Many tumour cells express on their surface proteins of endogenous retroviruses (ERVs) and there are suggestions to use these retroviral antigens as target for anti-tumour vaccines. However, until now there is no convincing data showing that this strategy works, in contrast, there are considerations suggesting that this strategy may be harmful if applied.
Background: Head and neck squamous cell carcinomas (HNSC) are among the most common malignant tumors with high incidence, relapse, and mortality rate. STAT proteins are implicated in various biological processes, including cell proliferation, metastasis, and immune regulation.
Method: Various bioinformatics tools were used to explore the role of the STAT family in HNSC.
Result: The mRNA levels of STAT1/2/4/5A/6 were significantly upregulated in HNSC tissues. The levels of STAT1/2/4/5A/6 could be used for the detection of HNSC. HNSC patients with a high level of STAT5A had a poor overall survival and relapse-free survival. A moderate to high correlation was obtained between the STAT family and HNSC. Genetic alteration revealed that STAT1/2/3/4/5A/5B/6 were altered in 6%, 5%, 7%, 8%, 6%, 6%, and 4% of the queried TCGA HNSC samples, respectively. Immune infiltrations analysis suggested a significant association between STAT5A expression and abundance of specific immune cells. Further, copy number alteration of STAT5A could certainly inhibit infiltration level. Moreover, a close correlation was obtained between STAT5A level and the expression of immune markers in HNSC. Several kinase targets and transcription factor targets of STAT5A in HNSC were also identified. Enrichment analysis suggested that STAT5A and co-expression genes were mainly responsible for adaptive immune response, T cell activation, cytokine-cytokine receptor interaction, chemokine signaling pathway, cell-adhesion molecules, and ribosome and RNA transport.
Conclusion: Our results provided additional data for the expression and clinical significance of the STAT family in HNSC, and further study should be performed to verify these.
Breast cancer is currently one of the most common malignant tumors in women. Our previous research found that thymic dysfunction has a certain relationship with the occurrence and development of breast cancer. In order to explore whether the functional status of thymus is related to the development and metastasis of breast cancer, we use BALB/c wild type mice (BALB wt), BALB/c nude mice (BALB nu), BALB wt mice implanted with 4T1 cells (wt 4T1), BALB nu with 4T1 (nu 4T1), D-galactose treatment wt 4T1 mice (D-Gal), Thymalfasin treatment wt 4T1 mice (Tα1), Cyclophosphamide treatment wt 4T1 mice (CTX), Doxorubicin treatment wt 4T1 mice (Dox) in the research. As a result, nu 4T1, D-Gal and DOX had earlier lung metastases. Gene chip results showed that PTMα and Tβ15b1 were the most up-regulated and down-regulated genes in thymosin-related genes, respectively. Overexpression or silencing of PTMα and Tβ15b1 genes did not affect the proliferation of 4T1 cells. PTMα gene silenced, cell migration and invasion ability enhanced, while PTMα gene overexpression, the cell invasion ability weaken. In vivo, PTMα gene overexpression promotes tumor growth and lung metastasis in the early stage, but has no significant effect in the later stage. Tβ15b1 overexpression also promotes tumor growth in the early stage, but suppresses in the later stage. Tβ15b1 gene silencing inhibits tumor lung metastasis. Thus, our findings demonstrated that thymic function affects breast cancer development and metastasis by regulating expression of thymus secretions PTMα and Tβ15b1. Our study provided new directions for breast cancer therapy.

