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Review
. 2024 May 15;14(5):2523-2537.
doi: 10.62347/WYKZ9784. eCollection 2024.

Unraveling role of ubiquitination in drug resistance of gynecological cancer

Affiliations
Review

Unraveling role of ubiquitination in drug resistance of gynecological cancer

Li Yu et al. Am J Cancer Res. .

Abstract

Chemotherapy is the principal treatment for advanced cancer patients. However, chemotherapeutic resistance, an important hallmark of cancer, is considered as a key impediment to effective therapy in cancer patients. Multiple signaling pathways and factors have been underscored to participate in governing drug resistance. Posttranslational modifications, including ubiquitination, glycosylation, acetylation and phosphorylation, have emerged as key players in modulating drug resistance in gynecological tumors, such as ovarian cancer, cervical cancer and endometrial cancer. In this review article, we summarize the role of ubiquitination in governing drug sensitivity in gynecological cancers. Moreover, we describe the numerous compounds that target ubiquitination in gynecological cancers to reverse chemotherapeutic resistance. In addition, we provide the future perspectives to fully elucidate the mechanisms by which ubiquitination controls drug resistance in gynecological tumors, contributing to restoring drug sensitivity. This review highlights the complex interplay between ubiquitination and drug resistance in gynecological tumors, providing novel insights into potential therapeutic targets and personalized treatment strategies to overcome the bottleneck of drug resistance.

Keywords: PTM; drug resistance; gynecological cancer; target; treatment; ubiquitination.

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Conflict of interest statement

None.

Figures

Figure 1
Figure 1
PTMs participate in drug resistance of gynecological cancers. These PTMs include ubiquitination, acetylation, glycosylation, phosphorylation, methylation and SUMOylation.
Figure 2
Figure 2
Ubiquitination plays a critical role in cisplatin resistance in ovarian cancer cells. Multiple compounds target ubiquitination to overcome the drug resistance of ovarian cancer cells.

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References

    1. Siegel RL, Miller KD, Wagle NS, Jemal A. Cancer statistics, 2023. CA Cancer J Clin. 2023;73:17–48. - PubMed
    1. Nishio S. PD4-2 - novel targeted therapies in uterine carcinosarcomas. Ann Oncol. 2019;30:vi50.
    1. Sun Q, Wang L, Zhang C, Hong Z, Han Z. Cervical cancer heterogeneity: a constant battle against viruses and drugs. Biomark Res. 2022;10:85. - PMC - PubMed
    1. Bhattacharjee R, Dey T, Kumar L, Kar S, Sarkar R, Ghorai M, Malik S, Jha NK, Vellingiri B, Kesari KK, Pérez de la Lastra JM, Dey A. Cellular landscaping of cisplatin resistance in cervical cancer. Biomed Pharmacother. 2022;153:113345. - PubMed
    1. Schmitz JC, Liu J, Lin X, Chen TM, Yan W, Tai N, Gollerkeri A, Chu E. Translational regulation as a novel mechanism for the development of cellular drug resistance. Cancer Metastasis Rev. 2001;20:33–41. - PubMed

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