MYC: unveiling novel therapeutic avenues for endometriosis

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This paper explores the role of MYC in endometriosis, identifying it as a potential therapeutic target for novel treatment strategies.

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This paper is a narrative review examining the role of MYC family members in regulating cell proliferation and metabolic activity in endometriosis, drawing on prior studies of MYC in cancer and other female reproductive system diseases. It highlights proposed links between MYC signaling and endometriosis processes including proliferation/invasion, hormone dependence, and epigenetic regulation, and it discusses MYC inhibitors and related molecules that could affect MYC expression. The main caveat is that it is a review without generating or analyzing new datasets. This paper is centrally about endometriosis — it specifically reviews how the MYC family may contribute to endometriosis biology and therapeutic targeting.

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Abstract

The 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.
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Abstract

The 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. Similar content being viewed by others Data availability No datasets were generated or analysed during the current study. Abbreviations - AMPK: - AMP-activated protein kinase - BET: - Bromodomain and extra terminal domain - BTG1: - B-cell translocation gene 1 - CTNNB1: - Catenin beta 1 - EMT: - Epithelial-mesenchymal transition - ERα: - Estrogen receptor alpha - ERβ: - Estrogen receptor beta - ESR1: - Estrogen receptor 1 - IFN: - Interferon - IGFBP1: - Insulin-like growth factor binding protein 1 - Ki-67: - Marker of cellular proliferation - MAPK: - Mitogen-activated protein kinase - MAX: - MYC-associated factor X - miRNA: - MicroRNA - mTOR: - Mammalian target of rapamycin - NDRG1: - N-MYC downstream regulated gene 1 - NMI: - N-MYC and STAT interactor - NR4A1: - Nuclear receptor subfamily 4 group A member 1 - PR: - Progesterone receptor - PR-A/B: - Progesterone receptor isoforms A and B - SPARC: - Secreted protein acidic and rich in cysteine - TF: - Transcription factor - TWIST1: - Twist family BHLH transcription factor 1 - WNT: - Wingless-type signaling pathway

References

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Acknowledgements

Not applicable. Funding The study was supported by research grants from National Natural Science Foundation of China (Grant no. 81972489). Author information Authors and Affiliations Contributions ZY, and XG conceived the review. ZY, AJ, XG, CY, MZ, MW and JL collected the related papers. 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. Corresponding authors Ethics declarations Consent for publication Not applicable. Competing interests The 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. Conflict of interest The authors declare that they have no conflict of interest. Ethical approval and consent to participate Not applicable. Additional information Publisher’s note Springer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations. 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. About this article Cite this article Ge, 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 Received: Accepted: Published: Version of record: DOI: https://doi.org/10.1007/s11033-026-11716-y

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