FQI1 inhibits the DNA-binding activity of LSF, a ubiquitous transcription factor that is up regulated in many hepatocellular carcinomas (HCC). FQI1 inhibits LSF-dependent luciferase reporter expression, blocks proliferation in cancer cell lines, and induces apoptosis in liver cancer cells but is not toxic to primary hepatocytes. FQI1 also inhibits tumor growth in a mouse HCC xenograft model.
FQI1 is an inhibitor of transcription factor LSF.
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The oncogene LSF (encoded by TFCP2) has been proposed as a novel therapeutic target for multiple cancers. LSF overexpression in patient tumors correlates with poor prognosis in particular for both hepatocellular carcinoma and colorectal cancer. The limited treatment outcomes for
Despite advances in precision oncology, cancer remains a global public health issue. In this report, proof-of-principle evidence is presented that a cell-penetrable peptide (ACP52C) dissociates transcription factor CP2c complexes and induces apoptosis in most CP2c oncogene-addicted cancer cells through transcription
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