Background: The family with sequence similarity 20-member C (Fam20C) kinase plays important roles in physiopathological process and is responsible for majority of the secreted phosphoproteome, including substrates associated with tumor cell migration. However, it remains unclear whether Fam20C plays a role in cancers. Here, we aimed to analyze the expression and prognostic value of Fam20C in pan-cancer and to gain insights into the association between Fam20C and immune infiltration. Methods: We analyzed Fam20C expression patterns and the associations between Fam20C expression levels and prognosis in pan-cancer via the ONCOMINE, TIMER (Tumor Immune Estimation Resource), PrognoScan, GEPIA (Gene Expression Profiling Interactive Analysis), and Kaplan–Meier Plotter databases. After that, GEPIA and TIMER databases were applied to investigate the relations between Fam20C expression and immune infiltration across different cancer types, especially BLCA (bladder urothelial carcinoma), LGG (brain lower grade glioma), and STAD (stomach adenocarcinoma). Results: Compared with adjacent normal tissues, Fam20C was widely expressed across many cancers. In general, Fam20C showed a detrimental role in pan-cancer, it was positively associated with poor survival of BLCA, LGG, and STAD patients. Specifically, based on TCGA (The Cancer Genome Atlas) database, a high expression level of Fam20C was associated with worse prognostic value in stages T2–T4 and stages N0–N2 in the cohort of STAD patients. Moreover, Fam20C expression had positive associations with immune infiltration, including CD4+ T cells, macrophages, neutrophils, and dendritic cells, and other diverse immune cells in BLCA, LGG, and STAD. Conclusion: Fam20C may serve as a promising prognostic biomarker in pan-cancer and has positive associations with immune infiltrates.

Introduction Aspirin is a common antipyretic, analgesic, and anti-inflammatory drug, which has been reported to extend life in animal models and application in the treatment of aging-related diseases. However, it remains unclear about the effects of aspirin on bone marrow-derived mesenchymal stromal cells (BM-MSCs). Here, we aimed to analyze the influence of aspirin on senescence and young BM-MSCs. Methods BM-MSCs were serially passaged to construct a replicative senescence model. SA-β-gal staining, PCR, western blot, and RNA-sequencing were performed on BM-MSCs with or without aspirin treatment, to examine aspirin’s impact on bone marrow-derived mesenchymal stem cells. Results SA-β-gal staining, PCR, and western blot revealed that aspirin could alleviate the cellular expression of senescence-related indicators of BM-MSCs, including a decrease of SA-β-gal-positive cells and staining intensity, and downregulation of p16, p21, and p53 expression after aspirin treatment. RNA-sequencing results shown in the biological processes related to aging, aspirin could influence cellular immune response and lipid metabolism. Conclusion The efficacy of aspirin for retarding senescence of BM-MSCs was demonstrated. Our study indicated that the mechanisms of this delay might involve influencing immune response and lipid metabolism.

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Brain low grade gliomas (LGG) often give serious clinical symptoms due to the invasion towards nervous system, affecting the life quality of patients. Collagen type I alpha 1(COL1A1) is the main component of type I collagen. Although there are many reports about abnormal expression of COL1A1 in various tumors, specific role and clinical significance of COL1A1 in LGG have not yet been elucidated. In this work, Tumor Immune Estimation Resource database was used for detecting the expression level of COL1A1 in cancer and normal tissues, and aimed to explore the relationship between COL1A1 and tumor immune infiltration. We applied Kaplan-Meier to analyze the role of COL1A1 in clinical prognosis. Univariate survival rate and multivariate Cox analysis were used to compare clinical characteristics and survival rate. The relativity between the expression of COL1A1 and the tumor microenvironment was evaluated using ESTIMATE algorithm. Finally, the relationship between expression level of COL1A1 and gene marker sets of immune cell infiltration was investigated via TIMER. According to TCGA, COL1A1 overexpression was correlated with overall survival (OS), progression free interval (PFI) and disease specific survival (DSS) of multiple tumors, especially in LGG. Multivariate analysis showed that COL1A1 expression was an independent prognostic factor for LGG. The expression of COL1A1 was positively correlated with the infiltration of CD4 + T and CD8 + T cells, neutrophils, macrophages and dendritic cells in LGG. In addition, there was a strong correlation between expression of COL1A1 and different immune marker sets in LGG. The results suggest that COL1A1 is related with tumor immune infiltration of LGG.

Stem cells from fetal tissue protect against aging and possess greater proliferative capacity than their adult counterparts. These cells can more readily expand in vitro and senesce later in culture. However, the underlying molecular mechanisms for these differences are still not fully understood. In this study, we used a robust rank aggregation (RRA) method to discover robust differentially expressed genes (DEGs) between fetal bone marrow mesenchymal stem cells (fMSCs) and aged adult bone marrow mesenchymal stem cells (aMSCs). Multiple methods, including gene set enrichment analysis (GSEA), Gene Ontology (GO) analysis, and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis were performed for functional annotation of the robust DEGs, and the results were visualized using the R software. The hub genes and other genes with which they interacted directly were detected by protein–protein interaction (PPI) network analysis. Correlation of gene expression was measured by Pearson correlation coefficient. A total of 388 up-regulated and 289 down-regulated DEGs were identified between aMSCs and fMSCs. We found that the down-regulated genes were mainly involved in the cell cycle, telomerase activity, and stem cell proliferation. The up-regulated DEGs were associated with cell adhesion molecules, extracellular matrix (ECM)–receptor interactions, and the immune response. We screened out four hub genes, MYC, KIF20A, HLA-DRA, and HLA-DPA1, through PPI-network analysis. The MYC gene was negatively correlated with TXNIP, an age-related gene, and KIF20A was extensively involved in the cell cycle. The results suggested that MSCs derived from the bone marrow of an elderly donor present a pro-inflammatory phenotype compared with that of fMSCs, and the HLA-DRA and HLA-DPA1 genes are related to the immune response. These findings provide new insights into the differences between aMSCs and fMSCs and may suggest novel strategies for ex vivo expansion and application of adult MSCs.