Simultaneous overactivation of Wnt/β-catenin and TGFβ signalling by miR-128-3p confers chemoresistance-associated metastasis in NSCLC

Junchao Cai(Sun Yat-sen University), Lishan Fang(Sun Yat-sen University), Yongbo Huang(Fudan University Shanghai Cancer Center), Rong Li(Sun Yat-sen University), Xiaonan Xu(Sun Yat-sen University), Zhihuang Hu(Sun Yat-sen University), Le Zhang(Sun Yat-sen University), Yi Yang(Sun Yat-sen University), Xun Zhu(Sun Yat-sen University), Heng Zhang(Sun Yat-sen University), Jueheng Wu(Sun Yat-sen University), Yan Huang(Sun Yat-sen University), Jun Li(Sun Yat-sen University), Mu‐Sheng Zeng(Sun Yat-sen University), Erwei Song(Sun Yat-sen University), Yukai He(Augusta University Health), Li Zhang(Sun Yat-sen University), Mengfeng Li(Sun Yat-sen University)
Nature Communications
June 19, 2017
Cited by 200Open Access
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Abstract

Cancer chemoresistance and metastasis are tightly associated features. However, whether they share common molecular mechanisms and thus can be targeted with one common strategy remain unclear in non-small cell lung cancer (NSCLC). Here, we report that high levels of microRNA-128-3p (miR-128-3p) is key to concomitant development of chemoresistance and metastasis in residual NSCLC cells having survived repeated chemotherapy and correlates with chemoresistance, aggressiveness and poor prognosis in NSCLC patients. Mechanistically, miR-128-3p induces mesenchymal and stemness-like properties through downregulating multiple inhibitors of Wnt/β-catenin and TGF-β pathways, leading to their overactivation. Importantly, antagonism of miR-128-3p potently reverses metastasis and chemoresistance of highly malignant NSCLC cells, which could be completely reversed by restoring Wnt/β-catenin and TGF-β activities. Notably, correlations among miR-128-3p levels, activated β-catenin and TGF-β signalling, and pro-epithelial-to-mesenchymal transition/pro-metastatic protein levels are validated in NSCLC patient specimens. These findings suggest that miR-128-3p might be a potential target against both metastasis and chemoresistance in NSCLC.


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