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a switch from canonical to noncanonical wnt signaling mediates drug resistance in colon cancer cells开关从规范中的wnt信号介导的耐药性结肠癌细胞
A Switch from Canonical to Noncanonical Wnt Signaling
Mediates Drug Resistance in Colon Cancer Cells
Michael Bordonaro, Shruti Tewari, Catherine E. Cicco, Wafa Atamna, Darina L. Lazarova*
Department of Basic Sciences, The Commonwealth Medical College, Scranton, Pennsylvania, United States of America
Abstract
Butyrate, a fermentation product of fiber in the colon, acts as a histone deacetylase inhibitor (HDACi) and induces apoptosis
in colon cancer (CC) cells in vitro. We have reported that the apoptotic effects of butyrate are dependent upon the
hyperactivation of the Wnt/beta-catenin pathway. However, prolonged exposure of CC cells to increasing concentrations of
butyrate results in the acquisition of resistance to the Wnt/beta-catenin- and apoptosis-inducing effects of this agent, as
well as cross-resistance to structurally different HDACis. Here we report that one mechanism whereby HDACi resistance
arises is through the increase of beta-catenin-independent (noncanonical) Wnt signaling. Compared to HDACi-sensitive
HCT-116 CC cells, HDACi-resistant HCT-R cells exhibit higher levels of AKT/PKB cell survival signaling, which is in part
induced by WNT5A and its receptor ROR2. The induction of AKT signaling by HDACis is also detected in other CC cell lines,
albeit to a lesser extent than in the drug-resistant HCT-R cells. The observations suggested that the apoptotic effect of
butyrate and other HDACis in CC cells can be augmented by inhibitors of pAKT. In agreement with the hypothesis, the
combination of MK2206, a pAKT inhibitor, and a HDACi (butyrate or LBH589) induced higher apoptosis in CC cells compared
to each agent alone. The exposure to both agents also re-sensitized the HCT-R cells to apoptosis. Finally, the concept of
simultaneously inducing canonical Wnt activity and suppressing AKT signaling
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