Background: Breast cancer has become one of the most prevalent malignant neoplasms among women, poses a significant threat to public health. As a member of the tetraspanin family of proteins, CD151 is implicated in tumor progression and has been shown to regulate various cellular and molecular mechanisms that drive malignancy. However, the specific functions of CD151 in triple-negative breast cancer (TNBC) remain unclear. In this study, we aimed to investigate the pro-tumorigenic role of CD151 in TNBC by focusing on its interaction with integrin α 3β 1, which often forms a complex with CD151. Methods: Our study first evaluated CD151 expression in clinical samples from TNBC patients and TNBC cell lines by immunohistochemistry and Western blotting analysis. Through RNA interference (RNAi) and constructed overexpressed plasmids, we further validated the impact of CD151 on the migration and invasion of TNBC cells. Then the differentially expressed genes were screened by single-cell RNA sequencing, and these genes were enriched and analyzed. Co-immunoprecipitation studies demonstrated the binding of CD151 with integrin α 3β 1. Western blotting analysis was used to evaluate the expression of proteins related to epithelial-mesenchymal transition (EMT) and Mitogen-activated protein kinase (MAPK) signaling pathway. Results: CD151 is highly expressed in TNBC tissues and cell lines. It enhanced the migration and invasive ability of TNBC cells by promoting EMT. Co-IP demonstrated the binding of CD151 and integrin α 3β 1. In addition, we found that knockdown of either integrin α 3β 1 or CD151 reduced the migration and invasion of TNBC cells in vitro. Western blot analysis revealed that the CD151-integrin α 3β 1 complex could activate the MAPK signaling pathway in TNBC cells, subsequently leading to EMT of these cells. Conclusion: Based on our findings, we propose a novel mechanism by which CD151 mediates tumor progression through the initiation of EMT. This suggests that CD151 could be considered a potential therapeutic target for TNBC.

As a member of the tetraspanin superfamily, CD151 plays a pivotal role in tumorigenesis, progression, and metastasis. CD151 is involved in various cellular processes, including cell-cell junction, signal transduction, epithelial-mesenchymal transition (EMT), cancer stem cell maintenance (CSCs), angiogenesis, and exosome regulation. Therefore, CD151 is a potential target for tumor therapy and may be valuable in tumor diagnosis and prognosis. Notably, while CD151 predominantly functions as an oncogene in most cancers, it can also exhibit tumor-suppressive roles in specific contexts, indicating that its function is context-dependent. Additionally, CD151 plays a significant role in modulating the immune microenvironment. For instance, CD151 supports the proliferation, activation, and migration of T cells. The CD151 peptide may function as a tumor vaccination by stimulating CD8 + IFNγ + lymphocytes and inducing cytotoxic effects. Thus, the function of CD151 in tumors is intricate and warrants further investigation. In this review, we discuss the diagnostic and prognostic potential of CD151, as well as its regulatory roles in solid cancers, including those of the digestive system, lung, breast, prostate, and gynecological tissues. Basic experiments and clinical data demonstrate the beneficial and detrimental effects of CD151 in malignancies and offer a path forward for future investigation.

Background The mechanism for ultraviolet A (UVA) involvement in age-related macular degeneration (AMD) is unclear. We examined the levels of autophagy-related proteins and ubiquitination of cell proteins after acute UVA exposure and determined whether UVA causes AMD by affecting autophagy in retinal pigment epithelium (RPE) cells. Methods Western blotting was used to determine the level of Beclin-1, LC3, and p62 in ARPE-19 cells exposed to UVA. Co-immunoprecipitation was used to detect the ubiquitination of proteins in cells. Cell viability was determined with a CGD1 assay. Results UVA irradiation increased the level of LC3 and the conversion of LC3-I to LC3-II in ARPE-19 cells within 24 h, inhibition of autophagy by NH4CL reversed the effect of UVA, and suppression of proteasomes by Epoxomicin (EPO) did not enhance the effect of UVA. UVA irradiation did not affect the level of Beclin-1. UVA up-regulated the expression of p62 and the ubiquitination of proteins in cells, especially k63-linked ubiquitination. ARPE-19 cells were lost in a short- time under exposure to UVA. Conclusion UVA induces autophagy in ARPE-19 cells in a short period, and promotes protein degradation through the autophagy pathway. However, acute UVA irradiation leads to cell death. Therefore, while acute UVA irradiation cannot cause protein degeneration by impairing autophagy in RPE cells, it is still a risk factor for AMD occurrence due to its effect on reducing cells.