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Background <p>Breast cancer (BC) patients have been threatened by distant metastasis and variations in treatment response for a long time. The mechanism urgently remains to be explored.</p> Methods <p>Bioinformatics analysis were performed to indicate the expression and function of related markers, and verified in BC tissues as well as adjacent tissues. Functional assays employed in vitro and in vivo with PSMD8 knockdown or overexpression. Mechanistic studies evaluated the ubiquitination degradation process via co-immunoprecipitation and rescue experiments.</p> Results <p>In the present study, PSMD8 was abnormally upregulated in BC tissues compared with adjacent tissues and was related to poor prognosis in BC patients. The knockdown of PSMD8 attenuated the biological effect and EMT progression in vitro and in vivo and augmented the sensitivity of BC cells to paclitaxel, whereas PSMD8 overexpression showed the opposite effects. Mechanistic analysis indicated that PSMD8 stabilized KIF10, and we observed its tumor-promoting effect in BC tumor cells. Moreover, KIF10 knockdown significantly antagonized the facilitating effect of PSMD8 on the EMT program and response to paclitaxel treatment. Finally, the PSMD8/KIF10 axis activated the ERK pathway. Inhibiting the ERK pathway in PSMD8-overexpressing cell lines partially blocked EMT progression and altered the cellular response to paclitaxel.</p> Conclusion <p>In conclusion, our results demonstrated that the PSMD8/KIF10 axis promoted BC development and modulated paclitaxel sensitivity via the ERK pathway. Our findings provide a theoretical basis for targeting PSMD8 to BC cells as a novel target for the treatment of BC.</p>

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PSMD8 promotes breast cancer progression and attenuates paclitaxel sensitivity by stabilizing KIF10

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年6月26日

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  • Chenyuan Li,
  • Xinyue Nie,
  • Shichong Liao,
  • Feng Yao

摘要

Background

Breast cancer (BC) patients have been threatened by distant metastasis and variations in treatment response for a long time. The mechanism urgently remains to be explored.

Methods

Bioinformatics analysis were performed to indicate the expression and function of related markers, and verified in BC tissues as well as adjacent tissues. Functional assays employed in vitro and in vivo with PSMD8 knockdown or overexpression. Mechanistic studies evaluated the ubiquitination degradation process via co-immunoprecipitation and rescue experiments.

Results

In the present study, PSMD8 was abnormally upregulated in BC tissues compared with adjacent tissues and was related to poor prognosis in BC patients. The knockdown of PSMD8 attenuated the biological effect and EMT progression in vitro and in vivo and augmented the sensitivity of BC cells to paclitaxel, whereas PSMD8 overexpression showed the opposite effects. Mechanistic analysis indicated that PSMD8 stabilized KIF10, and we observed its tumor-promoting effect in BC tumor cells. Moreover, KIF10 knockdown significantly antagonized the facilitating effect of PSMD8 on the EMT program and response to paclitaxel treatment. Finally, the PSMD8/KIF10 axis activated the ERK pathway. Inhibiting the ERK pathway in PSMD8-overexpressing cell lines partially blocked EMT progression and altered the cellular response to paclitaxel.

Conclusion

In conclusion, our results demonstrated that the PSMD8/KIF10 axis promoted BC development and modulated paclitaxel sensitivity via the ERK pathway. Our findings provide a theoretical basis for targeting PSMD8 to BC cells as a novel target for the treatment of BC.