Fig. 8: WPOI progression is not associated with the serum levels of the OXTR ligand.
Graphical representation of analysis of serum (a) OXT and (b) AVP levels from healthy, leukoplakia and (c, d) OSCC patients with WPOI 1–3 (n = 64) and 4–5 (n = 45) types as indicated and as determined by ELISA (n = 180). P = two-tailed t test. e, f Graphical representation of analysis of serum OXT and AVP levels from patients with WPOI 1–3 (n = 28) and 4–5 (n = 68) types in a validation group. P = two-tailed t test. g, h Graphical representation of analysis of OXT/AVP levels from patients with/without LNM (n = 85) and postoperative metastasis (n = 93). P = two-tailed t test. i Graphical representation of survival data from WPOI 4–5 OSCC patients stratified according to OXT level (low: n = 34 and high: n = 34). j Correlative index of OXTR, nuclear ERK5 and serum OXT levels from OSCC patient tissue (n = 96) by IHC and ELISA analysis using Pearson’s correlation test. k, l Graphical analysis of Lmax (invasion in 3D collagen matrix) of HN6 in heterotypic spheroids treated with OXT or AVP. n = 4/group, P = two-tailed t test. m Proposed working model depicting the mechanism of OXTR autoactivation-mediated ERK5 nucleus translocation for maintaining the function and phenotype of OXTRHigh CAFs in WPOI 4–5 type stroma. Results are shown as mean and standard deviation (SD). Source data are provided as a Source data file.
