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Compared to traditional platform environments in the online realm, the metaverse, as a three-dimensional (3D) virtual world, exposes more identity data to the network. Once these data are compromised, it leads to privacy breaches. Therefore, how to ensure identity security in the metaverse environment has become an urgent problem to be solved. Although research on identity authentication schemes can help improve identity security, traditional identity authentication schemes in network environments are studied based on their own environmental characteristics, which makes it difficult to meet the security needs in the metaverse environment. As a result, in this paper we propose an elliptic curve cryptography (ECC)-based identity authentication scheme to address identity authentication issues in the metaverse environment. This scheme ensures secure communication among users, avatars, and platform servers. The security of this scheme was demonstrated through informal security analysis and the automated validation of internet security protocols and applications (AVISPA) formal security analysis tools, and the results showed that it can resist various known attacks. Compared with existing identity authentication schemes, this scheme has lower computational and communication costs. [ABSTRACT FROM AUTHOR]

Background: Radioresistance is a primary factor contributing to the failure of rectal cancer treatment. Immune suppression plays a significant role in the development of radioresistance. We have investigated the potential role of phosphatidylinositol transfer protein cytoplasmic 1 (PITPNC1) in regulating immune suppression associated with radioresistance. Methods: To elucidate the mechanisms by which PITPNC1 influences radioresistance, we established HT29, SW480, and MC38 radioresistant cell lines. The relationship between radioresistance and changes in the proportion of immune cells was verified through subcutaneous tumor models and flow cytometry. Changes in the expression levels of PITPNC1, FASN, and CD155 were determined using immunohistochemistry and western blotting techniques. The interplay between these proteins was investigated using immunofluorescence co-localization and immunoprecipitation assays. Additionally, siRNA and lentivirus-mediated gene knockdown or overexpression, as well as co-culture of tumor cells with PBMCs or CD8+ T cells and establishment of stable transgenic cell lines in vivo, were employed to validate the impact of the PITPNC1/FASN/CD155 pathway on CD8+ T cell immune function. Results: Under irradiation, the apoptosis rate and expression of apoptosis-related proteins in radioresistant colorectal cancer cell lines were significantly decreased, while the cell proliferation rate increased. In radioresistant tumor-bearing mice, the proportion of CD8+ T cells and IFN-γ production within immune cells decreased. Immunohistochemical analysis of human and animal tissue specimens resistant to radiotherapy showed a significant increase in the expression levels of PITPNC1, FASN, and CD155. Gene knockdown and rescue experiments demonstrated that PITPNC1 can regulate the expression of CD155 on the surface of tumor cells through FASN. In addition, co-culture experiments and in vivo tumor-bearing experiments have shown that silencing PITPNC1 can inhibit FASN/CD155, enhance CD8+ T cell immune function, promote colorectal cancer cell death, and ultimately reduce radioresistance in tumor-bearing models. Conclusions: PITPNC1 regulates the expression of CD155 through FASN, inhibits CD8+ T cell immune function, and promotes radioresistance in rectal cancer. [ABSTRACT FROM AUTHOR]