Additional file 2 of Prmt5 deficiency inhibits CD4+ T-cell Klf2/S1pr1 expression and ameliorates EAE disease

Additional file 2. Materials information

Additional file 1 of Prmt5 deficiency inhibits CD4+ T-cell Klf2/S1pr1 expression and ameliorates EAE disease

Additional file 1. Supplementary figure

DataSheet_1_PRMT5 Inhibition Promotes PD-L1 Expression and Immuno-Resistance in Lung Cancer.pdf

Protein arginine transferase 5 (PRMT5) has been implicated as an important modulator of tumorigenesis as it promotes tumor cell proliferation, invasion, and metastasis. Studies have largely focused on PRMT5 regulating intrinsic changes in tumors; however, the effects of PRMT5 on the tumor microenvironment and particularly immune cells are largely unknown. Here we found that targeting PRMT5 by genetic or pharmacological inhibition reduced lung tumor progression in immunocompromised mice; however, the effects were weakened in immunocompetent mice. PRMT5 inhibition not only decreased tumor cell survival but also increased the tumor cell expression of CD274 in vitro and in vivo, which activated the PD1/PD-L1 axis and eliminated CD8+T cell antitumor immunity. Mechanistically, PRMT5 regulated CD274 gene expression through symmetric dimethylation of histone H4R3, increased deposition of H3R4me2s on CD274 promoter loci, and inhibition of CD274 gene expression. Targeting PRMT5 reduced this inhibitory effect and promoted CD274 expression in lung cancer. However, PRMT5 inhibitors represent a double-edged sword as they may selectively kill cancer cells but may also disrupt the antitumor immune response. The combination of PRMT5 inhibition and ani-PD-L1 therapy resulted in an increase in the number and enhanced the function of tumor-infiltrating T cells. Our findings address an unmet clinical need in which combining PRMT5 inhibition with anti-PD-L1 therapy could be a promising strategy for lung cancer treatment.</p

MOESM5 of Prognostic value of YKL-40 in solid tumors: a meta-analysis of 41 cohort studies

Additional file 5: Figure S5. Sensitivity analysis for the pooled hazard ratios in all patients with gastrointestinal tumors. The analysis was conducted by estimating the average hazard ratio in the absence of each study

MOESM2 of Prognostic value of YKL-40 in solid tumors: a meta-analysis of 41 cohort studies

Additional file 2: Figure S2. Sensitivity analysis for the pooled hazard ratios in overall survival in all patients. The analysis was conducted by estimating the average hazard ratio in the absence of each study

MOESM6 of Prognostic value of YKL-40 in solid tumors: a meta-analysis of 41 cohort studies

Additional file 6: Figure S6. Forest plot showing the meta-analysis of hazard ratio estimates for DFS/PFS in all patients. DFS, disease-free survival; PFS, progression-free survival

MOESM8 of Prognostic value of YKL-40 in solid tumors: a meta-analysis of 41 cohort studies

Additional file 8: Figure S7. Forest plots of the association between YKL-40 and clinicopathological parameters. (a)tumor stage (III-IVvs.I-II, C-D vs. A-B or extended vs. limited). Experimental, stage(III-IV, C-D or extended); Control, (I-II, A-B or limited). (b)metastasis status(lymph node or liver metastasis vs. no metastasis). Experimental, lymph node or liver metastasis. Control, no metastasis

MOESM4 of Prognostic value of YKL-40 in solid tumors: a meta-analysis of 41 cohort studies

Additional file 4: Figure S4. Contour-enhanced funnel plot of the association between serum/plasma YKL-40 and overall survival in gastrointestinal tumors

MOESM7 of Prognostic value of YKL-40 in solid tumors: a meta-analysis of 41 cohort studies

Additional file 7: Table S1. Results of meta-regression analyses exploring causes of heterogeneity with DFS/PFS in solid tumors

MOESM1 of Prognostic value of YKL-40 in solid tumors: a meta-analysis of 41 cohort studies

Additional file 1: Figure S1. Forest plot showing the meta-analysis of hazard ratio estimates for overall survival in all patients after the trim-and-fill method was applied