Solid organ transplantation is associated with increased risk of non-melanoma skin cancer.,Studies with short follow up times have suggested a reduced occurrence of these cancers in recipients treated with mammalian target of rapamycin inhibitors as maintenance immunosuppression.,We aimed to describe the occurrence of skin cancers in renal and liver transplant recipients switched from calcineurin inhibitor to sirolimus-based regimes.,We performed a retrospective study of sirolimus conversion within the Irish national kidney and liver transplant programs.,These data were linked with the National Cancer Registry Ireland to determine the incidence of NMSC among these recipients.,The incidence rate ratio (IRR) for post versus pre-conversion NMSC rates are referred in this study as an effect size with [95% confidence interval].,Of 4,536 kidney transplants and 574 liver transplants functioning on the 1 January 1994 or transplanted between 1 January 1994 and 01 January 1994 and 01 January 2015, 85 kidney and 88 liver transplant recipients were transitioned to sirolimus-based immunosuppression.,In renal transplants, the rate of NMSC was 131 per 1000 patient years pre-switch to sirolimus, and 68 per 1000 patient years post switch, with adjusted effect size of 0.48 [0.31 − 0.74] (p = .001) following the switch.,For liver transplant recipients, the rate of NMSC was 64 per 1,000 patient years pre-switch and 30 per 1,000 patient years post switch, with an adjusted effect size of 0.49 [0.22 − 1.09] (p .081).,Kidney transplant recipients were followed up for a median 3.4 years.,Liver transplants were followed for a median 6.6 years.,In this study, the conversion of maintenance immunosuppression from calcineurin inhibitors to mTOR inhibitors for clinical indications did appear to reduce the incidence of NMSC in kidney and liver transplant recipients.
Cutaneous squamous cell carcinoma (CSCC) is a common type of skin malignancy.,MicroRNA-221 (miRNA-221) is a critical non-coding RNA in tumor initiation and progression.,However, the molecular mechanisms of miRNA-221 in the development of CSCC remain unknown.,This study investigated the expression of miRNA-221 in CSCC and its potential tumor biological functions.,MTT assay, colony assay, PCR, and Western blot were adopted.,In this study, miRNA-221 expression was significantly higher in CSCC tissues and cell lines than in normal tissues and cells (P < 0.05).,Further functional experiments indicated that miRNA-221 knockdown inhibited the proliferation and cell cycle, while upregulation of miRNA-221 presented the opposite role.,The dual reporter gene assays indicated that PTEN is a direct target gene of miRNA-221.,PTEN protein or mRNA levels were decreased after the cells were transfected with miR-221 mimics.,Taken together, the obtained results indicated that miR-221 plays an oncogenic function in CSCC by targeting PTEN and further suggest that miR-221 may be a potential target for CSCC diagnosis and treatment.