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. 2016 Nov 12;8(11):3147-3150.
doi: 10.18632/aging.101123.

The Fhit protein: an opportunity to overcome chemoresistance

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The Fhit protein: an opportunity to overcome chemoresistance

Eugenio Gaudio et al. Aging (Albany NY). .
No abstract available

Keywords: Fragile Histidine Triad (FHIT); mimetic peptides; reactive oxygen species; targeted therapy; tumor suppressor.

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Figures

Figure 1
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).

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