High expression of TTC21A predict poor prognosis of colorectal cancer and influence the immune infiltrating level.

Background: Colorectal cancer (CRC) is the third most common malignancy. Immunoinvasion of tumor microenvironment was positively correlated with overall cancer survival. TTC21A is a little-reported gene in tumors, and its mechanism of action remains unclear. Our study used The Cancer Genome Atlas (TCGA) data to evaluate the role of TTC21A in CRC. Methods: Software R3.6.3 analyzed the expression of TTC21A in CRC. We assessed the impact of TTC21A on the survival of CRC patients through a survival module. The CRC data set was then downloaded from TCGA. Logistic regression was used to analyze the correlation between clinical information and TTC21A expression. Cox regression analysis showed that clinicopathological characteristics of TCGA patients were correlated with overall survival. In addition, we used ssGSEA to explore the correlation between TTC21A and tumor immune invasion. Results: High expression of TTC21A is significantly correlated with advanced pathological stage and poor overall survival. In multivariate analysis, the up-regulated TTC21A expression, high tumor stage, and distant metastasis are independent prognostic factors of poor prognosis. Moreover, a negative correlation between increased TTC21A expression and immune infiltrating T cells and neutrophils cells was established. Conclusions: High expression of TTC21A was associated with poor prognosis of CRC and affected the proportion of immune cells such as T cells, neutrophils, and NK cells. These results suggest that TTC21A can be used as a potential biomarker to evaluate the prognosis and level of immune invasion in CRC.

Delayed thrombocytopenia as a rare but serious adverse event secondary to immune checkpoint inhibitor: a case report.

Immune checkpoint inhibitors (ICIs) are a recent breakthrough in antitumor drugs, although their overall safety has not been fully defined. Compared to conventional chemotherapy, ICIs exhibit different patterns of immunotoxicity, and immune-related adverse events (irAEs) have an immunological basis that is more toxic than usual and have a broad spectrum of manifestations involving different organ systems. Early recognition of symptoms and timely intervention are very important in managing immune-related adverse events (irAEs). In this study, we report a case of delayed immune thrombocytopenia in a patient treated with nivolumab for small cell lung cancer (SCLC). We found that thrombocytopenia was associated with the presence of platelet antibodies, autoantibodies, and thyroglobulin antibodies, accompanied by a decrease in the number of helper T cells and regulatory T cells. Platelets returned to normal after the removal of antibodies by plasma exchanges and methylprednisolone. We hypothesized that thrombocytopenia in patients was an antibody-driven and T-cell-mediated process. Although these observations indirectly suggest that cytokine changes contribute to immune dysregulation during irAE, prospective validation is needed to explain the confounding etiologies that may contribute to cytokine dysregulation. Therefore, studying the relationship between T cell subpopulations, cytokines and irAE in a larger population may be crucial for identifying biomarkers for ICI.

MicroRNA-361-3p Inhibit the Progression of Lymphoma by the Wnt/ß-Catenin Signaling Pathway.

BACKGROUND: MicroRNA is involved in the development of lymphoma. It is reported that miR-361-3p has a tumor inhibitory effect, but its role in lymphoma is still unclear. The purpose of this study is to examine whether miR-361-3p can inhibit the development of lymphoma and further explore the related potential mechanism. METHODS: In this study, we first analyzed the biological function of miR-361-3p in transfected Raji that mimicked miRNA. We also analyzed the biological function of the whole population in stably expressed miR-361-3p transgenic cells. Next, we conducted a complete micro-gene network to test the genetic profile of differential expression of stable gene-modified cells. RESULTS: We found that miR-361-3p expression was often reduced in lymphoma cell lines. Cellular assays have shown a significant role in inhibiting the growth of miR-361-3p by inhibiting lymphoma proliferation and migration, and severely inhibiting the Wnt/ß-catenin series protein signal. Bioinformatics analysis shows that Wnt10A is a new target of miR-361-3p, which is confirmed by our mechanism research. It is confirmed that restoring Wnt10A can reduce the tumor inhibition of Wnt/ß-catenin during lymphoma progression and restore the normal signal of Wnt/ß-catenin series proteins. DISCUSSION: Our data indicate that miR-361-3p inhibits the Wnt/ß-catenin protein signal by locking Wnt10A, which is an important factor in inhibiting the tumor in the pathogenesis of lymphoma. The miR-361-3p/Wnt10A axis may be a promising target for the treatment of lymphoma.