Background: Breast cancer has overtaken lung cancer as the world's most common malignancy. Despite the development of some mRNA vaccines, no satisfactory vaccination for breast cancer has entered clinical application. Methods: In this study, we used multiple analyses of expression datasets from public sources to find new possible tumor antigens for breast cancer and to hunt for potential treatment-sensitive patients. Results: We identified the antigens DST, ANO6, LAMA3, and NEDD9 as putative candidates. Furthermore, we found five predictive genes to identify specific patients inclined for vaccination, namely TRBC2, CD3D, CD27, CD3E, and TRBV28. Following that, we discovered three immunological subtypes of breast cancer, Cluster 1 and Cluster 3, which were recognized as "cold tumors" with minimal immune activity and were more likely to respond to vaccination. We uncovered that Cluster 1 and Cluster 3 could be further separated into two subgroups, each with distinct immune cell infiltration patterns, suggesting that vaccine responses could differ among these patients. The findings of our study lay theoretical foundation for the development of mRNA vaccine and provide new opportunities for personalized treatment.

As recently reported by The International Agency for Research on Cancer (IARC), breast cancer has the highest incidence of all cancers in 2020. Many studies have revealed that golgi apparatus is closely associated with the development of breast cancer. However, the role of golgi apparatus in immune microenvironment is still not clear. In this study, using RNA-Seq datasets of breast cancer patients from the public database (n = 1080), we revealed that GOLT1B, encoding a golgi vesicle transporter protein, was significantly higher expressed in human breast cancer tissues versus normal tissues. Besides, we verified GOLT1B expression in five breast cancer cell line using our original data and found GOLT1B was significantly up-regulated in MDA-MB-231, MCF-7, SKBR3. Subsequently, we identified GOLT1B as a potential independent prognostic factor for breast cancer. After a multi-omics analysis, we uncovered that the higher expression of GOLT1B in breast cancer tissues versus normal tissues might be due to the amplification of GOLT1B and altered phosphorylation of its potential transcriptional factors, including JUN and SIN3A. Subsequently, we discovered that GOLT1B potentially regulated the immune microenvironment basing on the finding that its expression was closely related to the tumor microenvironment score and infiltration of immune cells. Moreover, we revealed that GOLT1B might affect the overall survival rates of breast cancer through regulating the immune cell infiltration. Finally, we disclosed the potential pathways involved in the functions of GOLT1B in breast cancer, including metabolism and ECM-receptor interaction pathways. To sum up, we identified GOLT1B as a potential prognostic gene for breast cancer and disclosed its role in regulating the immune microenvironment.

RC/BTB2 is a binding partner of sperm associated antigen 16S (SPAG16S), which is a regulator of spermiogenesis in mice, a process during which sperm flagella are formed. The expression of Rc/btb2 is also regulated by multicilin, a protein that controls ciliogenesis. Given that mouse Rc/btb2 mRNA is not only expressed in tissues bearing motile cilia, but also in tissues without motile cilia, we investigated whether RC/BTB2 plays a role in the general process of ciliogenesis by studying two cell lines that have primary cilia, NIH3T3, and IMCD3. We discovered that the subcellular localization of RC/BTB2 in the NIH3T3 and IMCD3 cells encompasses the pathway for ciliogenesis. RC/BTB2 was found in the Golgi bodies and centrosomes, two key structures essential for normal ciliogenesis. Knockdown of Rc/btb2 gene expression in these cell lines disrupted ciliogenesis. The percentage of cells with primary cilia was significantly reduced in stable cell lines transduced with specific Rc/btb2 shRNA viruses as compared to the control cells. When cilia were formed in the knockdown cells, they were significantly shorter than those in the control cells. Knockdown of Rc/btb2 expression did not affect cell proliferation and the cell cycle. Exogenous expression of RC/BTB2 in these stable knockdown cells restored ciliogenesis. These findings suggest that RC/BTB2 is a necessary component of the process of formation of primary cilia in somatic cells, perhaps through the transportation of cargos from Golgi bodies to centrosomes for cilia assembling. © 2015 Wiley Periodicals, Inc.