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Cocktail and Poster Display session

107P - Inhibition of hydrogen sulfide biosynthesis influences mitochondrial biogenesis in breast cancer

Date

26 Feb 2024

Session

Cocktail and Poster Display session

Topics

Tumour Site

Breast Cancer

Presenters

Kareem Elsayed

Citation

Annals of Oncology (2024) 9 (suppl_1): 1-4. 10.1016/esmoop/esmoop102329

Authors

K. Elsayed1, R.A. Youness2, H.M. Nafea3, D.A. Habashy4, T. Manie5, C. Bourquin6, C. Szabo7, R.M. Abdel-Kader8, M. Gad3

Author affiliations

  • 1 Biochemistry, GUC - German University in Cairo, 11432 - New Cairo/EG
  • 2 Molecular Biology And Biochemistry, German International University, 11835 - Cairo/EG
  • 3 Biochemistry Department, GUC - German University in Cairo, 11432 - New Cairo/EG
  • 4 Pharmacology And Toxicology, GUC - German University in Cairo, 11432 - New Cairo/EG
  • 5 Breast Surgery Department, Cairo University - Faculty Of Medicine, 11562 - Cairo/EG
  • 6 Department Of Anesthesiology, Pharmacology, Intensive Care And Emergency Medicine, UNIGE - Université de Genève - Centre Médical Universitaire (CMU), 1206 - Geneva/CH
  • 7 Pharmacology, University of Fribourg, 1712 - Fribourg/CH
  • 8 Pharmacology & Toxicology Dept., GUC - German University in Cairo, 11432 - New Cairo/EG

Resources

This content is available to ESMO members and event participants.

Abstract 107P

Background

In humans, cystathionine-β-synthase (CBS), cystathionine gamma-lyase (CSE), and 3-mercaptopyruvate sulfurtransferase (3-MST) biosynthesize Hydrogen Sulphide (H2S). The expression of these enzymes was found to be significantly upregulated in breast cancer (BC). H2S causes various alterations in cellular metabolism and plays a major role in metabolic reprogramming in several malignant tumors. At low concentrations H2S stimulates cellular bioenergetics and increases ATP production. It induces persulfidation of different transcription factors such as PGC1α and thus, promotes the mitochondrial biogenesis. Yet, the effect of endogenous H2S on other mitochondrial biogenesis signaling players such as PGC1α, Nrf1/2, TFAM and ND-1 is not well studied in BC. Thus, the main aim of this work was to unravel the expression profile of the mitochondrial biogenesis pathway in BC patients and the impact of knocking down of H2S synthesizing enzymes on the mitochondrial bioenergetic profile in BC cell lines.

Methods

Breast tissues were collected from 25 female BC patients. Aggressive BC cell line, MDA-MB-231 cells were transfected with CBS, CSE and 3MST siRNAs using lipofection technique. RNA extraction was done from BC tissues and cell lines followed by reverse transcription into cDNA. PGC1-α, Nrf1, NRF-2, TFAM and ND-1 expression was quantified using q-RT-PCR. Mitochondrial membrane potential was measured using Rhodamine 123.

Results

CBS, CSE, 3-MST and ND-1 were upregulated in BC tissues. However PGC1α, NRF1/2 and TFAM did not show a significant alteration in BC tissues compared to its normal counterparts. On the molecular level, knocking down of CBS and/or CSE in MDA-MB-231 cells resulted in a noticeable increase in the expression of PGC1α, NRF1/2 and ND-1. However, a significant increase in TFAM levels was observed only upon CBS silncing but not upon CSE silenecing. On the other hand, knocking down of 3-MST did not affect PGC1α, NRF1/2, TFAM and ND-1 levels in MDA-MB-231 cells. On the functional levels, Effecient knocking down of either CBS or CSE caused a reduction in the mitochondrial membrane potential of BC cells.

Conclusions

This study highlights a tangible influence of CBS and CSE-induced H2S production on mitochondrial biogenesis mediators in BC.

Clinical trial identification

Editorial acknowledgement

Legal entity responsible for the study

German University in Cairo.

Funding

Swiss National Science Foundation.

Disclosure

All authors have declared no conflicts of interest.

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