WNT16B, acting in a cell nonautonomous manner, promotes the survival of cancer cells after cytotoxic therapy.
Consistent with previous studies, transcripts encoding matrix metalloproteinases such as MMP1, chemokines such as CXCL3 and peptide growth factors such as amphiregulin were substantially elevated in PSC27 fibroblasts after genotoxic damage19,20.
Notably, the expression of WNT16B increased between eightfold and 64-fold as a result of these treatments (P < 0.005)
In other words, chemotherapy causes cancer.
WNT16B protein was substantially and significantly increased after chemotherapy in the periglandular stroma, which included fibroblasts and smooth muscle cells (P < 0.01)
We confirmed these findings in breast and ovarian carcinomas, two other malignancies commonly treated with cytotoxic chemotherapy.
In patients with prostate cancer treated with neoadjuvant chemotherapy, higher WNT16B immunoreactivity in prostate stroma after treatment was associated with a significantly greater likelihood of cancer recurrence