Ke Zheng
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
- 10 January 2020
- Published by Wiley in Journal of Cellular and Molecular Medicine
- Vol. 24 (3) , 2202-2214
Extracellular nanovesicles‐transmitted circular RNA has_circ_0000190 suppresses osteosarcoma progression
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.
- 10 January 2020
- Published by Wiley in Journal of Cellular and Molecular Medicine
- Vol. 24 (3) , 2202-2214
Open AccessExtracellular nanovesicles‐transmitted circular RNA has_circ_0000190 suppresses osteosarcoma progression
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.
- RetractedOpen Access
- 4 July 2019
- Published by Spandidos Publications in Oncology Letters
- Vol. 18 (3) , 2628-2638
Ursolic acid suppresses the biological function of osteosarcoma cells
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.
- 4 July 2019
- Published by Spandidos Publications in Oncology Letters
- Vol. 18 (3) , 2628-2638
RetractedOpen AccessUrsolic acid suppresses the biological function of osteosarcoma cells
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
- 10 April 2018
- Published by Tech Science Press in Oncology Research
- Vol. 26 (3) , 373-384
Histone Demethylase JARID1B Is Overexpressed in Osteosarcoma and Upregulates Cyclin D1 Expression via Demethylation of H3K27me3
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.
- 10 April 2018
- Published by Tech Science Press in Oncology Research
- Vol. 26 (3) , 373-384
Open AccessHistone Demethylase JARID1B Is Overexpressed in Osteosarcoma and Upregulates Cyclin D1 Expression via Demethylation of H3K27me3
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.