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Study on the Effect of High Expression of TRIML1 on Liver Cancer

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It was first discovered that the TRIML1 coding substance is highly similar to the TRIM family protein in acute mice. The literature has reported that the TRIM family plays a vital role in many types of cancer, among which TRIML1, TRIM31, TRIM52, and TRIM59 can promote the occurrence and development of liver cancer. An animal model of liver cancer for research was established through nude mouse tumor formation experiments to explore drugs and methods for treating liver cancer.

Triple motif protein (TRIM) is an E3 ubiquitin-protein ligase with a conserved structure and rapid evolution. It has been reported that the TRIM family plays a vital role in many types of cancer, among which TRIML1, TRIM31, TRIM52, and TRIM59 can promote The occurrence and development of liver cancer; TRIM16, TRIM26, and TRIM50 can inhibit the occurrence and growth of liver cancer.

Medicilon boasts nearly 300 tumor evaluation models. At the same time, we are empowering innovative therapies to comprehensively evaluate and study immuno-oncology. We have completed model establishment and efficacy evaluation of immuno-therapies such as CAR-T, TCR-T, CAR-NK, oncolytic virus, antibody (monoclonal antibody, double antibody, polyclonal antibody, etc.), siRNA, AAV.

USP5 is a deubiquitinating enzyme that interacts with Slug to remove its ubiquitination, extend its half-life, and promote Slug’s transcription of downstream target genes.

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SLUG protein plays a vital role in the malignant onset of liver cancer in epithelial-mesenchymal transition. As an essential transcription factor in the epithelial-mesenchymal change, SLUG protein can promote the epithelial-mesenchymal growth of tumor cells by inhibiting the expression of E-cadherin. . Therefore, SLUG and its interacting proteins can be used as potential targets for the development of anti-liver cancer drugs. At the level of cell function, USP5 can promote EMT of liver cancer, and it depends on the expression of Slug, which is also supported by data at the animal and clinicopathological levels. In conclusion. Studies have shown that USP5 can deubiquitinate the Slug to insert it stably. The cell experiment results on the page show that knocking down USP5 can inhibit the epithelial-mesenchymal transition of liver cancer.

Establish animal models of liver cancer through nude mouse tumor formation experiments, explore compounds that can inhibit the migration and invasion of liver cancer through in vivo and in vitro pharmacodynamic experiments, and promote the development of anti-tumor drugs. Primary research and experimental research on human cancer in medicine often use nude mouse tumor formation experiments. Medicilon Pharmacology Services can provide naked mouse tumor formation experiments to help customers conduct medical research.


USP5 is an oncogene of liver cancer, which can promote the occurrence and development of liver cancer, and TRIML1 can interact with USP5. Explore the effect of triple motif family-like 1 (TRIML1) on liver cancer, and provide new ideas for the treatment of liver cancer.

The researchers screened and identified stable strains overexpressing TRIML1 in HepG2 liver cancer cells, using the CCK8 method to detect the growth and reproduction activity of regular strains overexpressing TRIML1; soft agar clone formation experiments analyzed the cloning ability of stable strains overexpressing TRIML1 [1].

The tumorigenesis experiment in nude mice analyzed the tumorigenesis ability of animals overexpressing the stable TRIML1 strain. Using yeast cytokine TNF-α to stimulate overexpression of TRIML1 steady pressure and the opposite control for eighth, cell supernatant can be detected, and ELISA can see IL-6 secretion. Small interfering RNA (siRNA) was used to knock down TRIML1 in Huh7 liver cancer cells. The ball formation experiment was used to detect the effect of the knockdown of TRIML1 on the growth of Huh7 and cause the supernatant to see IL-6 secretion. The study found that TRIML1 can significantly promote the malignant growth of liver tumors in vivo and in vitro, and the effect may be related to the increased expression of IL-6.

Studies have also shown that TRIML1 promotes the malignant growth of liver cancer cells, and the role of TRIML1 in the migration, invasion, and drug resistance of liver cancer cells remains to be further studied.

TRIML1 is a molecular marker that can significantly promote the malignant growth of liver cancer in vivo and in vitro. Therefore, TRIML1 is expected to become the application of molecular markers for liver cancer and has guiding significance for subsequent clinical treatment. To prepare pharmaceutical compositions for the prevention or treatment of liver cancer to be used in the research of clinical applications such as gene therapy of liver cancer and drug treatment.

[1] The effect of TRIML1 on the malignant growth of hepatic fibrin[J].

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