ArticleAging2021
RNF168 is highly expressed in esophageal squamous cell carcinoma and contributes to the malignant behaviors in association with the Wnt/β-catenin signaling pathway.
Article in Aging, 2021. 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, 15 citations in OpenAlex.
- Ubiquitin System-Driven Proteostasis in DNA Damage Response.International journal of molecular sciences · 2026Review
- Long-term SiNPs exposure induced genetic instability and malignant transformation via SQSTM1/p62-mediated autophagy dysfunction in lungs.Materials today. Bio · 2025Article
- Review
- RNF126, 168 and CUL1: The Potential Utilization of Multi-Functional E3 Ubiquitin Ligases in Genome Maintenance for Cancer Therapy.Biomedicines · 2023Review
- Identification of hub genes and microRNAs with prognostic values in esophageal cancer by integrated analysis.Non-coding RNA research · 2023Article
- Ubiquitination Links DNA Damage and Repair Signaling to Cancer Metabolism.International journal of molecular sciences · 2023Review
- Roles of oncogenes in esophageal squamous cell carcinoma and their therapeutic potentials.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2023Review
- Emerging Roles of RNF168 in Tumor Progression.Molecules (Basel, Switzerland) · 2023Review
- Wnt signaling pathway-related gene PRICKLE1 is a prognostic biomarker for esophageal squamous cell carcinoma.Frontiers in oncology · 2022Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
E3 ubiquitin ligase RING finger protein 168 (RNF168) is one of the key proteins in DNA damage repair. Abnormal expression of RNF168 has recently been found in some tumors. However, the role of RNF168 in the development of esophageal squamous cell carcinoma (ESCC) has not been fully elucidated. Here we report that expression of RNF168 in esophageal squamous cell carcinoma is increased with respect to normal esophageal epithelial tissue. Notably, in ESCC patients, increased RNF168 expression was associated with tumor stage and depth of invasion. Knockdown of the RNF168 gene inhibited proliferation of esophageal cancer cells, promoted cell apoptosis, and interfered with cell movement, ultimately inhibiting tumor xenograft growth. Mechanistic studies showed that RNF168 influenced the malignant behavior of esophageal cancer cells by regulating the Wnt/ β-catenin signaling pathway. In addition, RNF168 expression was positively correlated with wingless-type MMTV integration site family member 3A (WNT3A) expression, and high expression of RNF168 and WNT3A predicted a low survival rate. In conclusion, our findings highlight the important role of RNF168 in ESCC tumorigenesis and provide new biomarkers and therapeutic targets for the treatment of ESCC.
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