Fig. 5: HMGA1 inhibits the transcription of STING.

a Western blot of STING in shNC-30 and shHMGA1-30-2 cells transfected with sicGAS. The samples derive from the same experiment but different gels for HMGA1, STING, cGAS, and another for β-actin were processed in parallel. b Western blot to determine the half-life of STING. Data were quantified using ImageJ. c Interaction between HMGA1 and STING in KYSE-30 cells was determined by co-IP. d EV-30 and oeSTING-30 were transduced with shNC and shHMGA1. Expression of exogenous STING (tagged with FLAG) was detected by western blot. The samples derive from the same experiment but different gels for HMGA1, FLAG-STING, and another for β-actin were processed in parallel. e, f Luciferase reporter assay to detect the effect of HMGA1 silencing (e) or overexpression (f) on the luciferase activity of the STING promoter in ESCC cells. g, h pGL3-STING promoter construct P3 (-372 bp/+376 bp from TSS of STING) with wild-type or mutated CREB binding site was co-transfected with a CREB expression vector into ESCC cells with HMGA1 silencing (g) or overexpression (h). Luciferase activities were measured after 48 h. I ChIP-qPCR detecting HMGA1 binding to the STING promoter. j ChIP-qPCR detecting CREB binding efficiency to the STING promoter in the presence or absence of HMGA1. k, l Co-IP to detect the interaction between HMGA1 and CREB. m Levels of STING in shNC-30 and shHMGA1-30-2 cells treated with siNC or sip300 were determined by qPCR. n, o Co-IP detects that HMGA1 competes with p300 for binding to CREB in ESCC cells with HMGA1 knockdown (n) or overexpression (o). Data are presented as mean ± SD. Statistical significance was determined by two-tailed unpaired t-test (e–j, m). Sample sizes: (a–o) n  =  3 independent experiments. Image in a–d, k, l, n, o shows representative results from three independent experiments. Source data are provided in the Source Data file.