Hai-Jing Liu

Publications (3)5.81 Total impact

• Article: The level of phosphorylated Akt predominantly reflects the expressive status of CerbB2 in invasive breast cancer.

  Yingkai Chi, Jing Zhao, Su-Ping Cui, Ping Jiang, Hua-Li Wang, Hong Zhang, Jing-Zhuo Mao, Hai-Jing Liu, Lin Hou, Bo Zhang
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  ABSTRACT: Although some evidence has been documented on EGFR/PI3K mediation of Akt activation in breast cancers, ILK and DNA-PK have not been investigated so far. The aim of this study was to analyze the expression of phosphorylated Akt (pAkt) in breast cancer, with respect to its upstream regulators. The immunostaining of pAkt (Ser473) in 70 invasive breast cancers revealed that status of CerbB2 could play a major role in Akt phosphorylation, while ILK was also involved in the stimulated level of pAkt. The results would provide an important clue for the activation of Akt and potential targeted therapy in breast cancer.
  Histology and histopathology 02/2013; · 2.48 Impact Factor
• Article: [Aberrant expression and correlative analysis of P16 in breast cancers].

  Su Ping Cui, Hua Li Wang, Wei Peng, Hai Jing Liu, Lin Hou, Bo Zhang
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  ABSTRACT: To evaluate the relationship between the aberrant expression of P16 and the clinic-pathological features in breast cancers. In our study, 72 cases of breast cancer were collected and the expressions of P16, HER-2 (human epidermal growth receptor-2), ER (estrogen receptor), PR (progesterone receptor), P53, Ki-67 were measured by immunohistochemistry. The correlations between the P16 and the clinic-pathological features(menstruation, tumor size, histological grade, lymph node metastasis)were statistically analyzed. Aberrant expression of P16 was detected in 36.1%(26/72)of breast cancers. Not only was the staining of P16 increased,but also the subcellular localization was changed from nuclear to cytoplasm or whole cell staining. In general, the occasional cell staining (+) usually presented in nuclear, as expression increased, P16 showed mainly in cytoplasm or whole cells(+++) even diffusive staining in extracellular, and the moderate staining was multi-focal both in nuclear and cytoplasm. The expression of P16 was significantly increased in ER negative group compared with ER positive group (78.6% vs. 9.1%,P=0.000). Statistical analysis showed a significant correlation of high Ki-67 index with the group of P16 positive (Z =-0.263, P=0.003). In addition, significant difference was calculated between pre- and post-menopause (55.6% vs. 24.4%, P=0.008)and P16 expressions were also more credited to the poor-differentiated group in histological grading: 11.8% (2/17) for highly differentiated group, 27.6% (8/29) for moderately differentiated group and 61.5% (16/26) for poorly differentiated group, respectively (P=0.002). The aberrant expression of P16 in breast cancers correlated closely with loss of estrogen receptor, high proliferation index or high histological grade, predisposed to the patients of pre-menopause, implicating that the aberrant expression of P16 should be a predictor of poor response to endocrine therapy or more aggressive behavior.
  Beijing da xue xue bao. Yi xue ban = Journal of Peking University. Health sciences 10/2012; 44(5):755-9.
• Article: Girdin locates in centrosome and midbody and plays an important role in cell division.

  Jing-Zhuo Mao, Ping Jiang, Su-Ping Cui, Ya-Li Ren, Jing Zhao, Xiu-Hua Yin, Atsushi Enomoto, Hai-Jing Liu, Lin Hou, Masahide Takahashi, Bo Zhang
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  ABSTRACT: Girdin is a downstream effector of epidermal growth factor receptor (EGFR)-AKT and interacts with actin and microtubule. Increasing evidence confirmed that Girdin played an important role in cell migration. Here we report that Girdin also regulates cell division. Overexpression or suppression of Girdin leads to attenuated cell proliferation. Imaging of mitotic cells revealed that Girdin is located in the cell division apparatus such as centrosome and midbody. The sub-cellular localization of Girdin was dependent on the domains, which interacted with actin or microtubules. Overexpression of Girdin lead to increased centrosome splitting and amplification. In addition, data show that pAKT also locates in both the centrosome and midbody, indicating the regulating role of AKT in Girdin-mediated cell division. To elucidate the effect of Girdin on tumor growth in vivo, HeLa cells infected with retrovirus harboring either control or Girdin shRNAs were injected subcutaneously into the immunocompromised nude mice. Downregulation of Girdin by shRNA markedly inhibited the cell growth of subcutaneously transplanted tumors in nude mice. These data demonstrate that Girdin is important for efficient cell division. Taking our previous data into consideration, we speculate that Girdin regulates both cell division and cell migration through cytoskeletal molecules.
  Cancer Science 07/2012; 103(10):1780-7. · 3.33 Impact Factor