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Cellular senescence is an initial barrier to tumor development that prevents the proliferation of premalignant cells. However, some of the features of senescent cells seem to promote tumor progression via senescence-associated secretory phenotype (SASP). Here, we demonstrated that the protein level of forkhead box Q1 (FOXQ1), which highly overexpresses in several kinds of tumors, was significantly downregulated during both replicative and oncogene-induced senescence. Moreover, overexpression of  FOXQ1  delayed senescence, whereas  FOXQ1  silence led to premature senescence in human fibroblasts. Furthermore, we identified that FOXQ1 upregulated SIRT1 expression through transcriptional regulation via directly binding to the  SIRT1  promoter. Finally, we showed that FOXQ1 remarkably inhibited the replicative senescence through depressing the expression of the inflammatory cytokines interleukin-6 (IL-6) and IL-8 via modulation of SIRT1-NF- κ B pathway. In addition, FOXQ1 overexpressed in human esophageal cancer cells and ablation of  FOXQ1  restrained the tumourigenic ability of the esophageal cancer cells (EC109 and EC9706) in a mouse xenograft model  in vivo . Taken together, these findings uncover a previously unidentified role of FOXQ1 regulating SASP and tumor development at same time.

FOXQ1 regulates senescence-associated inflammation via activation of SIRT1 expression