Yu‐Fan Chiu

National Chiayi University

Author Statistics

Papers

Citation

H-Index

i-10 index

Research Trends

Author Order

Document Type

Co-Authors

Min‐Shao Tsai

National Taiwan University

Ya‐Hsun Kuo

National Chiayi University

Yun‐Wei Lin

National Chiayi University

Shao‐Hsing Weng

National Chiayi University

Sheng-Chieh Tseng

National Chiayi University

Huang-Jen Chen

National Chiayi University

Ming-Han Kuo

National Tsing Hua University

Yu‐Ching Huang

National Chiayi University

An-Chun Lee

University of Kansas Medical Center

Shih-Hsin Hsiao

Taipei Medical University Hospital

Cooperative Institutions

National Taiwan University

National Tsing Hua University

National Chiayi University

National Applied Research Laboratories

National Yang Ming Chiao Tung University

Taiwan Semiconductor Manufacturing Company (Taiwan)

National Taipei University

National Chung Hsing University

Chang Gung University

Academia Sinica

Author Statistics

Papers

Citation

H-Index

i-10 index

Research Field

Supplementary Figure Legends 1-5 from Inhibition of p38 MAPK-Dependent Excision Repair Cross-Complementing 1 Expression Decreases the DNA Repair Capacity to Sensitize Lung Cancer Cells to Etoposide

Min‐Shao Tsai Shao‐Hsing Weng Huang-Jen Chen Yu‐Fan Chiu Yu‐Ching Huang

PDF file - 97K

10.1158/1535-7163.22497865.v1

Cite

Citations (0)

Supplementary Figure Legends 1-5 from Inhibition of p38 MAPK-Dependent Excision Repair Cross-Complementing 1 Expression Decreases the DNA Repair Capacity to Sensitize Lung Cancer Cells to Etoposide

Min‐Shao Tsai Shao‐Hsing Weng Huang-Jen Chen Yu‐Fan Chiu Yu‐Ching Huang

PDF file - 97K

10.1158/1535-7163.22497865

Cite

Citations (0)

Supplementary Materials and Methods from Cross-talk between SOX2 and TGFβ Signaling Regulates EGFR–TKI Tolerance and Lung Cancer Dissemination

Ming-Han Kuo An-Chun Lee Shih-Hsin Hsiao Sey‐En Lin Yu‐Fan Chiu

Supplementary Materials and Methods

10.1158/0008-5472.22424592

Cite

Citations (0)

Supplementary Table S1-S5 from Expression of Neuroendocrine Factor VGF in Lung Cancer Cells Confers Resistance to EGFR Kinase Inhibitors and Triggers Epithelial-to-Mesenchymal Transition

Wen Hwang Yu‐Fan Chiu Ming-Han Kuo Kuan-Lin Lee An-Chun Lee

'Table S1. Q-PCR primer and probe sequences for quantifying gene expression; Table S2. Q-PCR primer and probe sequences for quantifying gene amplification; Table S3. Antibodies for Western blot; Table S4. Antibodies for immunofluorescence; Table S5. Gene expression profiling data from the public domain used in this study.'

Immunofluorescence

Primer (cosmetics)

10.1158/0008-5472.22413930

Cite

Citations (0)

Supplementary Figure Legends for S1-S16 from Expression of Neuroendocrine Factor VGF in Lung Cancer Cells Confers Resistance to EGFR Kinase Inhibitors and Triggers Epithelial-to-Mesenchymal Transition

Wen Hwang Yu‐Fan Chiu Ming-Han Kuo Kuan-Lin Lee An-Chun Lee

'Figure S1. Lack of T790M and amplification of MET in HCC827GR cells; Figure S2. VGF-expressing cells are resistant to rociletinib; Figure S3. VGF expression in neuroendocrine carcinoma and EGFR-TKI resistant cells; Figure S4. VGF is expressed in the independently selected EGFR-TKI resistant HCC827 pool; Figure S5. Correlation of VGF levels with EGFR-TKI resistance and EMT in EGFR-TKI selected single cell clones; Figure S6. Effect of VGF expression on cell survival; Figure S7. VGF is highly expressed in small cell lung cancer; Figure S8. VGF is highly expressed in large cell neuroendocrine carcinoma; Figure S9. Correlation of VGF, CEACAM6, SYP, and CHGB expression levels with IC50 values of gefitinib in EGFR-mutated lung cancer cell lines; Figure S10. EGFR-TKI resistance in H1975 cells expressing differential VGF levels; Figure S11. VGF-TWIST1 signaling encourages EGFR-TKI resistance; Figure S12. Effect of conditioned medium from VGF expressing cells on low serum-mediated growth; Figure S13. Effect of doxycycline alone on tumor cell growth in vitro and in vivo; Figure S14. Correlation of VGF with EMT markers in lung adenocarcinoma; Figure S15. Correlation of neuroendocrine markers or TWIST1 with survival in lung adenocarcinoma; Figure S16. Correlation of neuroendocrine markers or VGF-TWIST1 signature with survival in EGFR-mutated lung adenocarcinoma.'

Neuroendocrine differentiation

10.1158/0008-5472.22413936.v1

Cite

Citations (0)

Modulation of Rad51, ERCC1, and thymidine phosphorylase by emodin result in synergistic cytotoxic effect in combination with capecitabine

Biochemical Pharmacology (2010)

Jen‐Chung Ko Min‐Shao Tsai Ya‐Hsun Kuo Yu‐Fan Chiu Shao‐Hsing Weng

Thymidine phosphorylase

ERCC1

10.1016/j.bcp.2010.12.008

Cite

Citations (27)

Supplementary Data 3 from Inhibition of p38 MAPK-Dependent Excision Repair Cross-Complementing 1 Expression Decreases the DNA Repair Capacity to Sensitize Lung Cancer Cells to Etoposide

Min‐Shao Tsai Shao‐Hsing Weng Huang-Jen Chen Yu‐Fan Chiu Yu‐Ching Huang

PDF file - 569K, etoposide structure

10.1158/1535-7163.22497883

Cite

Citations (0)

Supplementary Figures from Cross-talk between SOX2 and TGFβ Signaling Regulates EGFR–TKI Tolerance and Lung Cancer Dissemination

Ming-Han Kuo An-Chun Lee Shih-Hsin Hsiao Sey‐En Lin Yu‐Fan Chiu

Supplementary Figure S1-S23

10.1158/0008-5472.22424595

Cite

Citations (0)

Supplementary Table S1-S5 from Expression of Neuroendocrine Factor VGF in Lung Cancer Cells Confers Resistance to EGFR Kinase Inhibitors and Triggers Epithelial-to-Mesenchymal Transition

Wen Hwang Yu‐Fan Chiu Ming-Han Kuo Kuan-Lin Lee An-Chun Lee

Primer (cosmetics)

Immunofluorescence

Northern blot

10.1158/0008-5472.22413930.v1

Cite

Citations (0)

Data from Expression of Neuroendocrine Factor VGF in Lung Cancer Cells Confers Resistance to EGFR Kinase Inhibitors and Triggers Epithelial-to-Mesenchymal Transition

Wen Hwang Yu‐Fan Chiu Ming-Han Kuo Kuan-Lin Lee An-Chun Lee

<div>AbstractMutations in EGFR drive tumor growth but render tumor cells sensitive to treatment with EGFR tyrosine kinase inhibitors (TKI). Phenotypic alteration in epithelial-to-mesenchymal transition (EMT) has been linked to the TKI resistance in lung adenocarcinoma. However, the mechanism underlying this resistance remains unclear. Here we report that high expression of a neuroendocrine factor termed VGF induces the transcription factor TWIST1 to facilitate TKI resistance, EMT, and cancer dissemination in a subset of lung adenocarcinoma cells. VGF silencing resensitized EGFR-mutated lung adenocarcinoma cells to TKI. Conversely, overexpression of VGF in sensitive cells conferred resistance to TKIs and induced EMT, increasing migratory and invasive behaviors. Correlation analysis revealed a significant association of VGF expression with advanced tumor grade and poor survival in patients with lung adenocarcinoma. In a mouse xenograft model of lung adenocarcinoma, suppressing VGF expression was sufficient to attenuate tumor growth. Overall, our findings show how VGF can confer TKI resistance and trigger EMT, suggesting its potential utility as a biomarker and therapeutic target in lung adenocarcinoma. Cancer Res; 77(11); 3013–26. ©2017 AACR.</div>

10.1158/0008-5472.c.6508854

Cite

Citations (0)