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Wang, Fei

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Wang

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Fei

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Wang, Fei

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20162

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Author's Publications: search.filters.isAuthorOfPublication.bedfdc1f-0a6c-4481-9815-b9807bf1ff56

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    Targeting SALL4 by entinostat in lung cancer
    (Impact Journals LLC, 2016) Yong, Kol Jia; Li, Ailing; Ou, Wen-Bin; Hong, Clarice Kit Yee; Zhao, Wenxiu; Wang, Fei; Tatetsu, Hiro; Yan, Benedict; Qi, Lihua; Fletcher, Jonathan; Yang, Henry; Soo, Ross; Tenen, Daniel; Chai, Li
    The overall survival of lung cancer patients remains dismal despite the availability of targeted therapies. Oncofetal protein SALL4 is a novel cancer target. We herein report that SALL4 was aberrantly expressed in a subset of lung cancer patients with poor survival. SALL4 silencing by RNA interference or SALL4 peptide inhibitor treatment led to impaired lung cancer cell growth. Expression profiling of SALL4-knockdown cells demonstrated that both the EGFR and IGF1R signaling pathways were affected. Connectivity Map analysis revealed the HDAC inhibitor entinostat as a potential drug in treating SALL4-expressing cancers, and this was confirmed in 17 lung cancer cell lines. In summary, we report for the first time that entinostat can target SALL4-positive lung cancer. This lays the foundation for future clinical studies evaluating the therapeutic efficacy of entinostat in SALL4-positive lung cancer patients.
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    Leukemic survival factor SALL4 contributes to defective DNA damage repair
    (2016) Wang, Fei; Gao, Chong; Lu, Jiayun; Tatetsu, Hiro; Williams, David; Müller, Lars U; Cui, Wei; Chai, Li
    SALL4 is aberrantly expressed in human myelodysplastic syndromes (MDS) and acute myeloid leukemia (AML). We have generated a SALL4 transgenic (SALL4B Tg) mouse model with pre-leukemic MDS-like symptoms that transform to AML over time. This makes our mouse model applicable for studying human MDS/AML diseases. Characterization of the leukemic initiation population in this model leads to the discovery that Fancl (Fanconi anemia, complementation group L) is down-regulated in SALL4B Tg leukemic and pre-leukemic cells. Similar to the reported Fanconi anemia (FA) mouse model, chromosomal instability with radial changes that can be detected in pre-leukemic SALL4B Tg bone marrow (BM) cells after DNA damage challenge. Results from additional studies using DNA damage repair reporter assays support a role of SALL4 in inhibiting the homologous recombination pathway. Intriguingly, unlike the FA mouse model, after DNA damage challenge, SALL4B Tg BM cells can survive and generate hematopoietic colonies. We further elucidated that the mechanism by which SALL4 promotes cell survival is through Bcl2 activation. Overall, our studies demonstrate for the first time that SALL4 has a negative impact in DNA damage repair, and support the model of dual functional properties of SALL4 in leukemogenesis through inhibiting DNA damage repair and promoting cell survival.