SLC3A2 promotes integrin-dependent renal cancer growth [32] and loss of SLC3A2 inhibits Ras-driven tumorigenesis [33], Furthermore, we found that circSLC3A2, mainly localized in the cytoplasm, was upregulated in HCC tissues, associated with poor survival in patients with HCC, and facilitated cell proliferation and invasion by sponging miR-490-3p and upregulating PPM1F expression, but knockdown of circSLC3A2 reversed these effects (Fig. 10), suggesting that circSLC3A2 might function as an oncogenic factor in HCC via regulation of the miR-490-3p/PPM1F axis. Here, PPM1F is linked to renal carcinoma.