Abstract
Renal cell cancer (RCC) is the most common kidney cancer and has a poor prognosis (1). Although some achievements have been made to date, radical therapy for RCC remains challenging (2). It is now generally accepted that recurrence and metastasis are the main cause of reducing survival of RCC patients attributed to causing tumor resistance for conventional therapies. Recently, sunitinib is an important therapeutic option for advanced RCC patients. However, it is reported that 10–20% of advanced RCC patients are resistant to sunitinib therapy because of the patient’s inherent drug resistance (3). Emerging evidence have shown that the acquisition of sunitinib resistance was associated with the activation of compensatory signaling pathways (4), but the underlying mechanisms remain unclear. Further investigations of the mechanisms of resistance in RCC are necessary to clarify the pathogenesis and development of novel combination therapies (5).
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