Related Experiment Video

Updated: Jan 28, 2026

Mechanism of Kemeng Fang's Inhibition of Podocyte Apoptosis in Rats with Membranous Nephropathy through the PI3K/AKT Signaling Pathway
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Mechanism of Kemeng Fang's Inhibition of Podocyte Apoptosis in Rats with Membranous Nephropathy through the PI3K/AKT Signaling Pathway

Published on: August 23, 2024

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NFIB suppresses cell migration, invasion and EMT of bladder cancer through the PI3K-AKT signaling pathway

Lu Shen1, Chong Yu2, Yanqian Wu3

  • 1Department of Clinical Laboratory, The First Affiliated Hospital of Zhejiang Chinese Medical University (Zhejiang Provincial Hospital of Chinese Medicine), Hangzhou, 310006 Zhejiang China.

Cytotechnology
|January 27, 2026
PubMed

Insights

Nuclear factor I B (NFIB) acts as a tumor suppressor in bladder cancer. It inhibits cell migration, invasion, and metastasis by downregulating the PI3K-AKT pathway, offering a potential therapeutic target.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cancer Genetics

Background:

  • Nuclear factor I B (NFIB) has a dual role in tumorigenesis, acting as either an oncogene or tumor suppressor depending on cancer type.
  • The specific function of NFIB in bladder cancer pathogenesis is not well-defined.

Purpose of the Study:

  • To investigate the biological role and molecular mechanisms of NFIB in bladder cancer.
  • To determine NFIB's impact on bladder cancer cell behavior and metastasis.

Main Methods:

  • Analysis of NFIB protein levels in bladder cancer tissues versus adjacent noncancerous tissues.
  • In vitro functional assays (Wound healing, Transwell invasion, CCK8) to assess cell proliferation, migration, and invasion.
  • In vivo experiments (Xenograft, Nude mouse tail vein transfer) to evaluate metastatic potential.
  • Transcriptomic analysis to identify affected signaling pathways.

Main Results:

  • NFIB protein expression is downregulated in bladder cancer tissues.
  • NFIB suppresses bladder cancer cell migration, invasion, and epithelial-mesenchymal transition (EMT) in vitro.
  • NFIB inhibits lung metastasis in vivo without affecting primary tumor growth.
  • NFIB activation hinders the PI3K-AKT signaling pathway.

Conclusions:

  • NFIB functions as a tumor suppressor gene in bladder cancer.
  • NFIB inhibits bladder cancer cell migration, invasion, and EMT via the PI3K-AKT pathway.
  • NFIB is a potential biomarker for early metastasis detection and a therapeutic target for bladder cancer.
Keywords:
Bladder cancerEMTInvasionMigrationNFIBPI3K-AKT

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