Background HCC is an extremely malignant tumor with a very poor prognosis. In 2023, a brand-new kind of cell death known as disulfidptosis was identified. Although, the prognosis as well as expression of immune checkpoints that are closely connected with it in HCC remain unknown. Methods In this work, we identified 49 genes with abnormal expression in liver cancer and normal liver tissue, with 23 of them being differentially expressed genes. To create a signature, we classified all HCC cases into three subtypes and used the TCGA database to evaluate each relevant gene’s prognostic value for survival. Results Five gene signatures were identified using the LASSO Cox regression approach, while those diagnosed with HCC were split into either low- or high-risk groups. Patients having low-risk HCC showed a much greater likelihood of surviving than those with high risk (p < 0.05). Through immune cell infiltration analysis, it was found that immune-related genes were abundant in high-risk groups and had reduced immune status. Conclusion In conclusion, immune checkpoint genes highly associated with disulfidptosis contribute to tumor immunity and can be used to evaluate HCC prognosis. When it comes to predicting overall survival (OS) time in HCC, risk score has been set to be a separate predictor. Through immune cell infiltration analysis, it was found that immune-related genes were abundant in high-risk groups and had reduced immune status. It is possible to measure the prognosis of HCC based on immune checkpoints genes strongly linked to disulfidptosis.
Background Molecule interacting with CasL-like protein 2 (MICALL2) is believed to regulate cytoskeleton dynamics, tight junction formation, and neurite outgrowth. However, its biological role and the underlying mechanism in colorectal cancer (CRC) remain largely elusive. Methods qRT-PCR, Western blotting and immunohistochemistry assays were used to detect the expression levels of different genes. Next, mass spectrometry, co-immunoprecipitation and immunofluorescence staining were used to detect the interactions of proteins. Furthermore, MTT assay, colony formation assay, wound-healing assays and xenograft tumor models were performed to demonstrate the functions of MICALL2 in CRC. In addition, transcriptome sequencing and Western blotting were conducted to verify the mechanism of MICALL2 in CRC. Results We found that both mRNA and protein levels of MICALL2 are up-regulated in colorectal cancer tissues compared with non-tumor tissues and that its overexpression is closely correlated with poor prognosis. Ubiquitin E3 ligase Tripartite motif-containing protein 21 (TRIM21) mediated MICALL2 ubiquitination and proteasome-dependent degradation, negatively correlated with MICALL2 levels, and reversely regulated the tumorigenic activity of MICALL2 in CRC. Functional studies confirmed that MICALL2 promoted colorectal cancer cell growth and migration via the Wnt/β-catenin signaling pathway. Conclusions As a substrate of ubiquitinase TRIM21, MICALL2 enhances the growth and migration of colorectal cancer cells and activates the Wnt/β-catenin signaling pathway.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
hi@scite.ai
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
Copyright © 2024 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.