Laikui Liu

Nanjing Medical University, Nan-ching, Jiangsu Sheng, China

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Publications (5)16.87 Total impact

  • [Show abstract] [Hide abstract]
    ABSTRACT: The Hippo pathway has emerged as a fundamental regulator in tissue growth, organ size and stem cell functions, and tumorigenesis when deregulated. However, its roles and associated molecular mechanisms underlying oral squamous cell carcinoma (OSCC) initiation and progression remain largely unknown. Here, we identified TAZ, the downstream effector of Hippo signaling, as a novel bona fide oncogene by promoting cell proliferation, migration/invasion and chemoresistance in OSCC. TAZ promoted epithelial-to-mesenchymal transition (EMT) and also was involved in TGF-β1-induced EMT in oral cancer cells. Furthermore, enriched TAZ sustained self-renewal, maintenance, tumor-seeding potential of oral cancer stem cells (CSCs). Remarkably, enforced TAZ overexpression conferred CSCs-like properties on differentiated non-CSCs and fueled phenotypic transition from non-CSCs to CSCs-like cells. Mechanistically, TAZ-TEADs binding and subsequent transcriptional activation of EMT mediators and pluripotency factors are presumably responsible for TAZ-mediated EMT and non-CSCs-to-CSCs conversion. Importantly, aberrant TAZ overexpression was found to be associated with tumor size, pathological grade and cervical lymph node metastasis, as well as unfavorable prognosis. Pharmacological repression of TAZ by simvastatin resulted in potent anti-cancer effects against OSCC. Taken together, our findings have revealed critical links between TAZ, EMT and CSCs in OSCC initiation and progression, and also established TAZ as a novel cancer biomarker and viable druggable target for OSCC therapeutics. Copyright © 2015 Federation of European Biochemical Societies. Published by Elsevier B.V. All rights reserved.
    Molecular Oncology 02/2015; 9(6). DOI:10.1016/j.molonc.2015.01.007 · 5.33 Impact Factor
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    ABSTRACT: Previous studies have shown that craniofacial bone marrow stromal cells (BMSCs) have a strong osteogenic potential. However, the mechanism by which BMSCs of various embryonic origins develop diverse osteogenic potentials remains unclear. To investigate the mechanisms regulating osteoblast differentiation in two different types of BMSCs, we compared the temporal and spatial mRNA and protein expression patterns of Satb2 and its downstream gene Hoxa2 by using real-time polymerase chain reaction, Western blotting and fluorescent immunostaining in mandible BMSCs (M-BMSCs) and tibia BMSCs (T-BMSCs) undergoing osteoblast differentiation. Higher levels of alkaline phosphatase, greater calcium accumulation and earlier expression of Runx2 were observed in osteogenic-induced M-BMSCs compared with T-BMSCs. Low levels of Satb2 were detected in both types of uninduced BMSCs but the majority of SATB2 was located in the nuclei of M-BMSCs. Notably, Satb2 was expressed earlier in M-BMSCs and Hoxa2, a downstream target of Satb2, was not expressed in uninduced M-BMSCs or during osteoblast differentiation, just as during embryonic mandible development. In contrast, Hoxa2 was reactivated in T-BMSCs during osteoblast differentiation. Based on these results, we conclude that SATB2 plays a different role during osteoblast differentiation of M-BMSCs and T-BMSCs. The earlier activation of Satb2 expression in M-BMSCs compared with T-BMSCs might explain the stronger osteogenic potential of M-BMSCs.
    Cell and Tissue Research 09/2012; 350(3). DOI:10.1007/s00441-012-1487-4 · 3.57 Impact Factor
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    ABSTRACT: The purpose of this study is to investigate the effects of dexamethasone on repair of a critical size defect of the mandible in male Sprague-Dawley rats. Fifty rats were divided into 2 groups: saline control and dexamethasone-treated groups. A 1 mm × 3 mm full-thickness bone defect was created at the inferior border of the mandible. Saline or dexamethasone was administered once a day for 5 days after postoperative palinesthesia. On days 1, 3, 6, 10 and 17, after cessation of drug administration, 5 samples from each group were analysed. The bone defect healing process was examined and analysed by stereology, radiology, histology and histochemical staining for total collagen, tartrate-resistant acid phosphatase staining for osteoclasts and immunohistochemical staining for the COX-2, RUNX2 and osteocalcin antigens. The dexamethasone-treated rats exhibited significantly lower radiopacity properties compared to the control rats. Histological staining revealed that the osteogenic differentiation and maturation of a callus in the defect region was significantly delayed from day 1 to day 10 in the dexamethasone group after cessation of drug administration compared to the control group. Consistent with the histological data, the level of total collagen protein was significantly lower in the dexamethasone group than in the control group. However, there was no significant difference between the 2 groups at day 17. Immunohistochemical analysis of COX-2, RUNX2 and osteocalcin expression showed that, at day 1, COX-2 and RUNX2 expression in the dexamethasone group was significantly lower than in the control group. There was no significant difference in osteocalcin expression between the two groups at each time point. There was no significant difference in the number of osteoclasts between the two groups. In a model of bone healing of a mandible defect, dexamethasone-treated rats exhibited impaired osteogenic differentiation and maturation due to the inhibition of COX-2, osteogenic gene, RUNX2 and collagen protein expression, which resulted in delayed bone repair. Although perioperative short-term therapy did not exhibit long-term effects on wound healing of the maxillofacial bone, the application of glucocorticoids should be cautiously considered in the clinic.
    Injury 05/2012; 43(8):1284-9. DOI:10.1016/j.injury.2012.04.014 · 2.14 Impact Factor
  • Xue Wang · Yang Xia · Laikui Liu · Mei Liu · Ning Gu · Hanbing Guang · Feimin Zhang ·
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    ABSTRACT: In the present study, the cytotoxic effects of five prosthodontic materials on the L929 cell line were assessed by flow cytometry (FCM), reverse transcription PCR (RT-PCR), and MTT (3-(4,5-dimethylthiazole-2-yl)-2,5-diphenyltetrazoli-umbromide) assay. The cells were treated with eluates resin (RE), pressable ceramics (PC), Co-Cr alloy-porcelain (CC), Ni-Cr alloy-porcelain (NC), and diatomite ceramics (DC). The cytotoxicity of all the materials tested by the MTT assay was grade 1. By FCM analysis, apoptosis rates of DC and PC were low, with no significant difference from the control (p > 0.05). The rest of the groups induced much higher apoptosis rates (p < 0.05), with the highest in the RE group. The necrotic cell levels of RE was also significantly increased (p < 0.05). Bcl-2 and Bax mRNA expression were determined by RT-PCR, and the Bax/Bcl-2 ratio in the DC and PC groups were not significantly different from the control (p > 0.05), whereas CC, NC, and RE groups showed significant differences (p < 0.05). Taken together, the results suggest that FCM and RT-PCR analyses can supplement the traditional MTT assay in evaluating the cytotoxicity of prosthodontic materials for selecting highly biocompatible materials.
    Journal of Biomedical Materials Research Part B Applied Biomaterials 11/2010; 95(2):357-64. DOI:10.1002/jbm.b.31723 · 2.76 Impact Factor
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    ABSTRACT: The aims of the present study were to examine whether focal adhesion kinase (FAK) expression is correlated with cervical lymph node metastasis of tongue cancer and to investigate the roles of FAK in the process of cancer cell migration, invasion and anoikis resistance using the human tongue cancer cell line, Tca8113. FAK expression was evaluated in 5 normal oral mucosa, 10 premalignant lesions, 80 primary tongue cancers and 41 lymph node metastases using anti-FAK immunohistochemistry. The migration, invasion and anoikis resistance of tongue cancer cells were evaluated using wound healing assays, invasion assays and anoikis induction. The effect of FAK inhibition was evaluated using RNA interference (RNAi). In total, 55 of 80 primary tongue cancers (69%) showed high expression of FAK, and 25 of 80 tumors (31%) and all normal oral mucosa or premalignant lesions showed low expression of FAK. There was a significant correlation between FAK expression and the cervical lymph node metastasis of tongue cancer. Moreover, RNAi-mediated FAK reduction decreased tongue cancer cell migration, invasion and anoikis resistance. These results suggest that FAK may serve as a marker of cervical lymph node metastasis of tongue cancer and that RNAi targeting FAK could serve as a potential therapeutic for the treatment of tongue cancer.
    Journal of Cancer Research and Clinical Oncology 09/2010; 136(9):1295-302. DOI:10.1007/s00432-010-0780-4 · 3.08 Impact Factor

Publication Stats

40 Citations
16.87 Total Impact Points


  • 2010-2015
    • Nanjing Medical University
      • • Department of Oral and Maxillofacial Surgery
      • • School of Stomatology
      • • Department of Oral Pathology
      Nan-ching, Jiangsu Sheng, China