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Peer-reviewedCC BY 4.0Molecular & Cellular Oncology

Claudin 1 promotes blood-borne metastasis by modulating the Src/Ezrin signaling pathway in high-CLDN1 triple-negative breast cancer model

  • Huiping Yang1
  • Hong Lu2
  • Wei Wang1
  • Junchao Ma1
  • Ling Xiong1
  • Yong Zou1
  • Jianjiang Fu1,3
  1. 1Department of Pharmacology, School of Pharmacy, Jiangxi University of Chinese Medicine, Nanchang, Jiangxi Province, China
  2. 2Network and Information Technology Center, Jiangxi University of Chinese Medicine, Nanchang, Jiangxi Province, China
  3. 3Tumor Therapeutics Research Laboratory, Jiangxi Province Key Laboratory for Diagnosis, Treatment, and Rehabilitation of Cancer in Chinese Medicine, Nanchang, Jiangxi Province, China
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Abstract

This study aimed to elucidate the role and mechanism of CLDN1 in regulating migration and metastasis in triple‑negative breast cancer (TNBC). In vivo, an orthotopic TNBC model was used to evaluate circulating tumor cells and lung metastasis; in vitro, cell migration, F‑actin organization, and protein expression were examined in cultured TNBC cells. CLDN1 was knocked down or overexpressed via lentiviral constructs, and Ezrin was silenced by siRNA in CLDN1‑overexpressing cells. Pharmacological targeting of CLDN1 with PDS‑0330 specifically reduced migration in MDA‑MB‑468 cells but not in MDA‑MB‑231 cells; knock-down and knock‑in experiments further confirmed that CLDN1 critically determines the migratory and metastatic capacity of TNBC cells with high CLDN1 expression. Analysis of Ezrin and its interaction with podocalyxin revealed that Ezrin significantly contributes to CLDN1‑promoted migration, and our data also indicated that CLDN1 facilitates Src signaling activation. Collectively, these findings demonstrate that in TNBC with high CLDN1 expression, CLDN1 plays a pivotal role in regulating migration and hematogenous metastasis, likely through upregulating the Src/Ezrin pathway.

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Cite

BibTeXRIS
BibTeX
@article{yang2026claudin,
  title = {{Claudin 1 promotes blood-borne metastasis by modulating the Src/Ezrin signaling pathway in high-CLDN1 triple-negative breast cancer model}},
  author = {Huiping Yang and Hong Lu and Wei Wang and Junchao Ma and Ling Xiong and Yong Zou and Jianjiang Fu},
  journal = {Molecular \& Cellular Oncology},
  year = {2026},
  month = oct,
  doi = {10.1080/23723556.2026.2749929},
  url = {https://doi.org/10.1080/23723556.2026.2749929},
  note = {CC BY 4.0},
}
RIS
TY  - JOUR
TI  - Claudin 1 promotes blood-borne metastasis by modulating the Src/Ezrin signaling pathway in high-CLDN1 triple-negative breast cancer model
AU  - Huiping Yang
AU  - Hong Lu
AU  - Wei Wang
AU  - Junchao Ma
AU  - Ling Xiong
AU  - Yong Zou
AU  - Jianjiang Fu
PY  - 2026
DA  - 2026/10/23
JO  - Molecular & Cellular Oncology
DO  - 10.1080/23723556.2026.2749929
UR  - https://doi.org/10.1080/23723556.2026.2749929
AB  - This study aimed to elucidate the role and mechanism of CLDN1 in regulating migration and metastasis in triple‑negative breast cancer (TNBC). In vivo, an orthotopic TNBC model was used to evaluate circulating tumor cells and lung metastasis; in vitro, cell migration, F‑actin organization, and protein expression were examined in cultured TNBC cells. CLDN1 was knocked down or overexpressed via lentiviral constructs, and Ezrin was silenced by siRNA in CLDN1‑overexpressing cells. Pharmacological targeting of CLDN1 with PDS‑0330 specifically reduced migration in MDA‑MB‑468 cells but not in MDA‑MB‑231 cells; knock-down and knock‑in experiments further confirmed that CLDN1 critically determines the migratory and metastatic capacity of TNBC cells with high CLDN1 expression. Analysis of Ezrin and its interaction with podocalyxin revealed that Ezrin significantly contributes to CLDN1‑promoted migration, and our data also indicated that CLDN1 facilitates Src signaling activation. Collectively, these findings demonstrate that in TNBC with high CLDN1 expression, CLDN1 plays a pivotal role in regulating migration and hematogenous metastasis, likely through upregulating the Src/Ezrin pathway.
SN  - 2372-3556
ER  -