Research Perspectives:

Potential crosstalk between cofilin-1 and EGFR pathways in cisplatin resistance of non-small-cell lung cancer

Carolina Beatriz Müller, Marco Antônio De Bastiani, Matheus Becker, Fernanda Stapenhorst França, Mariane Araujo Branco, Mauro Antônio Alves Castro and Fábio Klamt _

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Oncotarget. 2015; 6:3531-3539. https://doi.org/10.18632/oncotarget.3471

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Carolina Beatriz Müller1,2,*, Marco Antônio De Bastiani1,2,*, Matheus Becker1,2, Fernanda Stapenhorst França1,2, Mariane Araujo Branco1,2, Mauro Antônio Alves Castro3 and Fábio Klamt1,2

1 Laboratory of Cellular Biochemistry, Department of Biochemistry, Federal University of Rio Grande do Sul (UFRGS), Porto Alegre (RS), Brazil

2 National Institutes for Science & Technology-Translational Medicine (INCT-TM), Porto Alegre (RS), Brazil

3 Programa de Pós-Graduação em Bioinformática, Federal University of Paraná (UFPR), Curitiba (PR), Brazil

* These authors contributed equally to this work

Correspondence to:

Fábio Klamt, email:

Keywords: NSCLC, EGFR, cofilin-1, chemotherapy resistance, personalized medicine

Received: December 02, 2014 Accepted: January 22, 2015 Published: February 28, 2015


Current challenge in oncology is to establish the concept of personalized medicine in clinical practice. In this context, non-small-cell lung cancer (NSCLC) presents clinical, histological and molecular heterogeneity, being one of the most genomically diverse of all cancers. Recent advances added Epidermal Growth Factor Receptor (EGFR) as a predictive biomarker for patients with advanced NSCLC. In tumors with activating EGFR mutations, tyrosine kinase inhibitors (TKI) are indicated as first-line treatment, although restricted to a very small target population. In this context, cofilin-1 (a cytosolic protein involved with actin dynamics) has been widely studied as a biomarker of an aggressive phenotype in tumors, and overexpression of cofilin-1 is associated with cisplatin resistance and poor prognosis in NSCLC. Here, we gather information about the predictive potential of cofilin-1 and reviewed the crosstalk between cofilin-1/EGFR pathways. We aimed to highlight new perspectives of how these interactions might affect cisplatin resistance in NSCLC. We propose that cofilin-1 quantification in clinical samples in combination with presence/absence of EGFR mutation could be used to select patients that would benefit from TKI’s treatment. This information is of paramount importance and could result in a possibility of guiding more effective treatments to NSCLC patients.

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