Oops, you're using an old version of your browser so some of the features on this page may not be displaying properly.

MINIMAL Requirements: Google Chrome 24+Mozilla Firefox 20+Internet Explorer 11Opera 15–18Apple Safari 7SeaMonkey 2.15-2.23

Poster display session: Biomarkers, Gynaecological cancers, Haematological malignancies, Immunotherapy of cancer, New diagnostic tools, NSCLC - early stage, locally advanced & metastatic, SCLC, Thoracic malignancies, Translational research

1290 - Application of CRISPR/Cas9 system for identification of genes involved in the regulation of pancreatic cancer cells platinum sensitivity

Date

20 Oct 2018

Session

Poster display session: Biomarkers, Gynaecological cancers, Haematological malignancies, Immunotherapy of cancer, New diagnostic tools, NSCLC - early stage, locally advanced & metastatic, SCLC, Thoracic malignancies, Translational research

Topics

Tumour Site

Pancreatic Adenocarcinoma

Presenters

Vera Skripova

Citation

Annals of Oncology (2018) 29 (suppl_8): viii14-viii57. 10.1093/annonc/mdy269

Authors

V. Skripova1, I. Serebriiskii1, R. Kiyamova1, I. Astsaturov2

Author affiliations

  • 1 Biochemistry And Biotechnology, Kazan Federal University, 420008 - Kazan/RU
  • 2 Institute For Cancer Research, Fox Chase Cancer Center, 19111 - Philadelphia/US

Resources

Login to access the resources on OncologyPRO.

If you do not have an ESMO account, please create one for free.

Abstract 1290

Background

Pancreatic cancer (PC) is an aggressive disease with high lethality rate due to multiple resistance mechanisms. We used in vitro CRISPR/Cas9 genetic drop-out screening to identify genes involved in the regulation of PC cell line sensitivity to platinum chemotherapy drugs.

Methods

We used two sgRNA libraries: 1) enriched for genes regulating cell cycle and nuclear proteins genes (CC, 50 000 sgRNA targeting 4 716 genes); 2) genome-wide (GW, 90 000 sgRNA targeting 18 164 genes). We performed screens in MIA PaCa-2 cells expressing doxycycline-inducible Cas9. Cells were treated with established IC30 of oxaliplatin (1 uM) or cisplatin (3 uM) for 9 cell divisions (12 days). Genomic DNA was extracted and sgRNA-containing regions were amplified and barcoded by PCR for further analysis by NGS. Statistical analysis for sgRNA enrichment or depletion was performed using R package comparing cells treated with the drugs vs. vehicle in the presence of Cas9/doxycycline.

Results

We identified 755 genes which significantly changed in cisplatin or oxaliplatin-treated cells (FDR 5%, p < 0.05). Candidate genes (n = 130) were further selected if at least 2 sgRNA per gene showed more than 2-fold change vs. vehicle. Among the 130 genes, 16 were known platinum sensitivity regulators involved in the double stranded break DNA repair pathway; 11 genes were positive platinum sensitivity regulators as their inactivation reduced sensitivity; 119 genes were negative platinum sensitivity regulators as their inactivation increased sensitivity. Gene Ontology analysis of the 130 candidate genes allowed us to identify regulators of cell cycle (n = 46), DNA replication and repair (n = 43), cellular compromise (n = 15), cellular assembly and organization (n = 35) and cell morphology (n = 48). Analysis of protein-protein interaction network showed that the majority of the hits (n = 74) are directly involved into cell cycle regulation and DNA repair processes.

Conclusions

We identified 130 candidate genes potentially involved in the modulation of platinum resistance most of which are regulating the cell cycle and DNA repair which is in keeping with the known DNA damaging mechanisms of action of platinum chemotherapy.

Clinical trial identification

Legal entity responsible for the study

Kazan Federal University.

Funding

The work is performed according to the Russian Government Program of Competitive Growth of Kazan Federal University.

Editorial Acknowledgement

Disclosure

All authors have declared no conflicts of interest.

This site uses cookies. Some of these cookies are essential, while others help us improve your experience by providing insights into how the site is being used.

For more detailed information on the cookies we use, please check our Privacy Policy.

Customise settings
  • Necessary cookies enable core functionality. The website cannot function properly without these cookies, and you can only disable them by changing your browser preferences.