From this cohort, we tested the predictive value of common clinicopathological parameters (ulceration, mitotic count and tumor regression) and FMNL-2, ezrin and BRAF V600E immunoreactivity, for sentinel node involvement and survival.
This study revealed functional and mechanistic links between miR-206 and oncogene FMNL2 and c-MET in the progression of CRC. miR-206 functioned as a tumor suppressor in the progression of CRC by targeting FMNL2 and c-MET.
Forced expression of FMNL2 caused a significant increase in tumour cell proliferation, motility, invasion in vitro, and metastasis in vivo, whereas FMNL2 depletion showed opposite effects.
In conclusion, these findings identify a novel EMT and tumor promoting function for FMNL2, which is involved in TGF-β-induced EMT and colorectal carcinoma cell invasion via Smad3 effectors, or in collaboration with MAPK/MEK pathway.
Paraffin-embedded specimens of CRC (including 75 primary CRC tumors and 45 corresponding metastatic lymph nodes) and normal colorectal mucosa (30 samples) were immunostained with a FMNL2 antibody.