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Your search keyword '"Chong, Qing Yun"' showing total 22 results
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22 results on '"Chong, Qing Yun"'

9. Long noncoding RNA Linc00460 promotes breast cancer progression by regulating the miR-489-5p/FGF7/AKT axis

Author

Zhu, Yong, Yang, Leiyan, Chong, Qing-Yun, Yan, Hong, Zhang, Weijie, Qian, Wenchang, Tan, Sheng, Wu, Zhengsheng, Lobie, Peter E, and Zhu, Tao

Subjects
breast cancer, Cancer Management and Research, miR-489-5p, AKT, FGF7, Linc00460, Original Research
Abstract

Yong Zhu,1 Leiyan Yang,1 Qing-Yun Chong,2 Hong Yan,3 Weijie Zhang,1 Wenchang Qian,1 Sheng Tan,1 Zhengsheng Wu,4 Peter E Lobie,5 Tao Zhu11Hefei National Laboratory for Physical Sciences at Microscale, the CAS Key Laboratory of Innate Immunity and Chronic Disease, School of Life Sciences, University of Science and Technology of China, Hefei, Anhui 230027, People’s Republic of China; 2Cancer Science Institute of Singapore and Department of Pharmacology, National University of Singapore, Singapore, Singapore; 3Department of Pathology, Anhui Provincial Cancer Hospital, The First Affiliated Hospital of University of Science and Technology of China, Hefei, Anhui, People’s Republic of China; 4Department of Pathology, Anhui Medical University, Hefei, Anhui 230032, People’s Republic of China; 5Tsinghua-Berkeley Shenzhen Institute, Tsinghua University, Shenzhen, Guangdong, People’s Republic of ChinaPurpose: Evidence indicates that long noncoding RNAs (lncRNA) possess important roles in various cellular processes and that dysregulation of lncRNAs promotes tumor progression. However, the expression patterns and biological functions of many specific lncRNAs in breast cancer remain to be determined.Methods: Quantitative real-time polymerase chain reaction was performed to detect Linc00460, miR-489-5p and FGF7 expression. Protein levels were determined using Western blot. MTT and colony formation assay were used to measure cell proliferation. Transwell assays were conducted to determine cell migration and invasion. Luciferase reporter assays were carried out to assess the interaction between miR-489-5p and Linc00460 or FGF7. Biotin pull-down assay was used to detect the direct interaction between miR-489-5p and Linc00460. In vivo experiments were performed to measure tumor formation and lung metastasis.Results: We demonstrated that lncRNA Linc00460 was upregulated in breast cancer, and its expression level was positively associated with lymphatic metastasis and poor overall survival. Forced expression of Linc00460 increased, whereas Linc00460 silencing decreased, breast cancer cell viability, migration and invasion both in vitro and in vivo. Linc00460 was identified as a direct target of miR-489-5p, which further targeted FGF7 and exerted oncogenic functions in breast cancer. Mechanistically, Linc00460 served as a competing endogenous RNA of FGF-7 mRNA by sponging miR-489-5p, resulting in upregulated FGF7 expression and AKT activity. Notably, forced expression of miR-489-5p abrogated Linc00460-mediated oncogenic behavior and activation of the FGF7-AKT pathway in breast cancer cells.Conclusion: We have demonstrated that Linc00460 promotes breast cancer progression partly through the miR-489-5p/FGF7/AKT axis.Keywords: Linc00460, miR-489-5p, breast cancer, FGF7, AKT

Published
2019

11. Loss of Estrogen-Regulated MIR135A1 at 3p21.1 Promotes Tamoxifen Resistance in Breast Cancer

Author

Zhang, Weijie, primary, Wu, Mingming, additional, Chong, Qing-Yun, additional, Zhang, Min, additional, Zhang, Xiao, additional, Hu, Lan, additional, Zhong, Yanghao, additional, Qian, Pengxu, additional, Kong, Xiangjun, additional, Tan, Sheng, additional, Li, Gaopeng, additional, Ding, Keshuo, additional, Lobie, Peter E., additional, and Zhu, Tao, additional

Published
2018
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13. Autocrine hGH stimulates oncogenicity, epithelial-mesenchymal transition and cancer stem cell-like behavior in human colorectal carcinoma

Author

Wang, Jing-Jing, primary, Chong, Qing-Yun, additional, Sun, Xin-Bao, additional, You, Ming-Liang, additional, Pandey, Vijay, additional, Chen, Yi-Jun, additional, Zhuang, Qiu-Shi, additional, Liu, Dong-Xu, additional, Ma, Lan, additional, Wu, Zheng-Sheng, additional, Zhu, Tao, additional, and Lobie, Peter E., additional

Published
2017
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14. Hypomethylation associated enhanced transcription of trefoil factor-3 mediates tamoxifen-stimulated oncogenicity of ER+ endometrial carcinoma cells

Author

Pandey, Vijay, primary, Zhang, Min, additional, Chong, Qing-Yun, additional, You, Mingliang, additional, Raquib, Ainiah Rushdiana, additional, Pandey, Amit K., additional, Liu, Dong-Xu, additional, Liu, Liang, additional, Ma, Lan, additional, Jha, Sudhakar, additional, Wu, Zheng-Sheng, additional, Zhu, Tao, additional, and Lobie, Peter E., additional

Published
2017
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15. Post-transcriptional regulation of ERBB2 by miR26a/b and HuR confers resistance to tamoxifen in estrogen receptor-positive breast cancer cells

Author

Tan, Sheng, primary, Ding, Keshuo, additional, Chong, Qing-Yun, additional, Zhao, Junsong, additional, Liu, Yuan, additional, Shao, Yunying, additional, Zhang, Yuanyuan, additional, Yu, Qing, additional, Xiong, Zirui, additional, Zhang, Weijie, additional, Zhang, Min, additional, Li, Gaopeng, additional, Li, Xiaoni, additional, Kong, Xiangjun, additional, Ahmad, Akhlaq, additional, Wu, Zhengsheng, additional, Wu, Qiang, additional, Zhao, Xiaodong, additional, Lobie, Peter E., additional, and Zhu, Tao, additional

Published
2017
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17. Release of HER2 repression of trefoil factor 3 (TFF3) expression mediates trastuzumab resistance in HER2+/ER+ mammary carcinoma

Author

Chong, Qing-Yun, primary, You, Ming-Liang, additional, Pandey, Vijay, additional, Banerjee, Arindam, additional, Chen, Yi-Jun, additional, Poh, Han-Ming, additional, Zhang, Mengyi, additional, Ma, Lan, additional, Zhu, Tao, additional, Basappa, Salundi, additional, Liu, Liang, additional, and Lobie, Peter E., additional

Published
2017
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19. Autocrine Prolactin Stimulates Endometrial Carcinoma Growth and Metastasis and Reduces Sensitivity to Chemotherapy

Author

Ding, Keshuo, primary, Yuan, Yan, additional, Chong, Qing-Yun, additional, Yang, Yulu, additional, Li, Rui, additional, Li, Xiaoni, additional, Kong, Xiangjun, additional, Qian, Pengxu, additional, Xiong, Zirui, additional, Pandey, Vijay, additional, Ma, Lan, additional, Wu, Zhengsheng, additional, Lobie, Peter E., additional, and Zhu, Tao, additional

Published
2017
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21. Pharmacological Inhibition of TFF3 Enhances Sensitivity of CMS4 Colorectal Carcinoma to 5-Fluorouracil through Inhibition of p44/42 MAPK.

Author

Chen, Ru-Mei, Chiou, Yi-Shiou, Chong, Qing-Yun, Poh, Han-Ming, Tan, Tuan-Zea, Zhang, Meng-Yi, Ma, Lan, Zhu, Tao, Pandey, Vijay, Basappa, Kumar, Alan Prem, and Lobie, Peter E.

Subjects
CANCER stem cells, FLUOROURACIL, TREFOIL factors, INHIBITION of cellular proliferation, CARCINOMA
Abstract

Increased expression of trefoil factor 3 (TFF3) has been reported in colorectal carcinoma (CRC), being correlated with distant metastasis and poor clinical outcomes. Amongst the CRC subtypes, mesenchymal (CMS4) CRC is associated with the worst survival outcome. Herein, the functional roles of TFF3 and the pharmacological inhibition of TFF3 by a novel specific small molecule TFF3 inhibitor—2-amino-4-(4-(6-fluoro-5-methylpyridin-3-yl)phenyl)-5-oxo-4H,5H-pyrano[3,2-c]chromene-3-carbonitrile (AMPC) in CMS4 CRC was explored. Forced expression of TFF3 in CMS4 CRC cells promoted cell proliferation, cell survival, foci formation, invasion, migration, cancer stem cell like behaviour and growth in 3D Matrigel. In contrast, siRNA-mediated depletion of TFF3 or AMPC inhibition of TFF3 in CMS4 CRC cells decreased oncogenic behaviour as indicated by the above cell function assays. AMPC also inhibited tumour growth in vivo. The TFF3-stimulated oncogenic behaviour of CMS4 CRC cells was dependent on TFF3 activation of the p44/42 MAPK (ERK1/2) pathway. Furthermore, the forced expression of TFF3 decreased the sensitivity of CMS4 CRC cells to 5-fluorouracil (5-FU); while depleted TFF3 expression enhanced 5-FU sensitivity in CMS4 CRC cells. 5-FU treatment induced TFF3 expression in CMS4 CRC cells. AMPC, when used in combination with 5-FU in CMS4 CRC cells exhibited a synergistic inhibitory effect. In summary, this study provides functional evidence for TFF3 as a therapeutic target in CMS4 CRC. [ABSTRACT FROM AUTHOR]

Published
2019
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22. Inhibition of TFF3 Enhances Sensitivity—and Overcomes Acquired Resistance—to Doxorubicin in Estrogen Receptor-Positive Mammary Carcinoma.

Author

Poh, Han Ming, Chiou, Yi Shiou, Chong, Qing Yun, Chen, Ru-Mei, Rangappa, Kanchugarakoppal S., Ma, Lan, Zhu, Tao, Kumar, Alan Prem, Pandey, Vijay, Basappa, Lee, Soo-Chin, and Lobie, Peter E.

Subjects
APOPTOSIS, BREAST tumors, DOXORUBICIN, DRUG resistance, ESTROGEN receptors, GENE expression, RNA, XENOGRAFTS, TREFOIL factors, IN vivo studies, CHEMICAL inhibitors, PHARMACODYNAMICS
Abstract

Dose-dependent toxicity and acquired resistance are two major challenges limiting the efficacious treatment of mammary carcinoma (MC) with doxorubicin. Herein, we investigated the function of Trefoil Factor 3 (TFF3) in the sensitivity and acquired resistance of estrogen receptor positive (ER+) MC cells to doxorubicin. Doxorubicin treatment of ER+MC cells increased TFF3 expression. The depletion of TFF3 by siRNA or inhibition with a small molecule TFF3 inhibitor (AMPC) synergistically enhanced the efficacy of doxorubicin in ER+MC through the suppression of doxorubicin-induced AKT activation and enhancement of doxorubicin-induced apoptosis. Elevated expression of TFF3 and increased activation of AKT were also observed using a model of acquired doxorubicin resistance in ER+MC cells. AMPC partially re-sensitized the doxorubicin resistant cells to doxorubicin-induced apoptosis. Indeed, doxorubicin resistant ER + MC cells exhibited increased sensitivity to AMPC as a single agent compared to doxorubicin sensitive cells. In vivo, AMPC attenuated growth of doxorubicin sensitive ER+MC xenografts whereas it produced regression of xenografts generated by doxorubicin resistant ER+MC cells. Hence, TFF3 inhibition may improve the efficacy and reduce required doses of doxorubicin in ER+MC. Moreover, inhibition of TFF3 may also be an effective therapeutic strategy to eradicate doxorubicin resistant ER+MC. [ABSTRACT FROM AUTHOR]

Published
2019
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