---
title: "MCL1 and BCL2L1 drive mitochondrial priming and therapy sensitivity in human germ cell tumors"
id: "biorxiv-0-mitochondrial-priming-in-human-germ-cell-tumors-is-dependent-on-mcl1-and-bcl2l1"
canonical_url: "https://medichelpline.com/clinical-feed/biorxiv-0-mitochondrial-priming-in-human-germ-cell-tumors-is-dependent-on-mcl1-and-bcl2l1"
content_type: "clinical_feed_article"
specialty: "Oncology"
source_name: "bioRxiv (Biomedical Preprints)"
source_url: "https://www.biorxiv.org/content/10.64898/2026.09.22.752028v1?rss=1"
published_at: "2026-09-26T11:54:25.000Z"
evidence_level: "Verified Feed"
license: "CC-BY-NC-4.0 / Informational Use"
---
# MCL1 and BCL2L1 drive mitochondrial priming and therapy sensitivity in human germ cell tumors
## Provenance & Clinical Metadata
- **Canonical URL:** https://medichelpline.com/clinical-feed/biorxiv-0-mitochondrial-priming-in-human-germ-cell-tumors-is-dependent-on-mcl1-and-bcl2l1
- **Specialty:** [Oncology](https://medichelpline.com/clinical-feed/oncology.md)
- **Primary Source:** bioRxiv (Biomedical Preprints)
- **Source URL:** [Original Journal Publication](https://www.biorxiv.org/content/10.64898/2026.09.22.752028v1?rss=1)
- **Published At:** 2026-09-26T11:54:25.000Z
- **Evidence Rating:** Verified Feed
## Executive GIST (TL;DR)
- Germ cell tumors (GCTs) display high apoptotic sensitivity to DNA-damaging chemotherapy; the study examined the role of BCL2 family members in this “apoptotic priming.” - Analysis of human primary GCTs and embryonic precursor cells found consistently elevated expression of the pro-survival factors **MCL1** and **BCL2L1 (BCLX)**. - These elevated pro-survival levels were often accompanied by copy-number gains at MCL1 and BCL2L1 loci and reciprocal losses of pro-apoptotic regulators **PMAIP1 (NOXA)** and **BAD**. - Pharmacologic co-inhibition of **MCL1** and **BCLX** with selective **BH3 mimetics** produced potent synthetic lethality in multiple embryonal carcinoma cell lines derived from GCTs. - In undifferentiated embryonal carcinoma cell lines, inhibition of MCL1 or BCLX potentiated apoptosis induced by DNA-damaging agents (cisplatin, etoposide); this potentiation was not seen after retinoic acid–induced differentiation. - Inhibition of MCL1 increased cisplatin sensitivity even in p53-deficient or p53-mutant cell lines, which are typically associated with therapy resistance. - An in ovo human xenograft model showed that combining cisplatin with MCL1 inhibition enhanced therapeutic response and led to elimination of tumor cells in that model. - The authors conclude **MCL1** and **BCLX** are critical for GCT viability and represent candidate therapeutic targets to increase responsiveness to DNA-damaging chemotherapy. - The report is a preprint and has not undergone peer review; the abstract does not provide detailed experimental protocols, dosages, or statistical metrics in this summary.
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Sirli Anniko 1 University of Bradford; * [Find this author on Google Scholar](https://www.biorxiv.org/lookup/google-scholar?link_type=googlescholar&gs_type=author&author%5B0%5D=Sirli%2BAnniko%2B "Open in new tab") * [Find this author on PubMed](https://www.biorxiv.org/lookup/external-ref?access_num=Anniko%20S&link_type=AUTHORSEARCH "Open in new tab") * [Search for this author on this site](https://www.biorxiv.org/search/author1%3ASirli%2BAnniko%2B) * [ORCID record for Sirli Anniko](http://orcid.org/0000-0003-0752-5056 "Open in new tab") Sonia Khan 1 University of Bradford; * [Find this author on Google Scholar](https://www.biorxiv.org/lookup/google-scholar?link_type=googlescholar&gs_type=author&author%5B0%5D=Sonia%2BKhan%2B "Open in new tab") * [Find this author on PubMed](https://www.biorxiv.org/lookup/external-ref?access_num=Khan%20S&link_type=AUTHORSEARCH "Open in new tab") * [Search for this author on this site](https://www.biorxiv.org/search/author1%3ASonia%2BKhan%2B) * [ORCID record for Sonia Khan](http://orcid.org/0009-0005-8040-0120 "Open in new tab") Jamie RJ Morton 1 University of Bradford; 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* [Find this author on Google Scholar](https://www.biorxiv.org/lookup/google-scholar?link_type=googlescholar&gs_type=author&author%5B0%5D=Peter%2BK%2BNicholls%2B "Open in new tab") * [Find this author on PubMed](https://www.biorxiv.org/lookup/external-ref?access_num=Nicholls%20PK&link_type=AUTHORSEARCH "Open in new tab") * [Search for this author on this site](https://www.biorxiv.org/search/author1%3APeter%2BK%2BNicholls%2B) * [ORCID record for Peter K Nicholls](http://orcid.org/0000-0002-5540-442X "Open in new tab") * For correspondence: p.nicholls@bradford.ac.uk * [Abstract](https://www.biorxiv.org/content/10.64898/2026.09.22.752028v1)[](https://www.biorxiv.org/panels_ajax_tab/biorxiv_tab_art/node:5813924/1) * [Info/History](https://www.biorxiv.org/content/10.64898/2026.09.22.752028v1.article-info)[](https://www.biorxiv.org/panels_ajax_tab/biorxiv_tab_info/node:5813924/1) * [Metrics](https://www.biorxiv.org/content/10.64898/2026.09.22.752028v1.article-metrics)[](https://www.biorxiv.org/panels_ajax_tab/article_tab_metrics/node:5813924/1) * [ Preview PDF](https://www.biorxiv.org/content/10.64898/2026.09.22.752028v1.full.pdf+html)[](https://www.biorxiv.org/panels_ajax_tab/biorxiv_tab_pdf/node:5813924/1) ![Loading](https://www.biorxiv.org/sites/all/modules/contrib/panels_ajax_tab/images/loading.gif) ## Abstract Germ cell tumors (GCTs) are highly sensitized to cell death in response to DNA damaging agents, a property that underlies the success of current chemotherapeutic regimens. To address the molecular basis for this, known as apoptotic priming, we evaluated how different BCL2 family members modulate the heightened sensitivity of GCTs to therapy. Our analysis of human GCTs finds consistently high expression of the pro-survival factors MCL1 and BCL2L1 (BCLX) in a cohort of primary tumors and in their embryonic precursor cells, frequently accompanied by copy number gains of these loci and reciprocal losses of their pro-apoptotic interaction partners and inhibitors, PMAIP1 (NOXA) and BAD. We find that co-inhibition of MCL1 and BCLX using selective BH3 mimetics results in a potent synthetic lethality in multiple GCT embryonal carcinoma cell lines. When these cell lines were cultured with the DNA damaging agents cisplatin or etoposide, inhibition of MCL1 or BCLX potentiated their apoptotic effect in undifferentiated embryonal carcinoma cell lines, but not in retinoic acid-differentiated cells. The inhibition of MCL1 also heightened cisplatin sensitivity in p53-deficient or -mutant cell lines, which is associated with resistance to therapy. Employing an in ovo human xenograft model, we validate that the combination of cisplatin and MCL1 inhibition enhanced the therapeutic response by eliminating tumor cells. Our findings identify MCL1 and BCLX as critical factors to maintain GCT viability and as putative therapeutic targets to further augment GCT responsiveness to DNA damaging agents. ### Competing Interest Statement The authors have declared no competing interest. ## Funder Information Declared Academy of Medical Sciences, SBF/008/1051 Children with Cancer UK, https://ror.org/04bac6g30, CwCPG25\100026 Copyright The cop
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