Fig 1: Depletion of PES1 increases head and neck squamous cell carcinoma cell sensitivity to CISPLATIN in PDX models. (A) Schematic flow chart of HNSCC PDX model (image partly retrieved from https://app.biorender.com/biorender‐templates). (B) Clinical information of the donor. (C–F) Twenty PDX models of P2 were randomly divided into four groups and treated with different combinations as indicated. Images of the tumour (C), tumour growth curves (D), tumour weight (E) and representative immunohistochemistry images staining for PES1 and Ki‐67 (F).
Fig 2: Relationship between PES1 expression and the abundance of tumour immune infiltrating cells, immune checkpoint genes and tumour microenvironment under different HPV statuses. (A) Correlation between PES1 expression and tumour immune infiltrating cells in HPV‐negative (left panel) and HPV‐positive groups (right panel). (B) There was an association between PES1 expression and immune checkpoint genes in HPV‐negative (left panel) and HPV‐positive groups (right panel). (C–F) Differences in ESTIMATE score (C), immune score (D), stromal score (E) and tumour purity (F) between PES1 high and low expression groups.
Fig 3: As a new diagnostic biomarker, PES1 is highly expressed in head and neck squamous cell carcinoma (HNSCC) and correlates with poorer prognosis. (A) Pan‐cancer expression of PES1 between tumour tissues and normal tissues from TCGA database. (B) The expression of PES1 in normal tissues and tumour tissues was obtained from the TCGA GSE59102 and the GSE127165 data sets. (C) The relationship between PES1 expression levels and HPV status. (D, E) Kaplan–Meier plot for overall survival (D) and disease‐specific survival (E) of HNSCC patients in TCGA data set based on PES1 expression. (F, G) PES1 protein expression levels in the paired HNSCC tissues and ANM tissues using western blot (F) and immunohistochemistry (G) analyses. Scale bar, low magnification: 200 μm, high magnification: 40 μm
Fig 4: PES1 may play a role in promoting the proliferation of head and neck squamous cell carcinoma (HNSCC) through the MYC targets V1 signalling pathway. (A) The correlation between PES1, DRG1, RRP7A, MCAT, FCHO2, KAT2B and MORC3 expression of HNSCC in the TCGA cohort. (B) The hallmark analysis of PES1‐related genes using the Metascape database. (C) Gene set enrichment analysis (GSEA) plot of MYC targets the V1 signal pathway in multiple cancers.
Fig 5: PES1 promotes head and neck squamous cell carcinoma cell proliferation and tumour growth. (A–I) TU177 and FaDu cells were transduced with PES1 shRNAs‐expressing (shPES1‐1 or shPES1‐2) lentiviruses or scrambled control (shSc) lentiviruses. (A, B) CCK8 (A) and colony formation (B) were used to evaluate cellular proliferation in vitro. Error bars represent mean ± SD for triplicate experiments. ***p < 0.001. (C–I) The indicated UT177 and FaDu cells were inoculated subcutaneously into the right flank of nude mice and the tumour growth was measured after the inoculation. Tumour images (C, F), tumour growth curves (D, G), tumour weight (E, H) and representative IHC images of PES1 and Ki‐67 (I). Scale bars, 1 cm (C, F), 40 μm (I).
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