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E-Poster Display

74P - Targeting mitochondria as a novel therapeutic strategy in biliary tract cancer

Date

17 Sep 2020

Session

E-Poster Display

Topics

Tumour Site

Hepatobiliary Cancers

Presenters

Pietro Carotenuto

Citation

Annals of Oncology (2020) 31 (suppl_4): S260-S273. 10.1016/annonc/annonc259

Authors

P. Carotenuto1, A. Barbato1, A. Indrieri1, M. Volpe1, P. Quadrano1, S. Brillante1, S. Riccardo1, L. Mirante1, D. Cacchiarelli1, I. Antonella1, B. Franco1, M. Salatiello2, G. Troncone2, L. Reggiani Bonetti3, M. Dominici4, M. Salati4

Author affiliations

  • 1 Genomic Medicine, TIGEM - Telethon Institute of Genetics and Medicine, 80078 - Pozzuoli/IT
  • 2 Department Of Public Health, University of Naples Federico II, 80131 - Naples/IT
  • 3 Section Of Pathology, Azienda Ospedaliero - Universitaria Policlinico di Modena, 4112 - Modena/IT
  • 4 Division Of Oncology, Department Of Oncology And Hematology, University Hospital of Modena, 40125 - Modena/IT

Resources

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Abstract 74P

Background

Mitochondria (Mi) are fundamentally implicated in cancer biology, including initiation, growth, metastasis, relapse, and acquired drug resistance. Mi are considered as the target organelles for therapeutic strategies of several cancers including CCA. The project aims to dissect the novel MiPa, to identify all molecular players, to functional characterize their role in CCA, to identify novel targeted therapies, to develop a gene signature exhibiting consistent prognostic power and predictive value as potential biomarker.

Methods

HTS has been performed by using Prestwick Chemical Library (Prestwick) and siGENOME Druggable-Genome-Library (Dharmacon). CASP9 activity has measured using the ApoAlert CASP9 assay (Clontech). Cell viability was monitored by CellTiter-Blue assay (Promega). The patient cohort consists of 100 patients retrospectively identified by Univeristy of Modena, IT. Lentiviral-based shRNA and CRISPR/Cas9 systems were utilized to establish stable gene knockdown and knockout model. FFPE-RNA extraction, RNAseq, WES and bioinformatic analyses will beperformed using protocols and pipeline available at TIGEM (2).

Results

Molecular players of the novel MiPa, which triggers APAF1-independent CASP-9 activation have been identified using a proteomic approach combined to siRNA library screening. HTS allowed to identify compounds targeting the novel MiPa. Two compounds were found to inhibit tumour growth in vitro and their anti-tumour efficacy has been assessed. Experiments in HuCCT-1, KMCH, CCLP, SW1, EGI, TFK1 cell lines revealed their effect on autophagy inhibition and apoptosis and correlated the MiPa pathway with drug treatment response and drug resistance. Whole-genome analysis is ongoing to profile the novel MiPa gene signature in cell lines treated and not with standard therapeutic approach and in a cohort of 100 CCA patients.

Conclusions

A novel MiPa has been identified regulating the apoptosis in CCA. Implication of the novel MiPa in drug resistance and sensitivity to classical therapeutic treatment has been assessed. Whole-transcriptome and exome analysis are ongoing to evaluate the clinical value of the MiPa gene signature in CCA patients. References: 1. Indrieri, A., et al., EMBO Mol Med, 2013. 2. Cacchiarelli D, et al., Cell. 2015.

Clinical trial identification

Editorial acknowledgement

Legal entity responsible for the study

The authors.

Funding

TIGEM - Telethon Institute of Genetics and Medicine.

Disclosure

All authors have declared no conflicts of interest.

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