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. 2023 Oct 14;13(10):e1443. doi: 10.1002/ctm2.1443

FIGURE 4.

FIGURE 4

Cullin‐associated and neddylation‐dissociated 1 (CAND1) functions by regulating the SCFFBXO11 complex to recruit hnRNPA2B1. (A) A coimmunoprecipitation (co‐IP) experiment detected binding between CAND1 and CUL1. (B) CUL1 knockdown partially reversed the CAND1 overexpression‐induced promotion of cell invasion. (C) CUL1 knockdown reduced colony formation in CAND1 overexpressing HCC‐LM3 cells. (D) CCK8 assay showing that CUL1 knockdown reduces the proliferation of CAND1‐overexpressing cells. (E) BODIPY staining showed that lipid accumulation clearly decreased in the CUL1 knockdown group. (F) CUL1 knockdown partially reversed the CAND1 overexpression‐induced increase in intracellular triglycerides and cholesterol. (G) Relative quantitative mass spectrometry (MS)‐based proteomic analysis. (H) A co‐IP experiment was performed to detect binding between CUL1 and different F‐box proteins. (I) A co‐IP experiment was performed to detect binding between FBXO11 and hnRNPA2B1, and binding between hnRNPA2B1 and other F‐box proteins. (J) GST pull‐down assay. (K) A co‐IP experiment was performed to detect binding between HA‐FBXO11 and Flag‐hnRNPA2B1. (L) FBXO11 immunolabeling shows colocalization with hnRNPA2B1. All cellular experiments were run in triplicate and repeated three times. p < .05(*), p < .01(**) or p < .001(***).