Research reveals Filamin A influences DLC1 levels in liver cancer, suggesting it may be a therapeutic target.
We identify a previously unknown interaction between the tumor suppressor DLC1 and Filamin A. Filamin A acts as a dual regulator of the RhoA-MRTF-A/SRF signaling axis, promoting gene transcription via MRTF-A or activating DLC1 to suppress transcription and induce senescence. This balance is controlled by phosphorylation of Filamin A at serine 2152, which determines whether Filamin A binds to DLC1 or MRTF-A. In hepatocellular carcinoma mouse models, high levels of phosphorylated FLNA correlate with reduced DLC1 expression. These findings highlight FLNA phosphorylation as a potential biomarker and therapeutic target, thereby providing new mechanistic insight into DLC1 downregulation in liver cancer.
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Michael Sergeev (2026) studied this question.
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