التفاصيل البيبلوغرافية
| العنوان: |
FOXP4 inhibits squamous differentiation of atypical cells in cervical intraepithelial neoplasia via an ELF3‐dependent pathway. |
| المؤلفون: |
Matsumoto, Takeo, Iizuka, Takashi, Nakamura, Mitsuhiro, Suzuki, Takuma, Yamamoto, Megumi, Ono, Masanori, Kagami, Kyosuke, Kasama, Haruki, Wakae, Kousho, Muramatsu, Masamichi, Horike, Shin‐ichi, Kyo, Satoru, Yamamoto, Yasuhiko, Mizumoto, Yasunari, Daikoku, Takiko, Fujiwara, Hiroshi |
| المصدر: |
Cancer Science; Oct2022, Vol. 113 Issue 10, p3376-3389, 14p |
| مستخلص: |
Although the human papillomavirus (HPV) vaccine is effective for preventing cervical cancers, this vaccine does not eliminate pre‐existing infections, and alternative strategies have been warranted. Here, we report that FOXP4 is a new target molecule for differentiation therapy of cervical intraepithelial neoplasia (CIN). An immunohistochemical study showed that FOXP4 was expressed in columnar epithelial, reserve, and immature squamous cells, but not in mature squamous cells of the normal uterine cervix. In contrast with normal mature squamous cells, FOXP4 was expressed in atypical squamous cells in CIN and squamous cell carcinoma lesions. The FOXP4‐positive areas significantly increased according to the CIN stages from CIN1 to CIN3. In monolayer cultures, downregulation of FOXP4 attenuated proliferation and induced squamous differentiation in CIN1‐derived HPV 16‐positive W12 cells via an ELF3‐dependent pathway. In organotypic raft cultures, FOXP4‐downregulated W12 cells showed mature squamous phenotypes of CIN lesions. In human keratinocyte‐derived HaCaT cells, FOXP4 downregulation also induced squamous differentiation via an ELF3‐dependent pathway. These findings suggest that downregulation of FOXP4 inhibits cell proliferation and promotes the differentiation of atypical cells in CIN lesions. Based on these results, we propose that FOXP4 is a novel target molecule for nonsurgical CIN treatment that inhibits CIN progression by inducing squamous differentiation. [ABSTRACT FROM AUTHOR] |
|
Copyright of Cancer Science is the property of Wiley-Blackwell and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.) |
| قاعدة البيانات: |
Complementary Index |
Full Text Finder