Senolytic and senescence-suppressing compounds in cisplatin-treated NSCLC cells
In this abstract, platinum drugs, mainly cisplatin, most strongly induced therapy-induced senescence in NSCLC cells; several compounds showed senolytic or senescence-suppressing activity, and senescence suppression increased sensitivity to venetoclax and auranofin. [1]
Automatic summary · not editorially reviewed
The key findings
Platinum-based chemotherapeutics, mainly cisplatin, were the most potent inducers of therapy-induced senescence in the tested NSCLC cells. [1]
Venetoclax, navitoclax, BTSA1 and auranofin showed selective senolytic activity, while amiloride and NECA suppressed the senescence phenotype. [1]
Suppressing senescence increased sensitivity to venetoclax and auranofin, and target expression was confirmed at protein level in cell lines and neo-adjuvant treated patient samples. [1]
The source at a glance
- Study type / format
- Laboratory study reported in an abstract
- Population / context
- Non-small cell lung cancer (NSCLC) cell lines and neo-adjuvant treated NSCLC patient samples.
- Summary based on
- Study abstract
- Publication status
- Preprint · peer-review status not confirmed
- Original publication
- August 20, 2026
Cisplatin as strongest senescence inducer in NSCLC cells
The abstract notes that platinum-based chemotherapy remains important in NSCLC, but response rates in advanced disease stay low at 15–30%. Using an in-house high-throughput senescence labeling and classification strategy, the authors tested multiple standard-of-care chemotherapy agents for therapy-induced senescence. Platinum-based drugs, mainly cisplatin, proved the most potent inducers. The senescence phenotype was then examined by transcriptomic analysis. These are cell-based laboratory findings; the abstract reports no patient outcomes from this step.
Supporting source [1]
Senolytic and suppressing compounds in treated cells
Transcriptomic drug connectivity analysis was used to identify potential senotherapeutic strategies. Live-cell imaging on a screening platform then examined responses of control and senescence conditions to candidate senolytics. Selective senolytic activity was shown for the Bcl-2 inhibitors venetoclax and navitoclax, the BAX activator BTSA1 and the thioredoxin reductase inhibitor auranofin. Potent suppression of the senescence phenotype was observed with amiloride, an epithelial sodium channel blocker, and NECA, a non-selective adenosine receptor agonist. Suppression was assessed by immunohistochemistry of SA-β-Gal, p21 and p53, with absence of the proliferation marker KI-67.
Supporting source [1]
Sensitivity change and protein confirmation in patient samples
Senescence suppression modulated treatment response and significantly increased sensitivity to venetoclax and auranofin. Expression of the targets of the novel senotherapeutic candidates was confirmed at protein level in cell lines and in NSCLC patient samples after neo-adjuvant treatment. The authors conclude that these agents, described as repurposable with well-established safety profiles, could serve as chemosensitizers or adjuvant senolytic therapy. This abstract reports laboratory and sample-level findings; it does not show improved survival in patients, and the proposed repurposing remains to be tested clinically.
Supporting source [1]
How to interpret this
This is an abstract only; the full text was not reviewed. Findings come from cell-based screening, transcriptomic analysis and protein confirmation in cell lines and patient samples. The abstract reports no clinical trial, no patient survival outcomes and no dosing; the proposed repurposing is a future strategy, not an established treatment.
Based on the study abstract; the full paper, tables and supplementary data were not reviewed.
Source & supporting passages
Verswyvel J, Domen A, Zaryouh H, De Waele J, Wuyts M, Hermans C, Lambrechts H, Siozopoulou V, Hoz ECDL, Janssens A, Wener R, Prenen H, Peeters M, Deben C, Lardon F, Wouters A. · europepmc.org · August 20, 2026