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Phosphoinositides play pivotal roles in the regulation of cancer cell phenotypes. Among them, phosphatidylinositol 3,4‐bisphosphate ( PI (3,4)P 2 ) localizes to the invadopodia, and positively regulates tumor cell invasion. In this study, we examined the effect of  PI (3,4)P 2  on focal adhesion dynamics in  MDA ‐ MB ‐231 basal breast cancer cells. Knockdown of  SHIP 2, a phosphatidylinositol 3,4,5‐trisphosphatase ( PIP  3 ) 5‐phosphatase that generates  PI (3,4)P 2 , in  MDA ‐ MB ‐231 breast cancer cells, induced the development of focal adhesions and cell spreading, leading to the suppression of invasion. In contrast, knockdown of  PTEN , a 3‐phosphatase that de‐phosphorylates  PIP  3  and  PI (3,4)P 2 , induced cell shrinkage and increased cell invasion. Interestingly, additional knockdown of  SHIP 2 rescued these phenotypes. Overexpression of the  TAPP 1  PH  domain, which binds to  PI (3,4)P 2 , and knockdown of Lpd, a downstream effector of  PI (3,4)P 2 , resulted in similar phenotypes to those induced by  SHIP 2 knockdown. Taken together, our results suggest that inhibition of  PI (3,4)P 2  generation and/or downstream signaling could be useful for inhibiting breast cancer metastasis.

PI (3,4)P 2 plays critical roles in the regulation of focal adhesion dynamics of MDA ‐ MB ‐231 breast cancer cells