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Updated: Oct 4, 2025

Purification of Ubiquitinated p53 Proteins from Mammalian Cells
Published on: March 21, 2022
PTBP3 modulates P53 expression and promotes colorectal cancer cell proliferation by maintaining UBE4A mRNA stability
Canbin Xie1, Fei Long1, Liang Li1
1Department of Gastrointestinal Surgery, The Third XiangYa Hospital of Central South University, Changsha, Hunan, 410013, China.
Abstract:
The RNA binding protein PTBP3 was recently reported to play a critical role in multiple cancers, and the molecular mechanisms involved RNA splicing, 3' end processing and translation. However, the role of PTBP3 in colorectal cancer (CRC) remains poorly explored. Herein, PTBP3 was upregulated in CRC and associated with a poor prognosis. PTBP3 knockdown in colorectal cancer cell lines restricted CRC proliferative capacities in vitro and in vivo. Mechanistically, PTBP3 regulated the expression of the E3 ubiquitin ligase UBE4A by binding the 3' UTR of its mRNA, preventing its degradation. UBE4A participated in P53 degradation, and PTBP3 knockdown in colorectal cancer cell lines showed increased P53 expression. UBE4A overexpression rescued PTBP3 knockdown-induced inhibition of CRC cell proliferation and P53 expression. Our results demonstrated that PTBP3 plays an essential role in CRC cell proliferation by stabilizing UBE4A to regulate P53 expression and may serve as a new prognostic biomarker and effective therapeutic target for CRC.
Insights
The RNA binding protein PTBP3 promotes colorectal cancer (CRC) growth by stabilizing UBE4A, which degrades P53. PTBP3 may serve as a prognostic biomarker and therapeutic target for CRC patients.
Area of Science:
- Molecular Oncology
- RNA Biology
Background:
- The RNA binding protein PTBP3 is implicated in various cancers.
- Its specific role in colorectal cancer (CRC) is not well understood.
Purpose of the Study:
- To investigate the role and molecular mechanisms of PTBP3 in colorectal cancer (CRC).
Main Methods:
- PTBP3 expression analysis in CRC tissues.
- PTBP3 knockdown in CRC cell lines (in vitro and in vivo).
- Analysis of UBE4A and P53 expression and interaction with PTBP3 mRNA.
Main Results:
- PTBP3 is upregulated in CRC and correlates with poor prognosis.
- PTBP3 knockdown inhibits CRC cell proliferation.
- PTBP3 stabilizes UBE4A mRNA, leading to P53 degradation.
- UBE4A overexpression rescues PTBP3 knockdown effects.
Conclusions:
- PTBP3 promotes CRC proliferation by stabilizing UBE4A and regulating P53.
- PTBP3 is a potential prognostic biomarker and therapeutic target for CRC.
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