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A renaissance for YES in cancer

Oncogene volume 42, pages 3385–3393 (2023)Cite this article

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Abstract

Most of our understanding regarding the involvement of SRC-family tyrosine kinases in cancer has stemmed from studies focused on the prototypical SRC oncogene. However, emerging research has shed light on the important role of YES signaling in oncogenic transformation, tumor growth, metastatic progression, and resistance to various cancer therapies. Clinical evidence indicates that dysregulated expression or activity of YES is a frequent occurrence in human cancers and is associated with unfavorable outcomes. These findings provide a compelling rationale for specifically targeting YES in certain cancer subtypes. Here, we review the crucial role of YES in cancer and discuss the challenges associated with translating preclinical observations into effective YES-targeted therapies.

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Fig. 1: Structure and activation of YES.
Fig. 2: Copy-number alterations of the YES1 gene in human cancer.
Fig. 3: YES is frequently overexpressed in human cancer.
Fig. 4: High expression of YES predicts shorter survival in different cancer types.
Fig. 5: Regulation, signaling, and pro-tumorigenic roles of YES in cancer.

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References

  1. Yeatman TJ. A renaissance for SRC. Nat Rev Cancer. 2004;4:470–80.

    Article  CAS  PubMed  Google Scholar 

  2. Rous P. A sarcoma of the fowl transmissible by an agent separable from the tumor cells. J Exp Med. 1911;13:397–411.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  3. Collett MS, Purchio AF, Erikson RL. Avian sarcoma virus-transforming protein, pp60src shows protein kinase activity specific for tyrosine. Nature. 1980;285:167–9.

    Article  CAS  PubMed  Google Scholar 

  4. Hunter T, Sefton BM. Transforming gene product of Rous sarcoma virus phosphorylates tyrosine. Proc Natl Acad Sci USA. 1980;77:1311–5.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  5. Levinson AD, Oppermann H, Varmus HE, Bishop JM. The purified product of the transforming gene of avian sarcoma virus phosphorylates tyrosine. J Biol Chem. 1980;255:11973–80.

    Article  CAS  PubMed  Google Scholar 

  6. Parsons SJ, Parsons JT. Src family kinases, key regulators of signal transduction. Oncogene. 2004;23:7906–9.

    Article  CAS  PubMed  Google Scholar 

  7. Shah NH, Amacher JF, Nocka LM, Kuriyan J. The Src module: an ancient scaffold in the evolution of cytoplasmic tyrosine kinases. Crit Rev Biochem Mol Biol. 2018;53:535–63.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  8. Kim LC, Song L, Haura EB. Src kinases as therapeutic targets for cancer. Nat Rev Clin Oncol. 2009;6:587–95.

    Article  PubMed  Google Scholar 

  9. Thomas SM, Brugge JS. Cellular functions are regulated by Src family kinases. Annu Rev Cell Dev Biol. 1997;13:513–609.

    Article  CAS  PubMed  Google Scholar 

  10. Klinghoffer RA, Sachsenmaier C, Cooper JA, Soriano P. Src family kinases are required for integrin but not PDGFR signal transduction. EMBO J. 1999;18:2459–71.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  11. Stein PL, Vogel H, Soriano P. Combined deficiencies of Src, Fyn, and Yes tyrosine kinases in mutant mice. Genes Dev. 1994;8:1999–2007.

    Article  CAS  PubMed  Google Scholar 

  12. Luton F, Verges M, Vaerman JP, Sudol M, Mostov KE. The SRC family protein tyrosine kinase p62yes controls polymeric IgA transcytosis in vivo. Mol Cell. 1999;4:627–32.

    Article  CAS  PubMed  Google Scholar 

  13. Summy JM, Sudol M, Eck MJ, Monteiro AN, Gatesman A, Flynn DC. Specificity in signaling by c- Yes. Front Biosci. 2003;8:s185–205.

    Article  CAS  PubMed  Google Scholar 

  14. Semba K, Yamanashi Y, Nishizawa M, Sukegawa J, Yoshida M, Sasaki M, et al. Location of the c-yes gene on the human chromosome and its expression in various tissues. Science. 1985;227:1038–40.

    Article  CAS  PubMed  Google Scholar 

  15. Bilal E, Alexe G, Yao M, Cong L, Kulkarni A, Ginjala V, et al. Identification of the YES1 kinase as a therapeutic target in basal-like breast cancers. Genes Cancer. 2010;1:1063–73.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  16. Rosenbluh J, Nijhawan D, Cox AG, Li X, Neal JT, Schafer EJ, et al. beta-Catenin-driven cancers require a YAP1 transcriptional complex for survival and tumorigenesis. Cell. 2012;151:1457–73.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  17. Sancier F, Dumont A, Sirvent A, Paquay de Plater L, Edmonds T, David G, et al. Specific oncogenic activity of the Src-family tyrosine kinase c-Yes in colon carcinoma cells. PloS One. 2011;6:e17237.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  18. Dubois F, Leroy C, Simon V, Benistant C, Roche S. YES oncogenic activity is specified by its SH4 domain and regulates RAS/MAPK signaling in colon carcinoma cells. Am J Cancer Res. 2015;5:1972–87.

    PubMed  PubMed Central  Google Scholar 

  19. Hamamura K, Tsuji M, Hotta H, Ohkawa Y, Takahashi M, Shibuya H, et al. Functional activation of Src family kinase yes protein is essential for the enhanced malignant properties of human melanoma cells expressing ganglioside GD3. J Biol Chem. 2011;286:18526–37.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  20. Sato A, Sekine M, Virgona N, Ota M, Yano T. Yes is a central mediator of cell growth in malignant mesothelioma cells. Oncol Rep. 2012;28:1889–93.

    Article  CAS  PubMed  Google Scholar 

  21. Yeung CL, Ngo VN, Grohar PJ, Arnaldez FI, Asante A, Wan X, et al. Loss-of-function screen in rhabdomyosarcoma identifies CRKL-YES as a critical signal for tumor growth. Oncogen. 2013;32:5429–38.

    Article  CAS  Google Scholar 

  22. Lewis-Tuffin LJ, Feathers R, Hari P, Durand N, Li Z, Rodriguez FJ, et al. Src family kinases differentially influence glioma growth and motility. Mol Oncol. 2015;9:1783–98.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  23. Je DW, O YM, Ji YG, Cho Y, Lee DH. The inhibition of SRC family kinase suppresses pancreatic cancer cell proliferation, migration, and invasion. Pancreas. 2014;43:768–76.

    Article  CAS  PubMed  Google Scholar 

  24. Miller RE, Brough R, Bajrami I, Williamson CT, McDade S, Campbell J, et al. Synthetic lethal targeting of ARID1A-mutant ovarian clear cell tumors with dasatinib. Mol Cancer Ther. 2016;15:1472–84.

    Article  CAS  PubMed  Google Scholar 

  25. Jin Y, Huang M, Wang Y, Yi C, Deng Y, Chen Y, et al. c-Yes enhances tumor migration and invasion via PI3K/AKT pathway in epithelial ovarian cancer. Exp Mol Pathol. 2016;101:50–7.

    Article  CAS  PubMed  Google Scholar 

  26. Garmendia I, Pajares MJ, Hermida-Prado F, Ajona D, Bertolo C, Sainz C, et al. YES1 Drives lung cancer growth and progression and predicts sensitivity to dasatinib. Am J Respir Crit Care Med. 2019;200:888–99.

    Article  CAS  PubMed  Google Scholar 

  27. Shen Y, Chen F, Liang Y. MicroRNA-133a inhibits the proliferation of non-small cell lung cancer by targeting YES1. Oncol Lett. 2019;18:6759–65.

    CAS  PubMed  PubMed Central  Google Scholar 

  28. Redin E, Garrido-Martin EM, Valencia K, Redrado M, Solorzano JL, Carias R, et al. YES1 is a druggable oncogenic target in SCLC. J Thorac Oncol. 2022;17:1387–403.

    Article  CAS  PubMed  Google Scholar 

  29. Mao L, Yuan W, Cai K, Lai C, Huang C, Xu Y, et al. EphA2-YES1-ANXA2 pathway promotes gastric cancer progression and metastasis. Oncogene. 2021;40:3610–23.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  30. Sun Y, Tian Y, He J, Tian Y, Zhang G, Zhao R, et al. Linc01133 contributes to gastric cancer growth by enhancing YES1-dependent YAP1 nuclear translocation via sponging miR-145-5p. Cell Death Dis. 2022;13:51.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  31. Guegan JP, Lapouge M, Voisin L, Saba-El-Leil MK, Tanguay PL, Levesque K, et al. Signaling by the tyrosine kinase Yes promotes liver cancer development. Sci Signal. 2022;15:eabj4743.

    Article  CAS  PubMed  Google Scholar 

  32. Konecny GE, Glas R, Dering J, Manivong K, Qi J, Finn RS, et al. Activity of the multikinase inhibitor dasatinib against ovarian cancer cells. Br J Cancer. 2009;101:1699–708.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  33. Hamanaka N, Nakanishi Y, Mizuno T, Horiguchi-Takei K, Akiyama N, Tanimura H, et al. YES1 Is a targetable oncogene in cancers harboring YES1 gene amplification. Cancer Res. 2019;79:5734–45.

    Article  CAS  PubMed  Google Scholar 

  34. Sato H, Kubota D, Qiao H, Jungbluth A, Rekhtman N, Schoenfeld AJ, et al. SRC family kinase inhibition targets YES1 and YAP1 as primary drivers of lung cancer and as mediators of acquired resistance to ALK and epidermal growth factor receptor inhibitors. JCO Precis Oncol. 2022;6:e2200088.

    Article  PubMed  PubMed Central  Google Scholar 

  35. Takeda H, Kawamura Y, Miura A, Mori M, Wakamatsu A, Yamamoto J, et al. Comparative analysis of human SRC-family kinase substrate specificity in vitro. J Proteome Res. 2010;9:5982–93.

    Article  CAS  PubMed  Google Scholar 

  36. Resh MD. Myristylation and palmitoylation of Src family members: the fats of the matter. Cell. 1994;76:411–3.

    Article  CAS  PubMed  Google Scholar 

  37. Slemmons KK, Yeung C, Baumgart JT, Juarez JOM, McCalla A, Helman LJ. Targeting Hippo-dependent and Hippo-independent YAP1 signaling for the treatment of childhood rhabdomyosarcoma. Cancer Res. 2020;80:3046–56.

    Article  CAS  PubMed  Google Scholar 

  38. Tamm C, Bower N, Anneren C. Regulation of mouse embryonic stem cell self-renewal by a Yes-YAP-TEAD2 signaling pathway downstream of LIF. J Cell Sci. 2011;124:1136–44.

    Article  PubMed  Google Scholar 

  39. Driskill JH, and Pan D. Control of stem cell renewal and fate by YAP and TAZ. Nat Rev Mol Cell Biol. 2023: https://doi.org/10.1038/s41580-023-00644-5.

  40. Garmendia I, Redin E, Montuenga LM, Calvo A. YES1: A novel therapeutic target and biomarker in cancer. Mol Cancer Ther. 2022;21:1371–80.

    Article  CAS  PubMed  Google Scholar 

  41. Ohkawa Y, Momota H, Kato A, Hashimoto N, Tsuda Y, Kotani N, et al. Ganglioside GD3 enhances invasiveness of gliomas by forming a complex with platelet-derived growth factor receptor alpha and Yes kinase. J Biol Chem. 2015;290:16043–58.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  42. Kleber S, Sancho-Martinez I, Wiestler B, Beisel A, Gieffers C, Hill O, et al. Yes, and PI3K bind CD95 to signal invasion of glioblastoma. Cancer Cell. 2008;13:235–48.

    Article  CAS  PubMed  Google Scholar 

  43. Han X, Zhang W, Yang X, Wheeler CG, Langford CP, Wu L, et al. The role of Src family kinases in growth and migration of glioma stem cells. Int J Oncol. 2014;45:302–10.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  44. Liu W, Monahan KB, Pfefferle AD, Shimamura T, Sorrentino J, Chan KT, et al. LKB1/STK11 inactivation leads to expansion of a prometastatic tumor subpopulation in melanoma. Cancer Cell. 2012;21:751–64.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  45. Weis S, Cui J, Barnes L, Cheresh D. Endothelial barrier disruption by VEGF-mediated Src activity potentiates tumor cell extravasation and metastasis. J Cell Biol. 2004;167:223–9.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  46. Campbell JD, Alexandrov A, Kim J, Wala J, Berger AH, Pedamallu CS, et al. Distinct patterns of somatic genome alterations in lung adenocarcinomas and squamous cell carcinomas. Nat Genet. 2016;48:607–16.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  47. Aramburu A, Zudaire I, Pajares MJ, Agorreta J, Orta A, Lozano MD, et al. Combined clinical and genomic signatures for the prognosis of early-stage non-small cell lung cancer based on gene copy number alterations. BMC Genom. 2015;16:752.

    Article  Google Scholar 

  48. Song Y, Li L, Ou Y, Gao Z, Li E, Li X, et al. Identification of genomic alterations in oesophageal squamous cell cancer. Nature. 2014;509:91–5.

    Article  CAS  PubMed  Google Scholar 

  49. Al-Harazi O, Kaya IH, El Allali A, Colak D. A network-based methodology to identify subnetwork markers for diagnosis and prognosis of colorectal cancer. Front Genet. 2021;12:721949.

    Article  CAS  PubMed  Google Scholar 

  50. Han NM, Curley SA, Gallick GE. Differential activation of pp60(c-src) and pp62(c-yes) in human colorectal carcinoma liver metastases. Clin Cancer Res. 1996;2:1397–404.

    CAS  PubMed  Google Scholar 

  51. Li N, Yu J, Luo A, Tang Y, Liu W, Wang S, et al. LncRNA and mRNA signatures associated with neoadjuvant chemoradiotherapy downstaging effects in rectal cancer. J Cell Biochem. 2019;120:5207–17.

    Article  CAS  PubMed  Google Scholar 

  52. Muro S, Takemasa I, Oba S, Matoba R, Ueno N, Maruyama C, et al. Identification of expressed genes linked to malignancy of human colorectal carcinoma by parametric clustering of quantitative expression data. Genome Biol. 2003;4:R21.

    Article  PubMed  PubMed Central  Google Scholar 

  53. Park J, Meisler AI, Cartwright CA. c-Yes, tyrosine kinase activity in human colon carcinoma. Oncogene. 1993;8:2627–35.

    CAS  PubMed  Google Scholar 

  54. Pena SV, Melhem MF, Meisler AI, Cartwright CA. Elevated c-yes tyrosine kinase activity in premalignant lesions of the colon. Gastroenterology. 1995;108:117–24.

    Article  CAS  PubMed  Google Scholar 

  55. Sirvent A, Benistant C, Pannequin J, Veracini L, Simon V, Bourgaux JF, et al. Src family tyrosine kinases-driven colon cancer cell invasion is induced by Csk membrane delocalization. Oncogene. 2010;29:1303–15.

    Article  CAS  PubMed  Google Scholar 

  56. Lee JH, Pyon JK, Kim DW, Lee SH, Nam HS, Kim CH, et al. Elevated c-Src and c-Yes expression in malignant skin cancers. J Exp Clin Cancer Res. 2010;29:116.

    Article  PubMed  PubMed Central  Google Scholar 

  57. Slack FJ, Chinnaiyan AM. The role of non-coding RNAs in oncology. Cell. 2019;179:1033–55.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  58. Chen L, Cao H, Feng Y. MiR-199a suppresses prostate cancer paclitaxel resistance by targeting YES1. World J Urol. 2018;36:357–65.

    Article  CAS  PubMed  Google Scholar 

  59. Gregersen LH, Jacobsen AB, Frankel LB, Wen J, Krogh A, Lund AH. MicroRNA-145 targets YES and STAT1 in colon cancer cells. PloS One. 2010;5:e8836.

    Article  PubMed  PubMed Central  Google Scholar 

  60. Majid S, Saini S, Dar AA, Hirata H, Shahryari V, Tanaka Y, et al. MicroRNA-205 inhibits Src-mediated oncogenic pathways in renal cancer. Cancer Res. 2011;71:2611–21.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  61. Fang Z, Yin S, Sun R, Zhang S, Fu M, Wu Y, et al. miR-140-5p suppresses the proliferation, migration, and invasion of gastric cancer by regulating YES1. Mol Cancer. 2017;16:139.

    Article  PubMed  PubMed Central  Google Scholar 

  62. Lee SA, Kim JS, Park SY, Kim HJ, Yu SK, Kim CS, et al. miR-203 downregulates Yes-1 and suppresses oncogenic activity in human oral cancer cells. J Biosci Bioeng. 2015;120:351–8.

    Article  CAS  PubMed  Google Scholar 

  63. Zhou Y, Wang C, Ding J, Chen Y, Sun Y, Cheng Z. miR-133a targets YES1 to reduce cisplatin resistance in ovarian cancer by regulating cell autophagy. Cancer Cell Int. 2022;22:15.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  64. Sen B, Johnson FM. Regulation of SRC family kinases in human cancers. J Signal Transduct. 2011;2011:865819.

    Article  PubMed  PubMed Central  Google Scholar 

  65. Masaki T, Okada M, Tokuda M, Shiratori Y, Hatase O, Shirai M, et al. Reduced C-terminal Src kinase (Csk) activities in hepatocellular carcinoma. Hepatology. 1999;29:379–84.

    Article  CAS  PubMed  Google Scholar 

  66. Fan PD, Narzisi G, Jayaprakash AD, Venturini E, Robine N, Smibert P, et al. YES1 amplification is a mechanism of acquired resistance to EGFR inhibitors identified by transposon mutagenesis and clinical genomics. Proc Natl Acad Sci USA. 2018;115:E6030–E8.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  67. Ichihara E, Westover D, Meador CB, Yan Y, Bauer JA, Lu P, et al. SFK/FAK signaling attenuates osimertinib efficacy in both drug-sensitive and drug-resistant models of EGFR-mutant lung cancer. Cancer Res. 2017;77:2990–3000.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  68. Yu HA, Suzawa K, Jordan E, Zehir A, Ni A, Kim R, et al. Concurrent alterations in EGFR-mutant lung cancers associated with resistance to EGFR kinase inhibitors and characterization of MTOR as a mediator of resistance. Clin Cancer Res. 2018;24:3108–18.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  69. Takeda T, Yamamoto H, Kanzaki H, Suzawa K, Yoshioka T, Tomida S, et al. Yes1 signaling mediates the resistance to Trastuzumab/Lapatinib in breast cancer. PloS One. 2017;12:e0171356.

    Article  PubMed  PubMed Central  Google Scholar 

  70. Yoshioka T, Shien K, Takeda T, Takahashi Y, Kurihara E, Ogoshi Y, et al. Acquired resistance mechanisms to afatinib in HER2-amplified gastric cancer cells. Cancer Sci. 2019;110:2549–57.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  71. Tao J, Sun D, Hou H. Role of YES1 amplification in EGFR mutation-positive non-small cell lung cancer: primary resistance to afatinib in a patient. Thorac Cancer. 2020;11:2736–9.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  72. Minari R, Valentini S, Madeddu D, Cavazzoni A, La Monica S, Lagrasta CAM, et al. YES1 and MYC amplifications as synergistic resistance mechanisms to different generation ALK tyrosine kinase inhibitors in advanced NSCLC: brief report of clinical and preclinical proofs. JTO Clin Res Rep. 2022;3:100278.

    PubMed  PubMed Central  Google Scholar 

  73. Fujihara M, Shien T, Shien K, Suzawa K, Takeda T, Zhu Y, et al. YES1 as a therapeutic target for HER2-positive breast cancer after trastuzumab and trastuzumab-emtansine (T-DM1) resistance development. Int J Mol Sci. 2021;22:12809.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  74. Takeda T, Yamamoto H, Suzawa K, Tomida S, Miyauchi S, Araki K, et al. YES1 activation induces acquired resistance to neratinib in HER2-amplified breast and lung cancers. Cancer Sci. 2020;111:849–56.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  75. Wang L, Wang Q, Xu P, Fu L, Li Y, Fu H, et al. YES1 amplification confers trastuzumab-emtansine (T-DM1) resistance in HER2-positive cancer. Br J Cancer. 2020;123:1000–11.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  76. Lun XK, Szklarczyk D, Gabor A, Dobberstein N, Zanotelli VRT, Saez-Rodriguez J, et al. Analysis of the human kinome and phosphatome by mass cytometry reveals overexpression-induced effects on cancer-related signaling. Mol Cell. 2019;74:1086–102. e5

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  77. Wang W, Cassidy J, O’Brien V, Ryan KM, Collie-Duguid E. Mechanistic and predictive profiling of 5-Fluorouracil resistance in human cancer cells. Cancer Res. 2004;64:8167–76.

    Article  CAS  PubMed  Google Scholar 

  78. Touil Y, Igoudjil W, Corvaisier M, Dessein AF, Vandomme J, Monte D, et al. Colon cancer cells escape 5FU chemotherapy-induced cell death by entering stemness and quiescence associated with the c-Yes/YAP axis. Clin Cancer Res. 2014;20:837–46.

    Article  CAS  PubMed  Google Scholar 

  79. Martellucci S, Clementi L, Sabetta S, Mattei V, Botta L, Angelucci A. Src family kinases as therapeutic targets in advanced solid tumors: what we have learned so far. Cancers. 2020;12:1448.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  80. Musumeci F, Greco C, Grossi G, Molinari A, Schenone S. Recent studies on ponatinib in cancers other than chronic myeloid leukemia. Cancers. 2018;10:430.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  81. Jabbour E, Kantarjian H. Chronic myeloid leukemia: 2018 update on diagnosis, therapy and monitoring. Am J Hematol. 2018;93:442–59.

    Article  PubMed  Google Scholar 

  82. Du G, Rao S, Gurbani D, Henning NJ, Jiang J, Che J, et al. Structure-based design of a potent and selective covalent inhibitor for SRC kinase that targets a P-loop cysteine. J Med Chem. 2020;63:1624–41.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  83. Temps C, Lietha D, Webb ER, Li XF, Dawson JC, Muir M, et al. A conformation selective mode of inhibiting SRC improves drug efficacy and tolerability. Cancer Res. 2021;81:5438–50.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  84. Verma R, Mohl D, Deshaies RJ. Harnessing the power of proteolysis for targeted protein inactivation. Mol Cell. 2020;77:446–60.

    Article  CAS  PubMed  Google Scholar 

  85. Manda S, Lee NK, Oh DC, Lee J. Design, synthesis, and biological evaluation of Proteolysis Targeting Chimeras (PROTACs) for the dual degradation of IGF-1R and Src. Molecules. 2020;25:1948.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  86. Dey A, Varelas X, Guan KL. Targeting the Hippo pathway in cancer, fibrosis, wound healing, and regenerative medicine. Nat Rev Drug Discov. 2020;19:480–94.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  87. Bartha A, Gyorffy B. TNMplot.com: a web tool for the comparison of gene expression in normal, tumor, and metastatic tissues. Int J Mol Sci. 2021;22:2622.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  88. Tang Z, Li C, Kang B, Gao G, Li C, Zhang Z. GEPIA: a web server for cancer and normal gene expression profiling and interactive analyses. Nucleic Acids Res. 2017;45:W98–W102.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

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Acknowledgements

We thank Christian Charbonneau for help with the preparation of the figures. Work performed in the laboratory of SM was supported by an Impact Grant from the Canadian Cancer Society.

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  1. Institute for Research in Immunology and Cancer, Montreal, QC, Canada

    Marjorie Lapouge & Sylvain Meloche

  2. Department of Pharmacology and Physiology, Université de Montréal, Montreal, QC, Canada

    Sylvain Meloche

  3. Molecular Biology Program, Faculty of Medicine, Université de Montréal, Montreal, QC, Canada

    Sylvain Meloche

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Correspondence to Sylvain Meloche.

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Lapouge, M., Meloche, S. A renaissance for YES in cancer. Oncogene 42, 3385–3393 (2023). https://doi.org/10.1038/s41388-023-02860-x

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