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Aberrant expression of claudin-6 contributes to malignant potentials and drug resistance of cervical adenocarcinoma.
Ito, Yui; Takasawa, Akira; Takasawa, Kumi; Murakami, Taro; Akimoto, Taishi; Kyuno, Daisuke; Kawata, Yuka; Shano, Kodai; Kirisawa, Kurara; Ota, Misaki; Aoyama, Tomoyuki; Murata, Masaki; Sugimoto, Kotaro; Chiba, Hideki; Saito, Tsuyoshi; Osanai, Makoto.
Afiliación
  • Ito Y; Department of Pathology, Sapporo Medical University School of Medicine, Sapporo, Japan.
  • Takasawa A; Department of Pathology, Sapporo Medical University School of Medicine, Sapporo, Japan.
  • Takasawa K; Department of Pathology, Sapporo Medical University School of Medicine, Sapporo, Japan.
  • Murakami T; Department of Pathology, Sapporo Medical University School of Medicine, Sapporo, Japan.
  • Akimoto T; Department of Obstetrics and Gynecology, Sapporo Medical University School of Medicine, Sapporo, Japan.
  • Kyuno D; Department of Pathology, Sapporo Medical University School of Medicine, Sapporo, Japan.
  • Kawata Y; Department of Pathology, Sapporo Medical University School of Medicine, Sapporo, Japan.
  • Shano K; Department of Pathology, Sapporo Medical University School of Medicine, Sapporo, Japan.
  • Kirisawa K; Department of Pathology, Sapporo Medical University School of Medicine, Sapporo, Japan.
  • Ota M; Department of Obstetrics and Gynecology, Sapporo Medical University School of Medicine, Sapporo, Japan.
  • Aoyama T; Department of Pathology, Sapporo Medical University School of Medicine, Sapporo, Japan.
  • Murata M; Department of Pathology, Sapporo Medical University School of Medicine, Sapporo, Japan.
  • Sugimoto K; Department of Basic Pathology, Graduate School of Medicine, Fukushima Medical University, Fukushima, Japan.
  • Chiba H; Department of Basic Pathology, Graduate School of Medicine, Fukushima Medical University, Fukushima, Japan.
  • Saito T; Department of Obstetrics and Gynecology, Sapporo Medical University School of Medicine, Sapporo, Japan.
  • Osanai M; Department of Pathology, Sapporo Medical University School of Medicine, Sapporo, Japan.
Cancer Sci ; 113(4): 1519-1530, 2022 Apr.
Article en En | MEDLINE | ID: mdl-35100472
Recent studies have revealed that aberrant expression of tight junction (TJ) proteins is a hallmark of various solid tumors and it is recognized as a useful therapeutic target. Claudin-6 (CLDN6), a member of the family of TJ transmembrane proteins, is an ideal therapeutic target because it is not expressed in human adult normal tissues. In this study, we found that CLDN6 is highly expressed in uterine cervical adenocarcinoma (ADC) and that high CLDN6 expression was correlated with lymph node metastasis and lymphovascular infiltration and was an independent prognostic factor. Shotgun proteome analysis revealed that cell-cell adhesion-related proteins and drug metabolism-associated proteins (aldo-keto reductase [AKR] family proteins) were significantly increased in CLDN6-overexpressing cells. Furthermore, overexpression of CLDN6 enhanced cell-cell adhesion properties and attenuated sensitivity to anticancer drugs including doxorubicin, daunorubicin, and cisplatin. Taken together, the results indicate that aberrant expression of CLDN6 enhances malignant potentials and drug resistance of cervical ADC, possibly due to increased cell-cell adhesion properties and drug metabolism. Our findings provide an insight into a new therapeutic strategy, a CLDN6-targeting therapy, against cervical ADC.
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Adenocarcinoma / Neoplasias del Cuello Uterino Tipo de estudio: Prognostic_studies Límite: Adult / Female / Humans Idioma: En Revista: Cancer Sci Año: 2022 Tipo del documento: Article País de afiliación: Japón Pais de publicación: Reino Unido
Texto completo
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Adenocarcinoma / Neoplasias del Cuello Uterino Tipo de estudio: Prognostic_studies Límite: Adult / Female / Humans Idioma: En Revista: Cancer Sci Año: 2022 Tipo del documento: Article País de afiliación: Japón Pais de publicación: Reino Unido