{"paper_id":"a3439fee-b174-4fe7-983c-5cddcc20d653","body_text":"Abstract\nThe MYC family has been the subject of extensive research in the field of cancer, yet the mechanisms by which these factors operate in the context of endometriosis remain unclear. Considering the existing studies on the MYC family and diseases of the female reproductive system, this review examines the role of MYC family members in regulating cell proliferation and metabolic activity in endometriosis. Furthermore, the study explores the potential association between the MYC family and endometriosis, drawing parallels with its established role in cancer and findings from other gynecological diseases. The primary areas of discussion include cell proliferation and invasion, hormone dependence, and epigenetic regulation. The review also considers inhibitors of the MYC family and other related molecules that may affect MYC expression. The findings of this study suggest significant potential for the MYC family to play a pivotal role in the context of endometriosis. It is anticipated that advancements in technology will stimulate further research in this area and facilitate the development of clinically applicable therapeutic strategies.\nSimilar content being viewed by others\nData availability\nNo datasets were generated or analysed during the current study.\nAbbreviations\n- AMPK:\n-\nAMP-activated protein kinase\n- BET:\n-\nBromodomain and extra terminal domain\n- BTG1:\n-\nB-cell translocation gene 1\n- CTNNB1:\n-\nCatenin beta 1\n- EMT:\n-\nEpithelial-mesenchymal transition\n- ERα:\n-\nEstrogen receptor alpha\n- ERβ:\n-\nEstrogen receptor beta\n- ESR1:\n-\nEstrogen receptor 1\n- IFN:\n-\nInterferon\n- IGFBP1:\n-\nInsulin-like growth factor binding protein 1\n- Ki-67:\n-\nMarker of cellular proliferation\n- MAPK:\n-\nMitogen-activated protein kinase\n- MAX:\n-\nMYC-associated factor X\n- miRNA:\n-\nMicroRNA\n- mTOR:\n-\nMammalian target of rapamycin\n- NDRG1:\n-\nN-MYC downstream regulated gene 1\n- NMI:\n-\nN-MYC and STAT interactor\n- NR4A1:\n-\nNuclear receptor subfamily 4 group A member 1\n- PR:\n-\nProgesterone receptor\n- PR-A/B:\n-\nProgesterone receptor isoforms A and B\n- SPARC:\n-\nSecreted protein acidic and rich in cysteine\n- TF:\n-\nTranscription factor\n- TWIST1:\n-\nTwist family BHLH transcription factor 1\n- WNT:\n-\nWingless-type signaling pathway\nReferences\nTsamantioti ES, Mahdy H (2025) Endometriosis, in StatPearls. 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ZY, and XG contributed to all tables and figures and were responsible for drafting the manuscript. ZY, AJ, CY, MZ, MW, and JL participated in the revision of the manuscript. All authors have thoroughly reviewed and approved the final version of the manuscript.\nCorresponding authors\nEthics declarations\nConsent for publication\nNot applicable.\nCompeting interests\nThe authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.\nConflict of interest\nThe authors declare that they have no conflict of interest.\nEthical approval and consent to participate\nNot applicable.\nAdditional information\nPublisher’s note\nSpringer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations.\nRights and permissions\nSpringer 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.\nAbout this article\nCite this article\nGe, X., Yue, C., Zhang, M. et al. MYC: unveiling novel therapeutic avenues for endometriosis. Mol Biol Rep 53, 535 (2026). https://doi.org/10.1007/s11033-026-11716-y\nReceived:\nAccepted:\nPublished:\nVersion of record:\nDOI: https://doi.org/10.1007/s11033-026-11716-y","source_license":"public-domain-us","license_restricted":false}