<![CDATA[Background: The ubiquitin system is one of the mechanisms that regulates cell function, signalling, and cancer cell growth. Ubiquitin involves the E3 ubiquitin ligase to help mark and degrade target proteins. Recent research has shown that tripartite motif-containing 56 (TRIM56), an E3 ubiquitin ligase, can modulate protein stability through a ubiquitination mechanism that contributes to the transformation and progression of cancer cells. Another protein that can act as an E3 ubiquitin ligase is the aryl hydrocarbon receptor (AhR), known to be involved in the development of various types of cancer through different molecular mechanisms. Although both have been reported to affect cancer growth, studies on the functional linkage between TRIM56 and AhR are limited. Therefore, this scoping review was conducted to focus on identifying the key concepts and analysing the knowledge gaps of the potential role of TRIM56 and AhR in cancer growth and their linkage. Thus, this review can serve as a reference for further research. Methods: This study was conducted through a literature review, using a combination of Boolean OR and AND operators to search the Scopus and PubMed databases from 2015 to 2025 with keywords ("ubiquitination" OR "ubiquitin ligase" OR "e3") AND TRIM56 OR AhR OR "arylhydrocarbon receptor" AND cancer. Result: The expression of TRIM56 and AhR can serve as biomarkers in several types of cancer. Both proteins have a dual role, either suppressing or promoting cell proliferation by mediating the degradation or modification of various target proteins, thereby influencing cancer progression. TRIM56 and AhR are expressed in multiple cancers and are involved in similar signalling pathways, including ubiquitin, STING, Toll-like Receptor, NF-kB, and Wnt signalling pathways. Conclusion: TRIM56 and AhR affect cancer cell proliferation within the same cancer type through the ubiquitin, STING, Toll-like receptor, NF-κB, and Wnt signalling pathways.]]>
