ArticleBioengineered2022
Overexpression of OTU domain-containing ubiquitin aldehyde-binding protein 1 exacerbates colorectal cancer malignancy by inhibiting protein degradation of β-Catenin via Ubiquitin-proteasome pathway.
Article in Bioengineered, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 15 citations in OpenAlex.
- METTL3‑mediated OTUB1 sustains PD‑L1 protein stability via deubiquitination and promotes immune evasion in oral squamous cell carcinoma.Molecular and cellular biochemistry · 2026Article
- Silencing OTUB1 induces pyroptosis to inhibit the growth of liver cancer HepG2 cells via the NLRP3/caspase/GSDM signaling pathway.Journal of gastrointestinal oncology · 2026Article
- OTU deubiquitinases in cancer pathogenesis and precision therapy.American journal of cancer research · 2025Review
- Dissecting the dual role of OTU family proteins in tumor progression and immune escape.Frontiers in immunology · 2025Review
- Review
- Role of protein degradation systems in colorectal cancer.Cell death discovery · 2024Review
- Review
- Target deubiquitinase OTUB1 as a therapeatic strategy for BLCA via β-catenin/necroptosis signal pathway.International journal of biological sciences · 2024Article
- OTUB1 Promotes Glioblastoma Growth by Inhibiting the JAK2/STAT1 Signaling Pathway.Journal of Cancer · 2024Article
- Inhibition of OTUB2 suppresses colorectal cancer cell growth by regulating β-Catenin signaling.American journal of cancer research · 2023Article
- TRIM9 Interacts with ZEB1 to Suppress Esophageal Cancer by Promoting ZEB1 Protein Degradation via the UPP Pathway.BioMed research international · 2023Article
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
Although major advances were achieved in colorectal cancer (CRC) therapy, major concerns still remain on proper control of cancer metastasis and chemo-resistance in order to achieve satisfactory general treatment response. Previous studies suggested that OTUB1 (OTU domain-containing ubiquitin aldehyde-binding protein 1) serves as regulator of gene ubiquitination and participates in the pathogenesis of multiple malignancies. Therefore, to discover its molecular mechanism in CRC tumor growth and metastasis will contribute in CRC treatment strategy development. Clinical tissues and CRC cancer cell lines were utilized to evaluate OTUB1 expression pattern. Functional tests including cellular proliferation, migration and invasion, as well as chemo-resistance, etc., were evaluated to investigate the role of OTUB1/β-catenin regulatory pathway on CRC malignant biological behaviors. Both CRC tumor tissues and CRC cell lines exhibited promoted OTUB1 expression level. Subsequent experiments further suggested that OTUB1 promoted CRC malignancy by enhancing protein stability of β-catenin, via inhibition of its protein degradation by UPP pathway, which indicated its crucial role in enhancement of CRC tumor cellular proliferative and chemo-resistant capabilities. This study reported that OTUB1 exhibited novel pro-survival and pro-metastatic function by interaction of β-Catenin via Ubiquitin-proteasome pathway. Our research indicated that OTUB1/β-Catenin regulatory axis might be potential druggable target for CRC cancer patients' treatment.
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