ArticleBioengineered2022
B7 family member H4 induces epithelial-mesenchymal transition and promotes the proliferation, migration and invasion of colorectal cancer cells.
Article in Bioengineered, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 11 citations in OpenAlex.
- The B7 family subgroup reflects tumor cell heterogeneity and patient post-operative prognosis in gallbladder cancer.Biology direct · 2026Article
- Investigation of the Effects of B7H4 (rs10754339 A>G) Gene Polymorphism and Serum Level on Breast Cancer Susceptibility.Asian Pacific journal of cancer prevention : APJCP · 2025Article
- Immune checkpoint blockade for cancer therapy: current progress and perspectives.Journal of Zhejiang University. Science. B · 2025Review
- B7H4 Role in Solid Cancers: A Review of the Literature.Cancers · 2024Review
- The loss of B7-H4 expression in breast cancer cells escaping from T cell cytotoxicity contributes to epithelial-to-mesenchymal transition.Breast cancer research : BCR · 2023Article
- Article
- Genomic landscape and expression profile of consensus molecular subtype four of colorectal cancer.Frontiers in immunology · 2023Article
- HHLA2 promotes tumor progression by long non‑coding RNA H19 in human gallbladder cancer.International journal of oncology · 2022Article
- The expression pattern of Immune checkpoints after chemo/radiotherapy in the tumor microenvironment.Frontiers in immunology · 2022Review
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Colorectal cancer (CRC) is a common malignancy of the gastrointestinal tract, which has the second highest incidence among gastrointestinal tumors. At present, due to the limitations of current CRC treatment strategies, there is an urgent need for developing more effective therapies. B7 family member H4 (B7-H4) is associated with the progression of a wide spectrum of cancers, but its functional role in CRC is unknown. The purpose of this study is to clarify the role of B7-H4 in CRC and the underlying mechanisms in controlling the progression of CRC. Our data showed that B7-H4 expression in CRC tissues and cell lines was significantly upregulated as compared with normal tissues and normal cell lines. High B7-H4 expression was correlated with a poor prognosis of CRC patients. B7-H4 overexpression promoted the proliferation and invasion of CRC cells, which could be suppressed by Wnt signaling inhibitor. In a mouse xenograft model, silencing B7-H4 suppressed tumor growth and epithelial-mesenchymal transition (EMT) of CRC cells. Collectively, our study demonstrated the oncogenic roles of B7-H4 in regulating the proliferation, EMT as well as the migration of CRC cells through Wnt signaling pathway. The heightened expression of B7-H4 could serve as a prognostic marker for CRC patients.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.