Preclinical data, and an increasing list of clinical investigations, show
anti-inflammatory agents to favourably influence the biology of
colorectal tumor. We have earlier reported on re-expression of activated immune cells after three days preoperative treatment of patients with
colorectal carcinoma, randomized to receive oral
NSAID (
indomethacin or
celebrex). Antisecretory prophylaxis (esomeprasol) was provided to all patients and served as
sham treatment. Concomittant to MHC locus activation, Prominin1/CD133, a marker associated with stemness and poor prognosis in several solid
tumors, was downregulated. The aim of the present study was to evaluate expression of additional regulators belonging to the stem cell niche, OCT4, SOX2 and BMP7, as well as some
microRNAs, reported to act as
tumor suppressors or oncomiRs. Peroperative
tumor biopsies were analyzed by microarrays, quantitative real-time PCR and immunohistochemistry (IHC). The stem cell master regulator SOX2 was increased by
NSAIDs (p<0.01), as well as the
tumor suppressor miR-630 (p<0.01), while BMP7, a marker for poor prognosis in CRC, was downregulated by
NSAID (
indomethacin, p<0.02). The upregulation of SOX2, but not of its heterodimer binding partner OCT4, could imply a negative feed-back loop, with a switch‑off for stemness preservation of
tumor cells. This is supported by the overall evaluation of gene expression profiles with subsequent events, indicating less aggressive
tumors following
NSAID treatment.