Rnal of Hepatocellular Carcinoma 2021:DovePressPowered by TCPDF (www.tcpdf.org)DovepressGuo et alFigure 6 Differential chemotherapeutic response among the higher and low DTYMK expression groups. (A) D3 Receptor Agonist manufacturer camptothecin, (B) vinblastine, (C) cisplatin, (D) cytarabine, (E) docetaxel, (F) vorinostat, (G) paclitaxel, (H) rapamycin, (I) sorafenib, (J) gemcitabine, (K) bortezomib, and (L) vinorelbine. The symbols and represent p0.01 and p0.001, respectively.Figure 7 (A) The proportion of higher and low DTYMK expression in HCC and adjacent typical tissues. (B) Representative images of DTYMK staining in HCC and normal liver tissues. (C and D) Kaplan-Meier general and disease-free survival evaluation of DTYMK expression based on data obtained from our validation cohort.Journal of Hepatocellular Carcinoma 2021:https://doi.org/10.2147/JHC.SDovePressPowered by TCPDF (www.tcpdf.org)Guo et alDovepressTable 4 Correlation Among DTYMK Expression and Clinicopathological Characteristics of HCC in Our Validation CohortClinicopathological Variables n DTYMK Expression High (63) Age Sex Male Female AFP, ng/L 200 200 Tumor size, cm five 5 Tumor number Solitary Many (2) PVTT Absence Presence TNM stage Early (I II) Advance (III IV) Differentiation grade Nicely Poor 59 27 39 24 20 three 50 Low (23) 47 0.369 1 73 13 53 10 20 3 0.226 42 44 28 35 14 9 0.468 50 36 35 28 15 eight 0.622 51 35 36 27 15 eight 0.427 60 26 42 21 18 5 0.808 45 41 32 31 13 ten 0.035 P-valueNotes: Bold text indicates a substantial difference. Abbreviations: AFP, alpha fetus protein; PVTT, portal vein tumor thrombosis.the essential role of DTYMK in HCC progression and mAChR1 Modulator manufacturer development. We carried out additional study to investigate the function of DTYMK in HCC by performing GSEA utilizing the TCGA information. GO term and KEGG pathway analyses suggested that upregulated DTYMK expression was closely associated for the cell cycle and acid metabolism in cancer. The results showed that DNA biosynthesis, condensed chromosome centromeric area, signal transduction involved within the cell cycle, checkpoint adverse regulation with the cell cycle in GO and base excision repair, pyrimidine metabolism, homologous recombination, DNA replication, and cell cycle in KEGG were differentially enriched in tissues with higher DTYMK expression. These results all indicated that DTYMK has the prospective to become a prognostic marker and therapeutic target for HCC patients.Moreover, we revealed the connection amongst DTYMK expression and immune infiltration levels in HCC tissues using the TIMER database. The heatmap of 22 immune infiltrating cells in HCC samples recommended that Tregs were correlated with resting NK cells. Our CIBERSORT evaluation showed a good correlation involving DTYMK expression and immune cell infiltration, particularly Tfhs, Tregs and M0 macrophages. HCC individuals with high DTYMK expression had a higher infiltration level of Tregs, which caused impaired functional activity of NK cells. Robinson et al reported that NK cells could release cytotoxic granules to kill tumor cells.16 Moreover, NK cells inhibit angiogenesis and tumor cell proliferation by secreting inflammatory cytokines.17 These findings revealed that Tfh cells, Tregs and M0 macrophages had larger infiltration levels inside the higher DTYMK expression group, which indicated a prospective regulatory pathway of DTYMK on the function of T cells and macrophages in HCC. Furthermore, we identified close links among DTYMK and CD4+ T cells, B cells, and myeloid dendritic cells, implying a achievable impact o.
