Here, we show that LPAR1 activation facilitates FLNA phosphorylation at S2152, complex formation with MRTF-A, stress fiber- and focal adhesion formation, whereas impairment of FLNA phosphorylation caused by LPAR1 depletion or blockade redistributes MRTF-A to the cytoplasm and drives HCC cells into senescence. This evidence concerns the gene LPAR1 and hepatocellular carcinoma.