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Updated: Jun 23, 2025

Dual CRISPR-Interference Strategy for Targeting Synthetic Lethal Interactions Between Non-Coding RNAs in Cancer Cells
Published on: May 30, 2025
Mitoferrin2 is a synthetic lethal target for chromosome 8p deleted cancers
Stephan Krieg1, Thomas Rohde2, Tobias Rausch3
1Helmholtz-University Group "Cell Plasticity and Epigenetic Remodeling", German Cancer Research Center (DKFZ), Institute of Pathology, University Hospital Heidelberg, Heidelberg, Germany.
Background:
Somatic copy number alterations are a hallmark of cancer that offer unique opportunities for therapeutic exploitation. Here, we focused on the identification of specific vulnerabilities for tumors harboring chromosome 8p deletions.
Methods:
We developed and applied an integrative analysis of The Cancer Genome Atlas (TCGA), the Cancer Dependency Map (DepMap), and the Cancer Cell Line Encyclopedia to identify chromosome 8p-specific vulnerabilities. We employ orthogonal gene targeting strategies, both in vitro and in vivo, including short hairpin RNA-mediated gene knockdown and CRISPR/Cas9-mediated gene knockout to validate vulnerabilities.
Results:
We identified SLC25A28 (also known as MFRN2), as a specific vulnerability for tumors harboring chromosome 8p deletions. We demonstrate that vulnerability towards MFRN2 loss is dictated by the expression of its paralog, SLC25A37 (also known as MFRN1), which resides on chromosome 8p. In line with their function as mitochondrial iron transporters, MFRN1/2 paralog protein deficiency profoundly impaired mitochondrial respiration, induced global depletion of iron-sulfur cluster proteins, and resulted in DNA-damage and cell death. MFRN2 depletion in MFRN1-deficient tumors led to impaired growth and even tumor eradication in preclinical mouse xenograft experiments, highlighting its therapeutic potential.
Conclusions:
Our data reveal MFRN2 as a therapeutic target of chromosome 8p deleted cancers and nominate MFNR1 as the complimentary biomarker for MFRN2-directed therapies.
Insights
Researchers identified MFRN2 as a vulnerability in cancers with chromosome 8p deletions. MFRN1 levels determine sensitivity, suggesting MFRN2 as a therapeutic target and MFRN1 as a biomarker.
Area of Science:
- Oncology
- Cancer Genomics
- Molecular Biology
Background:
- Somatic copy number alterations are key cancer features with therapeutic potential.
- Chromosome 8p deletions present specific vulnerabilities in cancer.
Purpose of the Study:
- To identify vulnerabilities specific to tumors with chromosome 8p deletions.
- To explore the therapeutic potential of targeting these vulnerabilities.
Main Methods:
- Integrative analysis of TCGA, DepMap, and CCLE datasets.
- In vitro and in vivo validation using gene knockdown and knockout strategies.
- Orthogonal gene targeting including shRNA and CRISPR/Cas9.
Main Results:
- SLC25A28 (MFRN2) identified as a vulnerability in chromosome 8p-deleted tumors.
- MFRN2 vulnerability is dependent on the expression of its paralog, SLC25A37 (MFRN1).
- MFRN1/2 deficiency impairs mitochondrial respiration, iron-sulfur cluster proteins, and induces DNA damage, leading to cell death. MFRN2 targeting eradicated tumors in mouse models.
Conclusions:
- MFRN2 is a therapeutic target for chromosome 8p deleted cancers.
- MFRN1 serves as a predictive biomarker for MFRN2-directed therapies.
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