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<p>Colorectal cancer (CRC) poses a threat to the health of people worldwide. Long noncoding RNAs (lncRNAs) have been reported to play a key role in regulating carcinogenesis, including CRC. In this study, the levels of lncRNA FOXP4-AS1 were analyzed in CRC specimens and cells via qRT-PCR. The impacts of FOXP4-AS1 on CRC cell metastasis were investigated. Then, the silver staining assay, western blot, RIP, Co-IP, and immunofluorescence were conducted to explore and validate the molecular mechanisms by which FOXP4-AS1 affects CRC progression. We discovered that FOXP4-AS1 expression was markedly elevated in CRC. Functionally, FOXP4-AS1 knockdown suppressed CRC cell migration, invasion, and EMT. Also, FOXP4-AS1 silencing weakened CRC tumor growth in vivo. Mechanistically, we identified that FOXP4-AS1 functioned as a scaffold to simultaneously bind USP7 and ZEB1, and regulated the ubiquitination and expression of ZEB1 by binding to USP7. Rescue experiments demonstrated that USP7 inhibitor P005091 abolished the promotion of cell metastasis by FOXP4-AS1 overexpression. Furthermore, ZEB1 overexpression reversed the impact of silencing FOXP4-AS1 on cell metastasis. Collectively, our work revealed the molecular mechanism and role of FOXP4-AS1-mediated USP7-ZEB1 axis in CRC.</p>

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LncRNA FOXP4-AS1 facilitates colorectal cancer invasion and migration by enhancing USP7 interaction with ZEB1

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年1月4日

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  • Xiaoling Yang,
  • Chenglong Shen,
  • Yuchen Yuan,
  • Jiazhe Shao,
  • Haichen Liu,
  • Yichen Li,
  • Guoqiang Zhou,
  • Zhiliang Shi

摘要

Colorectal cancer (CRC) poses a threat to the health of people worldwide. Long noncoding RNAs (lncRNAs) have been reported to play a key role in regulating carcinogenesis, including CRC. In this study, the levels of lncRNA FOXP4-AS1 were analyzed in CRC specimens and cells via qRT-PCR. The impacts of FOXP4-AS1 on CRC cell metastasis were investigated. Then, the silver staining assay, western blot, RIP, Co-IP, and immunofluorescence were conducted to explore and validate the molecular mechanisms by which FOXP4-AS1 affects CRC progression. We discovered that FOXP4-AS1 expression was markedly elevated in CRC. Functionally, FOXP4-AS1 knockdown suppressed CRC cell migration, invasion, and EMT. Also, FOXP4-AS1 silencing weakened CRC tumor growth in vivo. Mechanistically, we identified that FOXP4-AS1 functioned as a scaffold to simultaneously bind USP7 and ZEB1, and regulated the ubiquitination and expression of ZEB1 by binding to USP7. Rescue experiments demonstrated that USP7 inhibitor P005091 abolished the promotion of cell metastasis by FOXP4-AS1 overexpression. Furthermore, ZEB1 overexpression reversed the impact of silencing FOXP4-AS1 on cell metastasis. Collectively, our work revealed the molecular mechanism and role of FOXP4-AS1-mediated USP7-ZEB1 axis in CRC.