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2 results on '"Yan, Feifei"'

1. FGF19 genetic amplification as a potential therapeutic target in lung squamous cell carcinomas

Author

Zhang, Xiaochen, Kong, Mei, Zhang, Zhen, Xu, Suzhen, Yan, Feifei, Wei, Liyuan, and Zhou, Jianying

Subjects
Aged, 80 and over, Adult, Male, China, Lung Neoplasms, Smoking, Gene Amplification, Apoptosis, Original Articles, Middle Aged, Up-Regulation, Fibroblast Growth Factors, Gene Expression Regulation, Neoplastic, genetic amplification, Asian People, Cell Line, Tumor, Carcinoma, Squamous Cell, lung squamous cell carcinoma, Humans, Original Article, Female, In Situ Hybridization, Fluorescence, FGF 19, Aged, Cell Proliferation
Abstract

Background Although FGF 19 gene aberrations are associated with carcinogenesis and progression in human cancers, the roles of FGF 19 genetic amplification and expression in Chinese patients with lung squamous cell carcinoma (LSCC) and FGF 19 amplification as a potential therapeutic target for LSCC are not well understood. Methods Fluorescence in situ hybridization analysis and quantitative real‐time‐PCR was used to detect FGF 19 genetic amplification and FGF 19 messenger RNA expression in LSCC tumor and paired adjacent samples. Small interfering RNA and short hairpin RNA were used to knockdown FGF19 in vitro and in vivo. Results FGF 19 amplification was identified in a subset of LSCC patients (37.5%, 15/40), and upregulation of FGF 19 expression was found in 60% (24/40) of tumor tissues compared to adjacent non‐tumorous tissues. Correlation analysis with clinicopathologic parameters showed that FGF 19 upregulation was significantly associated with heavy smoking. Small interfering RNA knockdown of FGF 19 led to the significant inhibition of cell growth and induced apoptosis in LSCC cells carrying the amplified FGF 19 gene, but these effects was not observed in non‐amplified LSCC cells. Interfering FGF 19 expression with short hairpin RNA also resulted in tumor growth inhibition and induced apoptosis in LSCC xenografts with amplified FGF 19 in tumor cells. Conclusion Our results suggested that FGF 19 signaling activation is required for cell growth and survival of FGF 19 amplified LSCC cells, both in vitro and in vivo. Intervention of FGF 19 activation could be a potential therapeutic strategy for LSCC patients with FGF 19 amplification.

Published
2017

2. Tanshinone IIA Inhibits Osteosarcoma Growth through a Src Kinase-Dependent Mechanism.

Author

Hu, Chao, Zhu, Xiaobin, Zhang, Taogen, Deng, Zhouming, Xie, Yuanlong, Yan, Feifei, and Cai, Lin

Subjects
IN vitro studies, PROTEINS, FLOW cytometry, HERBAL medicine, STAINS & staining (Microscopy), OSTEOSARCOMA, ANIMAL experimentation, WESTERN immunoblotting, FLUOROIMMUNOASSAY, CANCER invasiveness, APOPTOSIS, LUNG tumors, HYDROCARBONS, GENE expression, CELL cycle, CELLULAR signal transduction, TRANSFERASES, CELL proliferation, CELL migration inhibition, CELL lines, POLYMERASE chain reaction, CHINESE medicine, MICE, DISEASE risk factors
Abstract

Introduction. Osteosarcoma is a malignant tumor associated with high mortality rates due to the toxic side effects of current therapeutic methods. Tanshinone IIA can inhibit cell proliferation and promote apoptosis in vitro, but the exact mechanism is still unknown. The aims of this study are to explore the antiosteosarcoma effect of tanshinone IIA via Src kinase and demonstrate the mechanism of this effect. Materials and Methods. Osteosarcoma MG-63 and U2-OS cell lines were stable transfections with Src-shRNA. Then, the antiosteosarcoma effect of tanshinone IIA was tested in vitro. The protein expression levels of Src, p-Src, p-ERK1/2, and p-AKt were detected by Western blot and RT-PCR. CCK-8 assay and BrdU immunofluorescence assay were used to detect cell proliferation. Transwell assay, cell scratch assay, and flow cytometry were used to detect cell invasion, migration, and cell cycle. Tumor-bearing nude mice with osteosarcoma were constructed. The effect of tanshinone IIA was detected by tumor HE staining, tumor inhibition rate, incidence of lung metastasis, and X-ray. Results. The oncogene role of Src kinase in osteosarcoma is reflected in promoting cell proliferation, invasion, and migration and in inhibiting apoptosis. However, Src has different effects on cell proliferation, apoptosis, and cell cycle regulation among cell lines. At a cellular level, the antiosteosarcoma effect of tanshinone IIA is mediated by Src downstream of the MAPK/ERK and PI3K/AKt signaling pathways. At the animal level, tanshinone IIA played a role in resisting osteosarcoma formation by Src downstream of the MAPK/ERK and PI3K/AKt signaling pathways. Conclusion. Tanshinone IIA plays an antiosteosarcoma role in vitro and in vivo and inhibits the progression of osteosarcoma mediated by Src downstream of the MAPK/ERK and PI3K/AKt signaling pathways. [ABSTRACT FROM AUTHOR]

Published
2021
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