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    Online Resource
    Online Resource
    American Association for Cancer Research (AACR) ; 2016
    In:  Cancer Research Vol. 76, No. 14_Supplement ( 2016-07-15), p. 2949-2949
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 76, No. 14_Supplement ( 2016-07-15), p. 2949-2949
    Abstract: REV3L, the catalytic subunit of DNA ploymerse zeta, is well known to participate in error-prone translesion synthesis (TLS) with less stringent and lower processivity. Recent evidence demonstrated that REV3L is involved in carcinogenesis and tumor progression. However, the function of REV3L remains unclear in esophageal squamous cell cancer (ESCC). In this study, we examined REV3L expression in ESCC tissues and its association with clinicopathological parameters. REV3L was found to be significantly up-regulated in ESCC tissues, which is correlated with lymph node metastasis and clinical stages of the patients. To further investigate the potential role of REV3L in esophageal cancer, stable ESCC cell lines with the suppression of REV3L expression were established. Down regulation of REV3L expression led to a decrease in cell proliferation and invasive tendency partly through suppressing cyclinD1 and survivin expression, and an increase in cellular sensitivity to 5-Fu by inducing G1 phase arrest and apoptosis. Therefore, REV3L plays an important role in ESCC progression and chemoresistance, and is a potential diagnostic marker and therapeutic target for ESCC. Citation Format: Jundong Zhou, Sitao Zou, Wei-Qun Ding, Jinchang Wu. REV3L, the catalytic subunit of pol ζ, is involved in the progression and chemoresistance of esophageal squamous cell cancer. [abstract]. In: Proceedings of the 107th Annual Meeting of the American Association for Cancer Research; 2016 Apr 16-20; New Orleans, LA. Philadelphia (PA): AACR; Cancer Res 2016;76(14 Suppl):Abstract nr 2949.
    Type of Medium: Online Resource
    ISSN: 0008-5472 , 1538-7445
    RVK:
    RVK:
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2016
    detail.hit.zdb_id: 2036785-5
    detail.hit.zdb_id: 1432-1
    detail.hit.zdb_id: 410466-3
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