Fig. 5

Illustration of the crosstalk of the Hippo pathway and BCSC-related pathways. Linc-OIP5 promotes transcription via forming a positive feedback circuit between YAP and Notch signaling [115]. IMP3 indirectly promotes Wnt5B via miR145-5p and facilitates TAZ-driven gene expression [116]. YAP and TAZ can promote the Wnt/β-catenin/TCF axis and induce target genes by interaction with β-catenin, while WBP2 integrates the Hippo, Wnt, and PI3K pathway [117,118,119]. Mir-613 inhibits EGFR via directly inhibiting WBP2 and positive correlation of EGFR and WBP2 is confirmed, while EGFR promotes WBP2 phosphorylation, contributing to integration of the Wnt/β-catenin and Hippo pathways [118, 119]. YAP/TAZ mediate the synergistic function and oncogene expression induced by the PI3K and dysregulated Hippo pathways [120]. The MAPK/ERK1 pathway negatively regulates breast cancer proliferation by inhibiting YAP/TEAD [121]. YAP induces gene transcription and promotes glycolysis by wiring up the Hh/GLI2 axis [108]. The SnoN oncoprotein exerts negative feedback regulation on TGF-β signaling, while promoting TAZ signaling and enhancing gene transcription in breast cancers [122]. Zyxin forms a ternary complex with LATS and Siah, which facilitates the degradation of LATS, activation of YAP and subsequently cell proliferation [123]. The tumor suppressor Merlin can inhibit YAZ/TAZ and maintain Smad7 stability, suppressing the adaptive glycolysis facilitated by the interaction between YAP/TAZ and Smads [124]. Ski inhibits breast cancer by suppressing TAZ in a LATS-dependent manner or in a LATS-independent manner, in which NCoR1 is recruited by Ski and suppresses TAZ by binding to the TEAD-TAZ complex [125]