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<p>Chemoresistance is a major challenge in effective chemotherapy for breast cancers. Unfortunately, the precise molecular mechanisms that confer resistance remain elusive so far. A remarkable feature in a multitude of breast cancers is the presence of clustered supernumerary centrosomes, which is a dysregulated condition that arises primarily through centrosome over-duplication. Normally, microtubule motor proteins (MiMos) maintain the integrity of centrosomes <i>via</i> regulating cohesion, separation and positioning of centrosomes. In the recent years, several MiMos have been reported to be differentially expressed in chemoresistant breast cancers. Such findings suggest a probable association of MiMos with chemoresistance. Here, we propose that MiMo-associated centrosomal dysregulation is involved in conferring chemoresistance in breast cancers. We corroborate the same with a systematic review of literature where we narrow down to sixteen MiMos (one dynein and fifteen kinesins). Our argument highlights a plausible decisive role of MiMo-mediated centrosomal anomalies in orchestrating chemoresistance in breast cancers.</p>

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Does microtubule motor-mediated centrosomal dyshomeostasis confer chemoresistance in breast cancer?

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  • 发表日期：

    2025年9月26日

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  • J. Priyanga,
  • Gunjan Guha,
  • Dipita Bhakta-Guha

摘要

Chemoresistance is a major challenge in effective chemotherapy for breast cancers. Unfortunately, the precise molecular mechanisms that confer resistance remain elusive so far. A remarkable feature in a multitude of breast cancers is the presence of clustered supernumerary centrosomes, which is a dysregulated condition that arises primarily through centrosome over-duplication. Normally, microtubule motor proteins (MiMos) maintain the integrity of centrosomes via regulating cohesion, separation and positioning of centrosomes. In the recent years, several MiMos have been reported to be differentially expressed in chemoresistant breast cancers. Such findings suggest a probable association of MiMos with chemoresistance. Here, we propose that MiMo-associated centrosomal dysregulation is involved in conferring chemoresistance in breast cancers. We corroborate the same with a systematic review of literature where we narrow down to sixteen MiMos (one dynein and fifteen kinesins). Our argument highlights a plausible decisive role of MiMo-mediated centrosomal anomalies in orchestrating chemoresistance in breast cancers.