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Poster display session: Basic science, Endocrine tumours, Gastrointestinal tumours - colorectal & non-colorectal, Head and neck cancer (excluding thyroid), Melanoma and other skin tumours, Neuroendocrine tumours, Thyroid cancer, Tumour biology & pathology

4177 - Macrophage migration inhibitory factor overexpression is a mechanism of acquired resistance to anti-EGFR inhibitor cetuximab in human colorectal cancer cell line

Date

21 Oct 2018

Session

Poster display session: Basic science, Endocrine tumours, Gastrointestinal tumours - colorectal & non-colorectal, Head and neck cancer (excluding thyroid), Melanoma and other skin tumours, Neuroendocrine tumours, Thyroid cancer, Tumour biology & pathology

Topics

Cancer Biology

Tumour Site

Colon and Rectal Cancer

Presenters

Nunzia Matrone

Citation

Annals of Oncology (2018) 29 (suppl_8): viii150-viii204. 10.1093/annonc/mdy281

Authors

N. Matrone1, A. Chambery2, R. Russo2, P.V. Pedone2, V. Belli1, S. Napolitano1, E. Martinelli1, E.F. Giunta1, V. De Falco1, N. Zanaletti1, P. Vitale1, M. Terminiello1, C. Cardone1, F. Ciardiello1, T. Troiani1

Author affiliations

  • 1 Precision Medicine, Università degli Studi della Campania Luigi Vanvitelli, 80131 - Napoli/IT
  • 2 Dipartimento Di Scienze E Tecnologie Ambientali, Biologiche E Farmaceutiche, Università degli Studi della Campania Luigi Vanvitelli, 80131 - Napoli/IT

Resources

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Abstract 4177

Background

The anti-epidermal growth factor receptor (EGFR) monoclonal antibodies (mAbs) cetuximab and panitumumab are effective in a subset of RAS/BRAF wild-type (WT) metastatic colorectal cancers (mCRCs) patients. Despite an accurate RAS-driven selection, not all patients will respond to EGFR inhibitors and the onset of secondary resistance limits their clinical benefit.

Methods

With the aim of developing effective preclinical models for testing possible strategies to overcome acquired resistance to EGFR blockade, we have generated a series of human colon cancer cell lines with in vitro and in vivo acquired resistance to anti-EGFR inhibitors. To better investigate the differentially expressed proteins involved in EGFR resistance, we applied an advanced quantitative proteomic approach based on TMT isobaric labeling and nano-liquid chromatography coupled with high resolution tandem mass spectrometry (MS/MS).

Results

To evaluate changes in protein expression we have used human CRC cell line cetuximab-sensitive GEO, as well as its derived cell line with acquired resistance to cetuximab GEO-CR. By MS/MS, we have identified and quantified 2455 proteins; 53 proteins were found to be differentially expressed in GEO-CR compared to GEO cells. Only 11 proteins were found to be high regulated in GEO-CR, among these we focused our attention on the inhibition factor of macrophage migration (MIF) for its relevance in CRC tumorigenesis. To explore its involvement in resistance to cetuximab in CRC cell line, we have performed an MTT assay with two MIF-antagonists, ISO1 a cell-permeable inhibitor of MIF tautomerase and 4-IPP, a selective MIF inhibitor that blocks MIF and its receptor, CD74, internalization. GEO-CR cell line was treated with two MIF antagonists alone and in combination with cetuximab. Only the combined treatment with cetuximab and 4-IPP induced a synergistic antiproliferative and apoptotic effects.

Conclusions

These results suggest that MIF overexpression is involved in acquired resistance to cetuximab and the inhibition of EGFR and MIF could be a strategy for overcoming anti-EGFR resistance in patients with CRC.

Clinical trial identification

Legal entity responsible for the study

Università Degli Studi della Campania "Luigi Vanvitelli".

Funding

Has not received any funding.

Editorial Acknowledgement

Disclosure

All authors have declared no conflicts of interest.

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