mkt-077 and Colorectal-Neoplasms

This study focused on the expression of mortalin in colorectal cancer (CRC). Mortalin activated the Wnt/β-catenin pathway to accelerate cell proliferation and the epithelial-mesenchymal transition (EMT) program. Data from online databases displayed that the expression of mortalin was high in CRC, which was further validated using clinical specimens. Meanwhile, high mortalin expression was positively associated with a poor overall survival rate. Suppression of mortalin inhibited CRC cell proliferation as evaluated by the 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2-H-tetrazolium bromide (MTT), colony formation, and immunofluorescence staining assays. In addition, depletion of mortalin inhibited CRC cell EMT progression and deactivated the Wnt/β-catenin pathway. Altogether, mortalin is highly expressed in CRC and may indicate a poor prognosis. Mortalin accelerated CRC progression by stimulating cell proliferation and the EMT program. This study may provide a potential clinical therapeutic target for CRC.

Topics: beta Catenin; Cell Line, Tumor; Cell Movement; Cell Proliferation; Colorectal Neoplasms; Epithelial-Mesenchymal Transition; HSP70 Heat-Shock Proteins; Humans; Prognosis; Pyridines; Thiazoles; Wnt Signaling Pathway