final paper.

Corresponding authors

Correspondence to Peng Huang or Yunfei Xia.

Ethics declarations

Competing interests

The authors declare no competing interests.

Ethics approval

The study was approved by the Sun Yat-sen University Cancer Center’s Institutional Ethical Review Board (GZR2018-100), and the informed consent was obtained from all patients. Animal experiments were approved by the Animal Research Ethics Committee of Sun Yat-sen University Cancer Center and complied with the relevant ethical guidelines (L102012020120M). All research protocols adhered to the Declaration of Helsinki.

Additional information

Publisher’s note Springer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations.

Supplementary information

Rights and permissions

Springer Nature or its licensor (e.g. a society or other partner) holds exclusive rights to this article under a publishing agreement with the author(s) or other rightsholder(s); author self-archiving of the accepted manuscript version of this article is solely governed by the terms of such publishing agreement and applicable law.

Reprints and permissions

About this article

Check for updates. Verify currency and authenticity via CrossMark

Cite this article

Feng, P., Wang, Y., Liu, N. et al. High expression of PPP1CC promotes NHEJ-mediated DNA repair leading to radioresistance and poor prognosis in nasopharyngeal carcinoma. Cell Death Differ (2024). https://doi.org/10.1038/s41418-024-01287-5

Download citation

  • Received:

  • Revised:

  • Accepted:

  • Published:

  • DOI: https://doi.org/10.1038/s41418-024-01287-5

Search

Advanced search

Quick links