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SALL4 is essential for cancer and leukemia. SALL4 is critical for cancer initiation, drug resistance, side-population, and metastases. Additional loss-of-function studies have demonstrated that SALL4 is essential for cancer cell survival.

Studies from our lab have explored and will continue to understand the oncogenic biology of SALL4 and its target genes in various cancer types, such as leukemia and liver cancer.

Yong et al. “Oncofetal gene SALL4 in aggressive hepatocellular carcinoma”, N Engl J Med, 2013.

SALL4 is a novel oncofetal protein in HCC. In healthy humans, SALL4 is expressed in fetal liver but silenced in mature adult liver. In a subgroup of HCC livers, SALL4 is re-activated and plays a functional role in hepatocarcinogenesis by silencing the tumor suppressor PTEN through the recruitment of the NuRD complex. A therapeutic peptide can be used to block the interaction between SALL4 and the NuRD complex, thereby activating PTEN transcription. Upregulation of PTEN expression leads to downregulation of pAKT level and silencing of the PI3K/AKT survival signaling, resulting in decreased HCC cell viability and tumorigenicity. We propose SALL4 to be a novel oncofetal protein that can be specifically targeted for treatment of a subgroup of aggressive HCCs with SALL4 expression.

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