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Its oncogenic potential is mediated by multiple mechanisms, including stimulation of cell proliferation [7, 9, 10, 13, 14], inhibition of cellular senescence [2,4] inhibition of apoptosis [8,10], resistance to oxidative stress [15], regulation of cellular metabolism [16], regulation of stem cell reprogramming [17,18], differentiation [6], and cancer stem cell maintenance [10]

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In addition to sorafenib, sunitinib and glycogen synthase 1 inhibitors can produce synthetic lethal effects in RCC cells (143)

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