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FBXW7 in gastrointestinal cancers: from molecular mechanisms to therapeutic prospects
Wanqing Wang1, Xue Liu1, Lingling Zhao1
1Cancer Center, The First Hospital of Jilin University, Changchun, China.
Abstract:
F-box and WD repeat domain-containing 7 (FBXW7), formerly known as hCdc4, hAGO Fbw7, or SEL10, plays a specific recognition function in SCF-type E3 ubiquitin ligases. FBXW7 is a well-established cancer suppressor gene that specifically controls proteasomal degradation and destruction of many key oncogenic substrates. The FBXW7 gene is frequently abnormal in human malignancies especially in gastrointestinal cancers. Accumulating evidence reveals that mutations and deletions of FBXW7 are participating in the occurrence, progression and treatment resistance of human gastrointestinal cancers. Considering the current therapeutic challenges faced by gastrointestinal cancers, elucidating the biological function and molecular mechanism of FBXW7 can provide new perspectives and references for future personalized treatment strategies. In this review, we elucidate the key molecular mechanisms by which FBXW7 and its substrates are involved in gastrointestinal cancers. Furthermore, we discuss the consequences of FBXW7 loss or dysfunction in tumor progression and underscore its potential as a prognostic and therapeutic biomarker. Lastly, we propose potential therapeutic strategies targeting FBXW7 to guide the precision treatment of gastrointestinal cancers.
Insights
The F-box and WD repeat domain-containing 7 (FBXW7) gene acts as a tumor suppressor, crucial for degrading oncoproteins. Its dysfunction in gastrointestinal cancers drives progression and treatment resistance, highlighting its therapeutic potential.
Area of Science:
- Oncology
- Molecular Biology
- Biochemistry
Background:
- F-box and WD repeat domain-containing 7 (FBXW7) is an SCF-type E3 ubiquitin ligase substrate recognition component.
- FBXW7 functions as a critical tumor suppressor by targeting oncogenic proteins for proteasomal degradation.
- Alterations in FBXW7 are frequently observed in human cancers, particularly gastrointestinal malignancies.
Purpose of the Study:
- To review the molecular mechanisms of FBXW7 in gastrointestinal cancers.
- To discuss the role of FBXW7 dysfunction in tumor progression and treatment resistance.
- To explore FBXW7 as a prognostic and therapeutic biomarker for precision medicine.
Main Methods:
- Literature review of studies on FBXW7 function in cancer.
- Analysis of molecular mechanisms involving FBXW7 and its substrates.
- Discussion of clinical implications and therapeutic strategies.
Main Results:
- FBXW7 regulates the degradation of key oncoproteins implicated in gastrointestinal cancer development.
- Loss or mutation of FBXW7 contributes to cancer occurrence, progression, and resistance to therapy.
- FBXW7 status correlates with patient outcomes and treatment response.
Conclusions:
- FBXW7 is a pivotal regulator in gastrointestinal carcinogenesis.
- Targeting FBXW7 offers a promising avenue for precision treatment strategies in gastrointestinal cancers.
- FBXW7 holds significant potential as a biomarker for prognosis and therapeutic guidance.
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