Loading
Life sciences · Journal article
Cells · October 15, 2026
No summary has been generated for this record yet. What follows is drawn from its source metadata only.
Journal article.
No findings were extractable from the material analysed.
Safety was not reported in the material analysed. Check the source before drawing any conclusion about harm.
The source did not state who this applies to in practice.
Graded across the dimensions that decide whether you should act, each from what the source actually supports. There is no single score, and where a dimension was not assessed it says so.
This record has not been graded across any dimension yet. Treat the label above as provisional and read the source.
What is missing. This record has no bottom line, key findings, reported figures, evidence dimensions. That is a gap in the analysis, not a judgement about the study.
Breast cancer (BC) and type 2 diabetes mellitus (T2DM) often co-occur and can contribute to poorer clinical outcomes after therapy compared to non-diabetic cases. It is assumed that glucose-lowering drugs like DPP4 inhibitors (DPP4-Is), e.g., sitagliptin, can affect the radiation responses of BC cells. In this study, parental and invasive (INV) MDA-MB-231 (triple-negative BC) and T47D (luminal A) cells were used. INV cells revealed a significant upregulation of DPP4/CD26 molecules compared to their parental counterparts. All investigated cells were treated with sitagliptin, ionizing radiation, or both. It was found that the specific inhibition of DPP4/CD26 molecules using sitagliptin can protect triple-negative BC cells from cytotoxic ionizing radiation or improve the radiation response in luminal A BC cells independently of their metastatic abilities. The protective and sensitizing effects of sitagliptin do not depend on the level of senescence and/or autophagy initiation after treatment.