Figure 1. Fhit protein or Fhit-mimetic peptide interaction with ANXA4 restores chemosensitivity to paclitaxel in lung cancer cells.

This simplistic drawing indicates that ANXA4, preferentially located in the cytosol of Fhit-negative lung cancer cells (A), undergoes overexpression (B) and translocation (C) to the inner side of plasma membrane following to paclitaxel treatment; this effect results in the chemoresistance to the drug (C). Fhit overexpression blocks ANXA4 translocation from cytosol to plasma membrane thus restoring sensitivity to paclitaxel (D). The Fhit peptide interacting with ANXA4 (E) recapitulates the effect of the wild-type Fhit protein on chemoresistance both in vitro and in vivo (F).