Lechuang Chen

Fuda Cancer Hospital, Shengcheng, Guangdong, China

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Publications (7)41.9 Total impact

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    Mei Liu · Chenfei Hu · Qing Xu · Lechuang Chen · Kai Ma · Ningzhi Xu · Hongxia Zhu ·
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    ABSTRACT: Esophageal squamous cell carcinoma (ESCC) occurs at a very high rates in certain regions of China. There are increasing evidences demonstrating that selenium could act as a potential anti-esophageal cancer agent, but the precise mechanisms involved are still not completely understood. Methylseleninicacid (MSA), as a potent second-generation selenium compound, is a promising chemopreventive agent. Previous studies demonstrated that the Kelch-like ECH-associated protein 1 (Keap1)/Nuclear factor E2-related factor 2 (Nrf2) system plays a critical role in cancer prevention, but little is known about its association with MSA in ESCC cells. In this study, we observed that MSA treatment significantly down-regulated Keap1, induced nuclear accumulation of Nrf2 and enhance the antioxidant response element (ARE) promoter activity in ESCC cells. MSA could also significantly induce microRNA-200a (miR-200a) expression and inhibit Keap1 directly. Antagomir-200a could attenuate MSA treatment-induced Keap1 down-regulation in ESCC cells. Moreover, MSA-induced miR-200a expression was dependent on the mediation of Krüpple-like factor 4 (KLF4). These results reaffirm the potential role of MSA as a chemopreventive agent via the regulation of KLF4/miR-200a/Keap1/Nrf2 axis in ESCC cells. Copyright 2015 The Author(s).
    Bioscience Reports 09/2015; DOI:10.1042/BSR20150092 · 2.64 Impact Factor
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    ABSTRACT: Aurora-A overexpression is common in various types of cancers and has been shown to be involved in tumorigenesis through different signaling pathways, yet how the deregulation affects cancer therapeutics remains elusive. Here we showed that overexpression of Aurora-A rendered esophageal cancer cells resistance to cisplatin (CDDP) by inhibiting apoptosis. By using an apoptosis array, we identified a downstream gene, p21-activated kinase 7 (PAK7). PAK7 was upregulated by Aurora-A overexpression at both mRNA and protein levels. Importantly, the expression levels of Aurora-A and PAK7 were correlated in ESCC primary samples. Chromatin immunoprecipitation (ChIP) assay revealed that binding of E2F1 to the promoter of PAK7 was significantly enhanced upon Aurora-A activation, and knockdown of transcription factor E2F1 decreased PAK7 expression, suggesting that Aurora-A regulated PAK7 through E2F1. Furthermore, we demonstrated that PAK7 knockdown led to increased apoptosis, and Aurora-A-induced resistance to CDDP was reversed by downregulation of PAK7, suggesting PAK7 was a downstream player of Aurora-A that mediated chemoresistance of ESCC cells to CDDP. Our data suggest that PAK7 may serve as an attractive candidate for therapeutics in ESCC patients with Aurora-A abnormality.
    PLoS ONE 12/2014; 9(12):e113989. DOI:10.1371/journal.pone.0113989 · 3.23 Impact Factor
  • Chenfei Hu · Wei Zhang · Qing Xu · Lechuang Chen · Kai Ma · Mei Liu · Hongxia Zhu · Ningzhi Xu ·

    Cancer Research 10/2014; 74(19 Supplement):427-427. DOI:10.1158/1538-7445.AM2014-427 · 9.33 Impact Factor
  • Chenfei Hu · Mei Liu · Wei Zhang · Qing Xu · Kai Ma · Lechuang Chen · Zaozao Wang · Shun He · Hongxia Zhu · Ningzhi Xu ·
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    ABSTRACT: Esophageal squamous cell carcinoma (ESCC) occurs at a very high frequency in certain areas of China. Supplementation with selenium-containing compounds was associated with a significantly lower cancer mortality rate in a study conducted in Linxia, China. Thus, selenium could be a potential anti-esophageal cancer agent. In this study, methylseleninic acid (MSA) could inhibit cell growth of ESCC cells in vitro and in vivo. Upon treated with MSA, the activity of histone deacetylases (HDACs) was decreased and general control nonrepressed protein 5 (GCN5) was upregulated in ESCC cells. Meanwhile, a significant increase of H3K9 acetylation (H3K9ac) was detected. Upregulation of Krüppel-like factor 4 (KLF4) was also observed after MSA treatment. Additionally, the acetylated histone H3 located more at KLF4 promoter region after MSA treatment, shown by chromatin immunoprecipitation (ChIP) assay. Moreover, knockdown of GCN5 decreased the protein level of both H3K9ac and KLF4, along with less cell growth inhibition. Taken all, our results indicated that MSA could inhibit ESCC cell growth, at least in part, by MSA-HDAC/GCN5-H3K9ac-KLF4 axis. To our best knowledge, this is the first report that MSA induced acetylation of histone H3 at Lys9, which might depend on the activities and the balance between HDACs and HATs. © 2014 Wiley Periodicals, Inc.
    Molecular Carcinogenesis 04/2014; 54(10). DOI:10.1002/mc.22174 · 4.81 Impact Factor
  • Lechuang Chen · Chenfei Hu · Qing Xu · Kai Ma · Mei Liu · Hongxia Zhu · Ningzhi Xu ·

    Cancer Research 08/2013; 73(8 Supplement):1550-1550. DOI:10.1158/1538-7445.AM2013-1550 · 9.33 Impact Factor
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    ABSTRACT: Esophageal squamous cell carcinoma (ESCC) is a leading cause of cancer-related death in China and has limited effective therapeutic options except for early surgery, since the underlying molecular mechanism driving its precursor lesions towards invasive ESCC is not fully understood. Cellular senescence is the state of the permanent growth arrest of a cell, and is considered as the initial barrier of tumor development. Human differentiated embryo chondrocyte expressed gene 1 (Dec1) is an important transcription factor that related to senescence. In this study, DEC1 immunohistochemical analysis was performed on tissue microarray blocks constructed from ESCC combined with adjacent precursor tissues of 241 patients. Compared with normal epithelia, DEC1 expression was significantly increased in intraepithelial neoplasia and DEC1 expression was significantly decreased in ESCC in comparison with intraepithelial neoplasia. In vitro, DEC1 overexpression induced cellular senescence, and it inhibited cell growth and colony formation in ESCC cell line EC9706. Fresh esophagectomy tissue sections from five ESCC patients were detected by immunohistochemistry of DEC1 and senescence-associated β-galactosidase (SA-β-Gal) activity, and strongly positive expression of DEC1 was correlated to more senescent cells in these fresh tissue sections. Kaplan-Meier method analysis of the 241 patients revealed that DEC1 expression levels were significantly correlated with the survival of ESCC patients after surgery. The expression levels of DEC1 were also correlated with age, tumor embolus, depth of invasion of ESCC, lymph metastasis status and pTNMs. These results suggest that DEC1 overexpression in precursor lesions of ESCC is a protective mechanism by inducing cellular senescence in ESCC initiation, and DEC1 may be a potential prognostic marker of ESCC.
    PLoS ONE 07/2012; 7(7):e41862. DOI:10.1371/journal.pone.0041862 · 3.23 Impact Factor

  • Cancer Research 06/2012; 72(8 Supplement):732-732. DOI:10.1158/1538-7445.AM2012-732 · 9.33 Impact Factor

Publication Stats

10 Citations
41.90 Total Impact Points


  • 2014-2015
    • Fuda Cancer Hospital
      Shengcheng, Guangdong, China
    • Chinese Academy of Medical Sciences
      Peping, Beijing, China
  • 2012
    • Chongqing Cancer Hospital and Institute
      Ch’ung-ch’ing-shih, Chongqing Shi, China