β-Catenin overexpression is associated with gefitinib resistance in non-small cell lung cancer cells

Impact of Small Molecules on β-Catenin and E-Cadherin Expression in HPV16-positive and -negative Squamous Cell Carcinomas

“…In non-small cell lung cancer cells, β-catenin overexpression has also been associated with increased chemoresistance to gefitinib by affecting the activation of EGFR and downstream intracellular signaling (49). In our study, we found the highest β-catenin concentration under gefitinib treatment in HPV16-positive CERV196 cells with an overall time-dependent increase after 96 hours but βcatenin expression was still significantly lower than that of the control cells.…”

Inhibition of β-Catenin Enhances the Anticancer Effect of Irreversible EGFR-TKI in EGFR-Mutated Non–small-cell Lung Cancer with a T790M Mutation

“…[36][37][38] Therefore, there is an increasing need to develop new molecular targeted agents. Although some previous studies have revealed that β-Catenin can affect the efficacy of EGFR-TKI therapy, [26][27][28] this is the first report to show that the inhibition of the β-Catenin signal enhances the antitumor effect of BIBW2992 for EGFRmutated NSCLC carrying the T790M mutation. The activated EGFR activates the β-Catenin signal.…”

“…[13][14][15] β-Catenin is a key component of the Wnt/β-Catenin signal and is an important oncogene that is involved in the pathogenesis and progression of malignant tumors including lung cancer. [26][27][28] However, the influence of the β-Catenin signal in EGFR-mutated NSCLC carrying the T790M mutation has not been previously reported. [19][20][21][22] A previous article has reported that excessive activation of the Wnt/β-Catenin signal exists in approximately 50% of the human NSCLC cell lines.…”

β-Catenin Contributes to Lung Tumor Development Induced by EGFR Mutations

“…Interestingly, somatic mutations of β-catenin with concomitant EGFR-T790M mutation have been detected in 5% of EGFR TKI-resistant tumors in one series (43) and in vitro overexpression of β-catenin (or expression of activated form of β-catenin) leads to resistant to reversible EGFR TKIs in EGFR mutant cell lines lacking the T790M mutation (44, 45). Furthermore, acquired resistance to TKIs in EGFR mutant cells that undergo epithelial-to-mesenchymal transition can be concurrently seen with β-catenin signaling activation (46).…”