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ADP-ribosylation factor-like protein 4C (ARL4C) is a member of the ARF family of small GTP-binding proteins within the Ras superfamily, involved in the regulation of actin cytoskeleton dynamics, cell morphology, migration, and membrane trafficking[1][5]. It localizes to cell membranes, cytoplasm, and nucleus, exhibits unusually high guanine nucleotide exchange rates, and interacts with regulators such as filamin-A and Cdc42 to drive filopodia formation and motility[5]. ARL4C participates in lipid and cholesterol metabolism through LXR-mediated pathways and is implicated in tumor progression, primarily by promoting cancer cell proliferation, migration, and invasion[1][3][5]. Elevated ARL4C expression is associated with cancer aggressiveness, making it both a potential biomarker and a therapeutic target candidate, particularly in renal cell carcinoma and atherosclerosis[1][2][3].
LXR agonists modulate ARL4C expression and thereby promote cholesterol efflux, alter lipid metabolism. Likely indirect inhibition of cancer cell growth/migration via ARL4C suppression; no direct inhibition described.
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