POSTN expression was significantly upregulated in renal cell carcinoma tissues, and its knockdown inhibited RCC cell proliferation, migration, and invasion via the ILK/AKT/mTOR pathway.
Does POSTN knockdown or overexpression affect proliferation, migration, invasion, and EMT in renal cell carcinoma cells?
POSTN promotes epithelial-mesenchymal transition and proliferation in renal cell carcinoma via the ILK/AKT/mTOR pathway, suggesting it as a potential therapeutic target.
p-value: p=<0.01
Periostin (POSTN) is an extracellular matrix (ECM) protein, involved in various diseases. This research focused on the detailed mechanisms study of periostin (POSTN) overexpression in renal cell carcinoma (RCC) invasion and migration. Western blot and RT-PCR were performed to explore POSTN expression in various RCC cells. Cells were transfected with siRNAs or lentivirus to regulate the expression of POSTN. The effects of POSTN on cell viability, apoptosis, migration, invasion and epithelial-to-mesenchymal transition (EMT) of RCC cells were determined by CCK-8, flow cytometry, migration and invasion assay and Western blot analysis. POSTN expression was significantly enhanced in RCC cells compared with renal tubular epithelial cells. In vitro experiments showed that POSTN knockdown could dramatically inhibit RCC cell proliferation, migration and invasion, while overexpression of POSTN could promote these biological behaviors. We further demonstrated that POSTN knockdown suppressed epithelial-mesenchymal transition (EMT), which was mediated via upregulation of E-cadherin and downregulation of N-cadherin and vimentin, through IKL/AKT/mTOR pathway. In contrast, overexpression of POSTN could promote EMT in RCC cells via the activation of IKL /AKT/mTOR pathway. Next, we demonstrated that higher POSTN expression promoted angiogenesis in vivo in an RCC xenograft tumor via activating IKL /AKT/mTOR pathway. Our study showed that POSTN could promote EMT through ILK/AKT/mTOR pathway and might be an alternative therapeutic strategy for RCC treatment.
Jia et al. (Fri,) conducted a other in Renal cell carcinoma (n=37). POSTN knockdown and overexpression vs. Control (si-NC/LV-NC or adjacent normal tissues) was evaluated on POSTN expression levels in RCC tissues compared to adjacent normal tissues (p=<0.01). POSTN expression was significantly upregulated in renal cell carcinoma tissues, and its knockdown inhibited RCC cell proliferation, migration, and invasion via the ILK/AKT/mTOR pathway.