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Your search keyword '"Yingyi Wang"' showing total 3 results
Start Over Author "Yingyi Wang" Journal molecular medicine reports
3 results on '"Yingyi Wang"'

1. Downregulation of osteopontin enhances the sensitivity of glioma U251 cells to temozolomide and cisplatin by targeting the NF-κB/Bcl-2 pathway

Author

Yingyi Wang, Wei Yan, Junxia Zhang, Yongping You, Chunfa Qian, Lei Shi, Ping Li, and Hongyi Liu

Subjects
Cancer Research, Small interfering RNA, Down-Regulation, Apoptosis, Biochemistry, stomatognathic system, Downregulation and upregulation, Cell Line, Tumor, Glioma, Temozolomide, Genetics, medicine, Humans, Osteopontin, RNA, Small Interfering, Molecular Biology, Cisplatin, Gene knockdown, biology, NF-kappa B, Cell cycle, medicine.disease, Dacarbazine, Enzyme Activation, Gene Expression Regulation, Neoplastic, Proto-Oncogene Proteins c-bcl-2, Oncology, Drug Resistance, Neoplasm, Cancer research, biology.protein, Molecular Medicine, Signal Transduction, medicine.drug
Abstract

Glioma is resistant to the apoptotic effects of chemotherapy and the mechanism underlying its chemoresistance is not currently understood. In a previous study, we reported that osteopontin (OPN) was overexpressed in glioma tissues and had an important anti‑apoptotic effect. Furthermore, overexpression of OPN was observed following chemotherapy. To elucidate whether OPN plays a role in chemotherapy resistance and to investigate its downstream signaling pathway, this study used small interfering RNA (siRNA) to silence the expression of OPN in U251 human neuronal glioma astrocytoma cells. OPN downregulation in U251 cells enhanced the apoptotic effects induced by temozolomide (TMZ) and cisplatin (DDP). Furthermore, OPN siRNA suppressed the nuclear factor κ‑light‑chain‑enhancer of activated B cells (NF‑κB) activation and B cell lymphoma 2 (Bcl‑2) expression that was induced by chemotherapy. Taken together, these results demonstrated that the expression levels of OPN are involved in glioma chemoresistance. Knockdown of OPN through siRNA enhanced the effects of TMZ and DDP chemotherapy by targeting the NF‑κB/Bcl‑2 pathway.

Published
2014

2. Combination of tamoxifen and antisense human telomerase RNA inhibits glioma cell proliferation and anti-apoptosis via suppression of telomerase activity

Author

Yingyi Wang, Ning Liu, Zhifeng Wu, Weifeng Miu, Jiong Geng, Zhengxiang Yang, Yongping You, Hui Luo, Zhimin Zhou, and Yi Pu

Subjects
Cancer Research, Telomerase, Oncogene, Cell growth, Cell, Cell cycle, Biology, medicine.disease, Biochemistry, Molecular biology, medicine.anatomical_structure, stomatognathic system, Oncology, Glioma, Genetics, medicine, Cancer research, Molecular Medicine, Telomerase reverse transcriptase, Signal transduction, skin and connective tissue diseases, Molecular Biology, hormones, hormone substitutes, and hormone antagonists
Abstract

Accumulating evidence indicates that telomerase activity and human telomerase RNA (hTR) play a potentially crucial role in maintaining the malignant progression of human gliomas. Tamoxifen (TAM) induces cell growth inhibition by modulating several cellular activities, including signaling pathways and the cell cycle. In this study, we aimed to evaluate the effect of combination therapy with TAM and antisense hTR on malignant glioma growth in vitro. TAM treatment and the down-regulation of hTR expression by antisense hTR resulted in a significant suppression of cell growth and the induction of cell apoptosis through the inhibition of telomerase activity. The antitumor effect of treatment with TAM alone was found to be mediated in part by the down-regulation of telomerase activity and of PKC and IGF-1 expression. Our results indicate that TAM and antisense hTR may serve as a novel strategy for glioma therapy.

Published
2010

3. Downregulation of osteopontin enhances the sensitivity of glioma U251 cells to temozolomide and cisplatin by targeting the NF-κB/Bcl-2 pathway.

Author

CHUNFA QIAN, PING LI, WEI YAN, LEI SHI, JUNXIA ZHANG, YINGYI WANG, HONGYI LIU, and YONGPING YOU

Subjects
OSTEOPONTIN, TEMOZOLOMIDE, CISPLATIN, APOPTOSIS, CANCER chemotherapy, SMALL interfering RNA
Abstract

Glioma is resistant to the apoptotic effects of chemotherapy and the mechanism underlying its chemoresistance is not currently understood. In a previous study, we reported that osteopontin (OPN) was overexpressed in glioma tissues and had an important anti-apoptotic effect. Furthermore, overexpression of OPN was observed following chemotherapy. To elucidate whether OPN plays a role in chemotherapy resistance and to investigate its downstream signaling pathway, this study used small interfering RNA (siRNA) to silence the expression of OPN in U251 human neuronal glioma astrocytoma cells. OPN downregulation in U251 cells enhanced the apoptotic effects induced by temozolomide (TMZ) and cisplatin (DDP). Furthermore, OPN siRNA suppressed the nuclear factor κ-light-chain-enhancer of activated B cells (NF-κB) activation and B cell lymphoma 2 (Bcl-2) expression that was induced by chemotherapy. Taken together, these results demonstrated that the expression levels of OPN are involved in glioma chemoresistance. Knockdown of OPN through siRNA enhanced the effects of TMZ and DDP chemotherapy by targeting the NF-κB/Bcl-2 pathway. [ABSTRACT FROM AUTHOR]

Published
2015
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