Its primary mechanism is senescence-associated secretory phenotype (SASP), involving the release of a large number of biologically active proteins containing prominent pro-inflammatory cytokines and chemokines [145], which can transmit signals in a paracrine manner to nearby living cancer cells and other cells in the TME, thereby promoting tumor progression [146,147].For example, upregulated miR-335 in senescent normal fibroblasts and cancer-associated fibroblasts regulates SASP factor secretion and induces cancer cell motility in co-cultures by inhibiting PTEN expression [148]. This evidence concerns the gene PTEN and cancer.