ArticleBritish journal of cancer2024
Tumorigenic role of tacrolimus through mTORC1/C2 activation in post-transplant renal cell carcinomas.
Article in British journal of cancer, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 8 citations in OpenAlex.
- SPOP-mediated ZMYND8 ubiquitination and phase separation exclusion drives mTOR inhibitor resistance in kidney cancer.Nature communications · 2026Article
- Post-transplant malignancies in Taiwanese kidney transplant recipients: incidence, temporal trends, and immunosuppressive risk factors in a two-decade single-center cohort.Frontiers in immunology · 2026Article
- Tacrolimus modulates the PI3K AKT mTOR pathway in retinal epithelial cells under inflammatory stress.Scientific reports · 2025Article
- The mTOR pathway controls phosphorylation of BRAF at T401.Cell communication and signaling : CCS · 2024Article
- EZH2 overexpression is associated with aggressive behavior and promotes cell proliferation in CNS WHO grade 3 meningiomas.Neuro-oncology advancesArticle
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Authors and funding
13 authors at 1 institution in 1 country.
Funding
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Abstract
backgroundKidney transplant recipients (KTRs) face an increased risk of renal cell carcinoma (RCC), in which the immunosuppressive regimen plays an important role. This study aimed to identify intracellular signalling alterations associated with post-transplant (post-tx) tumour formation.
methodsExpression of mTOR-related proteins were analysed in kidneys obtained from end-stage renal disease (ESRD) patients and RCCs developed in KTRs or non-transplant patients. The effects of tacrolimus (TAC) and rapamycin (RAPA) on mTOR activity, proliferation, and tumour growth were investigated through different in vitro and in vivo experiments.
resultsElevated mTORC1/C2 activity was observed in post-tx RCCs and in kidneys of TAC-treated ESRD patients. In vitro experiments demonstrated that TAC increases mTOR activity in a normal tubular epithelial cell line and in the investigated RCC cell lines, moreover, promotes the proliferation of some RCC cell line. In vivo, TAC elevated mTORC1/C2 activity in ischaemic kidneys of mice and enhanced tumour growth in xenograft model.
conclusionsWe observed significantly increased mTOR activity in ischaemic kidneys and post-tx RCCs, which highlights involvement of mTOR pathway both in the healing or fibrotic processes of kidney and in tumorigenesis. TAC-treatment further augmented the already elevated mTOR activity of injured kidney, potentially contributing to tumorigenesis during immunosuppression.
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