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Articles by LiMei Xu
Total Records ( 2 ) for LiMei Xu
  Qiang Wan , Limei Xu and Feng Yang
  The envelopment of the nucleocapsid is an important step in white spot syndrome virus (WSSV) assembly. Previous studies showed that VP26, a major envelope protein of WSSV, can interact with viral nucleocapsid. In this study, using the biotin label transfer technique, we found that the biotin label was transferred from Bio-rVP26 to the viral capsid protein VP51 or from Bio-MBP-VP51 to VP26. Far-Western analyses provided further evidence for direct interaction between VP26 and VP51. Therefore, we conclude that VP26 functions as a matrix-like linker protein between the viral envelope and nucleocapsid, which suggests that VP26 is a key factor in the envelopment of WSSV virion.
  George Z. Cheng , WeiZhou Zhang , Mei Sun , Qi Wang , Domenico Coppola , Mena Mansour , LiMei Xu , Carliann Costanzo , Jin Q. Cheng and Lu-Hai Wang
  To explore the basis of metastasis, we compared the human breast cancer lines MCF-7 and MDA-MB453, which have low invasive ability, with their sublines MCF7-I4 and MDA-MB453-I4 with high invasive ability for gene expression and signaling pathways. We previously showed that the I4 lines had dramatically elevated levels of Twist compared with their parental lines. In this study, we observed significantly increased STAT3 Tyr705 phosphorylation, but not the STAT3 protein levels, in the I4 lines. Activation of STAT3 by interleukin-6 or expression of activated Src induced Twist expression at protein and mRNA levels. Inhibiting STAT3 by a small molecule inhibitor, JSI-124, STAT3 small hairpin RNAs, or dominant negative STAT3 resulted in significant reduction of Twist protein and mRNA expression. STAT3 directly bound to the second proximal STAT3-binding site on the human Twist promoter and activated its transcriptional activity. Inhibition of STAT3 reduced migration, invasion, and colony formation of the I4 cells. Ectopic expression of Twist significantly rescued those phenotypes. Ten normal and 46 tumor specimens of breast tissues were examined for activation of STAT3 and expression of Twist. There was a strong correlation between Tyr705 p-STAT3 and Twist level in the late stage tumor tissues. Our results indicate that activated STAT3 transcriptionally induces Twist, which plays an important role in promoting migration, invasion, and anchorage-independent growth. Together with our previous observation that Twist transcriptionally induces AKT2 to mediate Twist-promoted oncogenic functions, we conclude that STAT3, Twist, and AKT2 form a functional signaling axis to regulate pivotal oncogenic properties of cancer cells.
 
 
 
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