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Peer-reviewedCC BYPLOS One

Enhanced enfortumab vedotin sensitivity in a cisplatin-resistant bladder cancer model

  • Taisuke Tobe1
  • Jun Teishima1
  • Takuto Hara1
  • Yusuke Shiraishi1
  • Hideto Ueki1
  • Naoto Wakita1
  • Yasuyoshi Okamura1
  • Yukari Bando1
  • Kotaro Suzuki1
  • Tomoaki Terakawa1
  • Akihisa Yao1
  • Koji Chiba1
1 more authors
  • Hideaki Miyake1
  1. 1Division of Urology, Department of Surgery Related, Kobe University Graduate School of Medicine, Japan.
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Abstract

Objective: Enfortumab vedotin (EV) and cisplatin (CDDP) are central treatments for advanced urothelial carcinoma, yet the influence of prior CDDP exposure on subsequent EV efficacy remains unclear. In this report, we characterized EV-related drug responses in a CDDP-resistant bladder cancer subline. Methods: A CDDP-resistant subline (HT1376-CR) was generated from parental bladder cancer cell (HT1376/P) through continuous exposure to CDDP. Sensitivities to CDDP, EV, and the EV payload monomethyl auristatin E (MMAE) were compared between HT1376-CR and HT1376/P. Nectin-4 expression, EV binding, and drug-resistance-related gene expression were evaluated. The effect of ABCB1 silencing on drug response was also examined. In vivo EV responses were explored using xenograft models. Results: HT1376-CR cells showed increased sensitivity to EV in vitro and in vivo. HT1376-CR cells were more sensitive to MMAE and showed greater G2/M accumulation after MMAE exposure. In contrast, cell-surface nectin-4 expression and EV binding were reduced. ABCB1 was markedly upregulated in HT1376-CR, and ABCB1 silencing increased sensitivity to CDDP, MMAE, and EV within the resistant subline. Conclusion: The CDDP-resistant HT1376 subline showed enhanced sensitivity to EV, and ABCB1 suppression further increased EV sensitivity within this resistant subline.

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Cite

BibTeXRIS
BibTeX
@article{tobe2026enhanced,
  title = {{Enhanced enfortumab vedotin sensitivity in a cisplatin-resistant bladder cancer model}},
  author = {Taisuke Tobe and Jun Teishima and Takuto Hara and Yusuke Shiraishi and Hideto Ueki and Naoto Wakita and Yasuyoshi Okamura and Yukari Bando and Kotaro Suzuki and Tomoaki Terakawa and Akihisa Yao and Koji Chiba and Hideaki Miyake},
  journal = {PLOS One},
  year = {2026},
  month = oct,
  doi = {10.1371/journal.pone.0361593},
  url = {https://doi.org/10.1371/journal.pone.0361593},
  note = {CC BY},
}
RIS
TY  - JOUR
TI  - Enhanced enfortumab vedotin sensitivity in a cisplatin-resistant bladder cancer model
AU  - Taisuke Tobe
AU  - Jun Teishima
AU  - Takuto Hara
AU  - Yusuke Shiraishi
AU  - Hideto Ueki
AU  - Naoto Wakita
AU  - Yasuyoshi Okamura
AU  - Yukari Bando
AU  - Kotaro Suzuki
AU  - Tomoaki Terakawa
AU  - Akihisa Yao
AU  - Koji Chiba
AU  - Hideaki Miyake
PY  - 2026
DA  - 2026/10/29
JO  - PLOS One
DO  - 10.1371/journal.pone.0361593
UR  - https://doi.org/10.1371/journal.pone.0361593
AB  - Objective: Enfortumab vedotin (EV) and cisplatin (CDDP) are central treatments for advanced urothelial carcinoma, yet the influence of prior CDDP exposure on subsequent EV efficacy remains unclear. In this report, we characterized EV-related drug responses in a CDDP-resistant bladder cancer subline. Methods: A CDDP-resistant subline (HT1376-CR) was generated from parental bladder cancer cell (HT1376/P) through continuous exposure to CDDP. Sensitivities to CDDP, EV, and the EV payload monomethyl auristatin E (MMAE) were compared between HT1376-CR and HT1376/P. Nectin-4 expression, EV binding, and drug-resistance-related gene expression were evaluated. The effect of ABCB1 silencing on drug response was also examined. In vivo EV responses were explored using xenograft models. Results: HT1376-CR cells showed increased sensitivity to EV in vitro and in vivo. HT1376-CR cells were more sensitive to MMAE and showed greater G2/M accumulation after MMAE exposure. In contrast, cell-surface nectin-4 expression and EV binding were reduced. ABCB1 was markedly upregulated in HT1376-CR, and ABCB1 silencing increased sensitivity to CDDP, MMAE, and EV within the resistant subline. Conclusion: The CDDP-resistant HT1376 subline showed enhanced sensitivity to EV, and ABCB1 suppression further increased EV sensitivity within this resistant subline.
SN  - 1932-6203
ER  -