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: Annexin, a calcium-dependent phospholipid binding protein, can affect tumor cell adhesion, proliferation, apoptosis, invasion and metastasis, as well as tumor neovascularization in different ways. Recent studies have shown that annexin exists not only as an intracellular protein in tumor cells, but also in different ways to be secret outside the cell as a “crosstalk” tool for tumor cells and tumor microenvironment, thus playing an important role in the development of tumors, such as participating in epithelial-mesenchymal transition, regulating immune cell behavior, promoting neovascularization and so on. The mechanism of annexin secretion in the form of extracellular vesicles and its specific role is still unclear. This paper summarizes the main role of annexin secreted into the extracellular space in the form of extracellular vesicles in tumorigenesis and drug resistance and analyzes its possible mechanism.

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Background RAC1 is involved in many physiological processes such as cytoskeleton regulation, and is highly related to the occurrence and development of various tumors. The global characterization of RAC1 in different tumor backgrounds is necessary to understand the mechanism of RAC1 involved in tumor progression Methods Based on the data of The Cancer Genome Atlas (TCGA), Gene Expression Omnibu (GEO), Human Protein Atlas (HPA), Genotype-Tissue Expression (GTEx) and so on, this paper comprehensively expounded the expression and prognosis of RAC1 in different tumors, and further analyzed the effects of genetic changes (gene mutation, epigenetic changes) of RAC1 on expression and immune infiltration on prognosis. Results RAC1 was highly expressed in most tumors and was associated with poor prognosis. Gene mutation, alternative splicing events and methylation of RAC1 may affect the abnormal expression of RAC1 in tumors. Interestingly, we found that RAC1-related immune cell infiltration was consistent between endothelial cells and fibroblasts, and RAC1-related macrophage infiltration in LIHC and LUAD was consistent with poor patient outcomes. Conclusions We have enriched the tumor-promoting role of RAC1 in different tumor profiles as a whole and speculated the intrinsic link, providing a basis for the search for potential biomarker.