KZKe Zheng

Ke Zheng

*This is an algorithmically generated author record based on publicly available information.

Current Organizations / Institutes

The organizations/institutes from the scholar's latest article

Previous Organizations / Institutes

The organizations / institutes from the scholar's other articles in the past ten years


Ke Zheng has a total of 10 co-authors. Here are the top co-authors by number of shared publications:

  • Xiaojing Zhang

    Department of Bone and Soft Tissue Surgery, Cancer Hospital of China Medical University, Liaoning Cancer Hospital and Institute, Shenyang, Liaoning 110042, P.R. China

    3 shared publications
  • Yi Pei

    Department of Bone and Soft Tissue Tumor Surgery Cancer Hospital of China Medical University Liaoning Cancer Hospital & Institute Shenyang Liaoning Province China

    3 shared publications
  • Wei Wang

    Affiliated Oncology Hospital of Guizhou Medical University, Guiyang, China

    2 shared publications
  • Enduo Qiu

    Department of Bone and Soft Tissue Surgery, Cancer Hospital of China Medical University, Liaoning Cancer Hospital and Institute, Shenyang, Liaoning 110042, P.R. China

    1 shared publication
  • Fei Liu

    Research Center, the Fourth Hospital of Hebei Medical University, Shijiazhuang, Hebei, China

    1 shared publication
  • Guanning Shang

    Department of Orthopedics, Shengjing Hospital of China Medical University, Shenyang, Liaoning 110004, China

    1 shared publication

Latest Publications

  • Open Access

    Extracellular nanovesicles‐transmitted circular RNA has_circ_0000190 suppresses osteosarcoma progression

    by Shenglong Li, Yi Pei, Wei Wang, Fei Liu, Ke Zheng, Xiaojing Zhang

    Under the microenvironment, tumour progression is substantially affected by cell‐cell communication. In spite of the mediating effect of extracellular nanovesicles (EVs) on cell‐cell communication by packaging into circRNAs, the effect of EVs circRNA hsa_circ_0000190 (circ‐0000190) in osteosarcoma is still not clear. Circ‐0000190 expressions in tissues and EVs from plasma were compared between osteosarcoma patients and controls. Thereafter, receiver operating characteristic (ROC) curve was drawn and area under the curve was calculated to examine whether the diagnostic results were accurate, and the effect of EVs circ‐0000190 was dug out via the determination of cell phenotypes and animal assays. Results showed circ‐0000190 exhibited an obvious reduction in EVs and tissues of osteosarcoma patients (P < .05). It was also discovered that EVs encapsulated the majority of circ‐0000190, and EVs‐encapsulated circ‐0000190 could be applied to make a distinction between osteosarcoma patients and controls. Besides, EVs circ‐0000190 in osteosarcoma cells transported from normal cells weakened the capacities of osteosarcoma cells to migrate, proliferate and invade, so as to block their biological malignant behaviours (P < .05). In addition, under the action of EVs circ‐0000190, tumour growth was impeded and the expression of TET1 was inhibited via the competitive binding to miR‐767‐5p. In all, EVs circ‐0000190 has a good prospect as it can be regarded as a new biomarker for detecting osteosarcoma. EVs circ‐0000190 transported from normal cells to osteosarcoma cells impeded the in vitro and in vivo development of osteosarcoma, implying that EVs circ‐0000190 exerts an effect on communication between normal cells and osteosarcoma cells in the carcinogenesis process of osteosarcoma.


  • Retracted
    Open Access

    Ursolic acid suppresses the biological function of osteosarcoma cells

    by Yi Pei, Yueyan Zhang, Ke Zheng, Guanning Shang, Yuming Wang, Wei Wang, Enduo Qiu, Xiaojing Zhang

    Osteosarcoma is a highly malignant tumour that occurs in adolescents. Upregulation or the constitutive activation of epidermal growth factor receptor (EGFR) is a hallmark of osteosarcoma. To investigate the effect of ursolic acid on the biological function of osteosarcoma, MTT assay was used to detect the effect of ursolic acid on the proliferation of HOS and MG63 cells, while flow cytometry was used to analyse the effect on the cell cycle and apoptosis. Transwell and Matrigel assays were used to detect the effect of ursolic acid on cell migration and invasion, respectively. Western blot analysis and reverse transcription‑quantitative polymerase chain reaction were used to detect the effects of different concentrations of ursolic acid on EGFR signaling pathway‑related proteins, cell cycle, apoptosis and cell migration‑related proteins. After overexpression or silencing of EGFR, the effects of ursolic acid on EGFR pathway and cell biological function were subsequently detected, using the same methods. The present study identified that ursolic acid had inhibitory effects on the growth and metastatic ability of osteosarcoma cells by suppressing EGFR.


  • Open Access

    Histone Demethylase JARID1B Is Overexpressed in Osteosarcoma and Upregulates Cyclin D1 Expression via Demethylation of H3K27me3

    by Wei Wang, Ke Zheng, Yi Pei, XiaoJing Zhang

    JARID1B has been proven to be upregulated in many human malignancies and is correlated with tumor progression. However, its expression and clinical significance in osteosarcoma are still unclear. Thus, the aim of this study was to explore the effects of JARID1B in osteosarcoma tumorigenesis and development. In this study, we found that the expression levels of JARID1B in osteosarcoma tissues were significantly higher than those in corresponding noncancerous bone tissues. In addition, JARID1B upregulation occurred more frequently in osteosarcoma specimens from patients with a poor prognosis. After JARID1B transfection in osteosarcoma cells, cell proliferation was significantly promoted in vitro and in vivo. On the contrary, knockdown of JARID1B inhibited cell proliferation in vitro and tumor growth in vivo. JARID1B can also decrease the G0/G1phase cell numbers and increase the S and G2/M phase cell numbers. We further demonstrated that JARID1B regulates cyclin D1 expression through H3K27me3. These findings indicate that JARID1B may act not only as a novel diagnostic and prognostic marker but also as a potential target for molecular therapy in osteosarcoma.