Role of Pten Phosphatase Activity in Migration of Renal Cancer Cells

Brenner, Walburgis; Schneider, Elke; Lausch, Ekkehard; Roos, Frederik C.; Thüroff, Joachim W.

doi:10.1016/s0022-5347(09)60109-9

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“…It has been shown that in renal cell carcinoma, PTEN was commonly mutated or down-regulated (1,11,17,26,39); and PI3K activation and Akt activation were increased in renal cell carcinoma and were associated with poor prognosis (16,32). Furthermore, in vitro studies suggested that inhibition of PI3K by specific inhibitor could inhibit renal cell carcinoma (14); Overexpression of PTEN in renal cell carcinoma cell lines inhibits cell migration (5). So, these results cepin on microRNA-21 expression was studied.…”

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confidence: 99%

“…In addition, phosphatase and tensin homolog (PTEN) was a target of microRNA-21 and could be down-regulated by microRNA-21 (22,42). PTEN is a tumor suppressor in renal cell carcinoma and inhibits tumor cell proliferation and migration in renal cell carcinoma (2,5,39). Nonetheless, PTEN gene is often mutated or down-regulated in renal cell carcinoma (1,11,17,26,39).…”

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Cordycepin induces apoptotic cell death and inhibits cell migration in renal cell carcinoma via regulation of microRNA-21 and PTEN phosphatase

et al. 2017

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Cordycepin is an active component extracted from Traditional Chinese medical herb Cordyceps militaris. Many reports demonstrated that cordycepin harbors antitumor activity in a broad spectrum of cancer types. In this study the actions and the underneath molecular mechanisms of cordycepin were investigated in renal cell carcinoma Caki-1 cell line. Results showed that cordycepin induced apoptotic cell death and inhibited cell migration in Caki-1 cells. Quantitative real-time PCR results and western blot analyses indicated cordycepin dose-dependently decreased microRNA-21 expression and Akt phosphorylation levels in Caki-1 cells, but increased PTEN phosphatase levels. Block of cordycepin-induced microRNA-21 decrease or PTEN increase in Caki-1 cells by transfection of microRNA-21 mimic or PTEN siRNA significantly attenuated cordycepin-induced cell death and inhibition of cell migration. Taken together, findings in present study suggested that cordycepin induced apoptotic cell death in renal cell carcinoma through regulation of microRNA-21 and PTEN phosphatase. Furthermore, present study also firstly illustrated that cordycepin inhibited cell migration of renal cell carcinoma, which also involved micro-RNA-21 and PTEN phosphatase.Renal cell carcinoma (RCC) is the most lethal urological cancer, accounting for 87% of all renal malignancies and 2-3% of all cancers (4). In the past two decades, the global incidence of RCC has increased by 2% per year (4). Worldwide, the agestandardized incidence and mortality of RCC were 6 per 100,000 and 2.1 per 100,000 respectively (43). Despite advance in diagnostic techniques, up to 20-30% of patients with RCC present with metastasis (4). The prognosis of RCC has historically been poor, with 5-year survival rate of 8% among patients with metastatic RCC (9). Although recent progress about understanding of the pathogenesis of RCC has led to novel immune-based and targeted treatments for this chemoresistant cancer, no one drug obtains overall response rate of 100% and durable complete responses (4, 9). Development of neo-adjuvant therapy is still in a demand at present. Cordycepin is a main active composition extracted from Cordyceps militaris and has been reported to harbor anti-tumor activity in a broad spectrum of cancer types, including lung cancer (50), ovarian cancer (46), leukemia (30), breast cancer (47), and so on (33). Two recent reports firstly demonstrated that cordycepin could induce apoptosis in renal cell carcinoma through Erk-JNK signaling pathway (20,48) and indicated the potential application of cordycepin in treating renal cell carcinoma. However, the actions and the underneath molecular mechanisms of cordycepin in renal cell carcinoma are not definitely clear and warrant extensive and further investigations. Recently, a comprehensive molecular analysis

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