Aldehyde Dehydrogenase 1B1 Is Associated with Altered Cell Morphology, Proliferation, Migration and Chemosensitivity in Human Colorectal Adenocarcinoma Cells

Aldehyde dehydrogenases (ALDHs) are NAD(P)+-dependent enzymes that catalyze the oxidation of endogenous and exogenous aldehydes to their corresponding carboxylic acids. ALDHs participate in a variety cellular mechanisms, such as metabolism, cell proliferation apoptosis, well differentiation stemness. Over last few years, have emerged cancer stem markers wide spectrum solid tumors hematological malignancies. In this study, pathophysiological role ALDH1B1 human colorectal adenocarcinoma was investigated. Human colon HT29 cells were stably transfected either with green fluorescent protein (GFP)-tagged or an empty lentiviral expression vector. The overexpression correlated altered morphology, decreased rate reduced clonogenic efficiency. Additionally, triggered G2/M arrest at 24 h post-cell synchronization, probably through p53 p21 upregulation. Furthermore, ALDH1B1-overexpressing exhibited enhanced resistance against doxorubicin, fluorouracil (5-FU) etoposide. Finally, induced increased migratory potential displayed epithelial–mesenchymal transition (EMT) upregulation ZEB1 vimentin consequent downregulation E-cadherin. Taken together, confers alterations cycle progression gene expression, accompanied by significant changes chemosensitivity cells, underlying its significance progression.