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2. Supplementary Figure 1 from Another Surprise from Metformin: Novel Mechanism of Action via K-Ras Influences Endometrial Cancer Response to Therapy

Author

Iglesias, David A., primary, Yates, Melinda S., primary, van der Hoeven, Dharini, primary, Rodkey, Travis L., primary, Zhang, Qian, primary, Co, Ngai Na, primary, Burzawa, Jennifer, primary, Chigurupati, Sravanthi, primary, Celestino, Joseph, primary, Bowser, Jessica, primary, Broaddus, Russell, primary, Hancock, John F., primary, Schmandt, Rosemarie, primary, and Lu, Karen H., primary

Published
2023
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3. Supplementary Figure Legend from Another Surprise from Metformin: Novel Mechanism of Action via K-Ras Influences Endometrial Cancer Response to Therapy

Author

Iglesias, David A., primary, Yates, Melinda S., primary, van der Hoeven, Dharini, primary, Rodkey, Travis L., primary, Zhang, Qian, primary, Co, Ngai Na, primary, Burzawa, Jennifer, primary, Chigurupati, Sravanthi, primary, Celestino, Joseph, primary, Bowser, Jessica, primary, Broaddus, Russell, primary, Hancock, John F., primary, Schmandt, Rosemarie, primary, and Lu, Karen H., primary

Published
2023
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4. Supplementary Figure 2 from Another Surprise from Metformin: Novel Mechanism of Action via K-Ras Influences Endometrial Cancer Response to Therapy

Author

Iglesias, David A., primary, Yates, Melinda S., primary, van der Hoeven, Dharini, primary, Rodkey, Travis L., primary, Zhang, Qian, primary, Co, Ngai Na, primary, Burzawa, Jennifer, primary, Chigurupati, Sravanthi, primary, Celestino, Joseph, primary, Bowser, Jessica, primary, Broaddus, Russell, primary, Hancock, John F., primary, Schmandt, Rosemarie, primary, and Lu, Karen H., primary

Published
2023
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7. Supplementary Figure 4 from Identification of FGFR4 as a Potential Therapeutic Target for Advanced-Stage, High-Grade Serous Ovarian Cancer

Author

Zaid, Tarrik M., primary, Yeung, Tsz-Lun, primary, Thompson, Melissa S., primary, Leung, Cecilia S., primary, Harding, Tom, primary, Co, Ngai-Na, primary, Schmandt, Rosie S., primary, Kwan, Suet-Ying, primary, Rodriguez-Aguay, Cristian, primary, Lopez-Berestein, Gabriel, primary, Sood, Anil K., primary, Wong, Kwong-Kwok, primary, Birrer, Michael J., primary, and Mok, Samuel C., primary

Published
2023
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8. Supplementary Figure 3 from Identification of FGFR4 as a Potential Therapeutic Target for Advanced-Stage, High-Grade Serous Ovarian Cancer

Author

Zaid, Tarrik M., primary, Yeung, Tsz-Lun, primary, Thompson, Melissa S., primary, Leung, Cecilia S., primary, Harding, Tom, primary, Co, Ngai-Na, primary, Schmandt, Rosie S., primary, Kwan, Suet-Ying, primary, Rodriguez-Aguay, Cristian, primary, Lopez-Berestein, Gabriel, primary, Sood, Anil K., primary, Wong, Kwong-Kwok, primary, Birrer, Michael J., primary, and Mok, Samuel C., primary

Published
2023
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9. Supplementary Table 1 from Identification of FGFR4 as a Potential Therapeutic Target for Advanced-Stage, High-Grade Serous Ovarian Cancer

Author

Zaid, Tarrik M., primary, Yeung, Tsz-Lun, primary, Thompson, Melissa S., primary, Leung, Cecilia S., primary, Harding, Tom, primary, Co, Ngai-Na, primary, Schmandt, Rosie S., primary, Kwan, Suet-Ying, primary, Rodriguez-Aguay, Cristian, primary, Lopez-Berestein, Gabriel, primary, Sood, Anil K., primary, Wong, Kwong-Kwok, primary, Birrer, Michael J., primary, and Mok, Samuel C., primary

Published
2023
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10. Supplementary Table 2 from Identification of FGFR4 as a Potential Therapeutic Target for Advanced-Stage, High-Grade Serous Ovarian Cancer

Author

Zaid, Tarrik M., primary, Yeung, Tsz-Lun, primary, Thompson, Melissa S., primary, Leung, Cecilia S., primary, Harding, Tom, primary, Co, Ngai-Na, primary, Schmandt, Rosie S., primary, Kwan, Suet-Ying, primary, Rodriguez-Aguay, Cristian, primary, Lopez-Berestein, Gabriel, primary, Sood, Anil K., primary, Wong, Kwong-Kwok, primary, Birrer, Michael J., primary, and Mok, Samuel C., primary

Published
2023
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11. Supplementary Table 3 from Identification of FGFR4 as a Potential Therapeutic Target for Advanced-Stage, High-Grade Serous Ovarian Cancer

Author

Zaid, Tarrik M., primary, Yeung, Tsz-Lun, primary, Thompson, Melissa S., primary, Leung, Cecilia S., primary, Harding, Tom, primary, Co, Ngai-Na, primary, Schmandt, Rosie S., primary, Kwan, Suet-Ying, primary, Rodriguez-Aguay, Cristian, primary, Lopez-Berestein, Gabriel, primary, Sood, Anil K., primary, Wong, Kwong-Kwok, primary, Birrer, Michael J., primary, and Mok, Samuel C., primary

Published
2023
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12. Supplementary Figure 2 from Identification of FGFR4 as a Potential Therapeutic Target for Advanced-Stage, High-Grade Serous Ovarian Cancer

Author

Zaid, Tarrik M., primary, Yeung, Tsz-Lun, primary, Thompson, Melissa S., primary, Leung, Cecilia S., primary, Harding, Tom, primary, Co, Ngai-Na, primary, Schmandt, Rosie S., primary, Kwan, Suet-Ying, primary, Rodriguez-Aguay, Cristian, primary, Lopez-Berestein, Gabriel, primary, Sood, Anil K., primary, Wong, Kwong-Kwok, primary, Birrer, Michael J., primary, and Mok, Samuel C., primary

Published
2023
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13. Data from Identification of FGFR4 as a Potential Therapeutic Target for Advanced-Stage, High-Grade Serous Ovarian Cancer

Author

Zaid, Tarrik M., primary, Yeung, Tsz-Lun, primary, Thompson, Melissa S., primary, Leung, Cecilia S., primary, Harding, Tom, primary, Co, Ngai-Na, primary, Schmandt, Rosie S., primary, Kwan, Suet-Ying, primary, Rodriguez-Aguay, Cristian, primary, Lopez-Berestein, Gabriel, primary, Sood, Anil K., primary, Wong, Kwong-Kwok, primary, Birrer, Michael J., primary, and Mok, Samuel C., primary

Published
2023
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14. Supplementary Figure Legend from Identification of FGFR4 as a Potential Therapeutic Target for Advanced-Stage, High-Grade Serous Ovarian Cancer

Author

Zaid, Tarrik M., primary, Yeung, Tsz-Lun, primary, Thompson, Melissa S., primary, Leung, Cecilia S., primary, Harding, Tom, primary, Co, Ngai-Na, primary, Schmandt, Rosie S., primary, Kwan, Suet-Ying, primary, Rodriguez-Aguay, Cristian, primary, Lopez-Berestein, Gabriel, primary, Sood, Anil K., primary, Wong, Kwong-Kwok, primary, Birrer, Michael J., primary, and Mok, Samuel C., primary

Published
2023
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15. Supplementary Figure 1 from Identification of FGFR4 as a Potential Therapeutic Target for Advanced-Stage, High-Grade Serous Ovarian Cancer

Author

Zaid, Tarrik M., primary, Yeung, Tsz-Lun, primary, Thompson, Melissa S., primary, Leung, Cecilia S., primary, Harding, Tom, primary, Co, Ngai-Na, primary, Schmandt, Rosie S., primary, Kwan, Suet-Ying, primary, Rodriguez-Aguay, Cristian, primary, Lopez-Berestein, Gabriel, primary, Sood, Anil K., primary, Wong, Kwong-Kwok, primary, Birrer, Michael J., primary, and Mok, Samuel C., primary

Published
2023
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24. Exosomal transfer of stroma-derived miR21 confers paclitaxel resistance in ovarian cancer cells through targeting APAF1

Author

Au Yeung, Chi Lam, primary, Co, Ngai-Na, additional, Tsuruga, Tetsushi, additional, Yeung, Tsz-Lun, additional, Kwan, Suet-Ying, additional, Leung, Cecilia S., additional, Li, Yong, additional, Lu, Edward S., additional, Kwan, Kenny, additional, Wong, Kwong-Kwok, additional, Schmandt, Rosemarie, additional, Lu, Karen H., additional, and Mok, Samuel C., additional

Published
2016
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28. Viral-Human Chimeric Transcript Predisposes Risk to Liver Cancer Development and Progression

Author

Lau, Chi-Chiu, primary, Sun, Tingting, additional, Ching, Arthur K.K., additional, He, Mian, additional, Li, Jing-Woei, additional, Wong, Alissa M., additional, Co, Ngai Na, additional, Chan, Anthony W.H., additional, Li, Pik-Shan, additional, Lung, Raymond W.M., additional, Tong, Joanna H.M., additional, Lai, Paul B.S., additional, Chan, Henry L.Y., additional, To, Ka-Fai, additional, Chan, Ting-Fung, additional, and Wong, Nathalie, additional

Published
2014
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30. Another Surprise from Metformin: Novel Mechanism of Action via K-Ras Influences Endometrial Cancer Response to Therapy

Author

Iglesias, David A., primary, Yates, Melinda S., additional, van der Hoeven, Dharini, additional, Rodkey, Travis L., additional, Zhang, Qian, additional, Co, Ngai Na, additional, Burzawa, Jennifer, additional, Chigurupati, Sravanthi, additional, Celestino, Joseph, additional, Bowser, Jessica, additional, Broaddus, Russell, additional, Hancock, John F., additional, Schmandt, Rosemarie, additional, and Lu, Karen H., additional

Published
2013
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33. Identification of FGFR4 as a Potential Therapeutic Target for Advanced-Stage, High-Grade Serous Ovarian Cancer

Author

Zaid, Tarrik M., primary, Yeung, Tsz-Lun, additional, Thompson, Melissa S., additional, Leung, Cecilia S., additional, Harding, Tom, additional, Co, Ngai-Na, additional, Schmandt, Rosie S., additional, Kwan, Suet-Ying, additional, Rodriguez-Aguay, Cristian, additional, Lopez-Berestein, Gabriel, additional, Sood, Anil K., additional, Wong, Kwong-Kwok, additional, Birrer, Michael J., additional, and Mok, Samuel C., additional

Published
2013
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43. HPV-16 E6 upregulation of DNMT1 through repression of tumor suppressor p53.

Author

Au Yeung CL, Tsang WP, Tsang TY, Co NN, Yau PL, and Kwok TT

Subjects
Carcinoma etiology, Carcinoma genetics, Carcinoma metabolism, Cell Line, Tumor, Cell Proliferation drug effects, DNA (Cytosine-5-)-Methyltransferase 1, DNA (Cytosine-5-)-Methyltransferases metabolism, Down-Regulation drug effects, Down-Regulation genetics, Female, Gene Expression Regulation, Neoplastic drug effects, Gene Knockdown Techniques, Human papillomavirus 16 metabolism, Human papillomavirus 16 physiology, Humans, Oncogene Proteins, Viral genetics, Oncogene Proteins, Viral metabolism, Papillomavirus Infections complications, Papillomavirus Infections genetics, RNA, Small Interfering pharmacology, Repressor Proteins genetics, Repressor Proteins metabolism, Tumor Suppressor Protein p53 metabolism, Up-Regulation drug effects, Up-Regulation physiology, Uterine Cervical Neoplasms etiology, Uterine Cervical Neoplasms genetics, Uterine Cervical Neoplasms metabolism, DNA (Cytosine-5-)-Methyltransferases genetics, Oncogene Proteins, Viral physiology, Repressor Proteins physiology, Tumor Suppressor Protein p53 antagonists & inhibitors, Tumor Suppressor Protein p53 genetics
Abstract

The HPV-16 early proteins E6 and E7 are considered to function as oncoproteins in cervical cancer. DNA methyltransferase 1 (DNMT1) is one of the enzymes involved in epigenetic silencing of tumor suppressor genes. In the present study, the functional role and regulation of DNMT1 in HPV-16 E6 associated cervical cancer development were examined. Knockdown of E6 in HPV-16 positive human cervical carcinoma SiHa and CaSki cells led to the increase in p53, repression of DNMT1 protein and promoter activity. Moreover, p53 knockdown increased the DNMT1 protein as well as promoter activity, indicating that p53 may mediate E6 upregulation of DNMT1. In addition, E6 knockdown induced growth retardation in SiHa cells, and the effect was partially reverted by DNMT1 overexpression. The results suggest that HPV-16 E6 may act through p53/ DNMT1 to regulate the development of cervical cancer.

Published
2010
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44. AF1q enhancement of gamma irradiation-induced apoptosis by up-regulation of BAD expression via NF-kappaB in human squamous carcinoma A431 cells.

Author

Co NN, Tsang WP, Tsang TY, Yeung CL, Yau PL, Kong SK, and Kwok TT

Subjects
Apoptosis drug effects, Base Sequence, Blood Proteins antagonists & inhibitors, Blood Proteins genetics, Carcinoma, Squamous Cell genetics, Carcinoma, Squamous Cell metabolism, Cell Line, Tumor, Gamma Rays, Gene Expression Regulation, Neoplastic drug effects, Gene Expression Regulation, Neoplastic radiation effects, Humans, Molecular Sequence Data, NF-kappa B antagonists & inhibitors, NF-kappa B genetics, NF-kappa B metabolism, Neoplasm Proteins antagonists & inhibitors, Neoplasm Proteins genetics, Promoter Regions, Genetic, Protein Binding, Proto-Oncogene Proteins, RNA, Small Interfering pharmacology, Transcription, Genetic drug effects, Transcription, Genetic genetics, Up-Regulation drug effects, Up-Regulation genetics, bcl-Associated Death Protein metabolism, Apoptosis genetics, Apoptosis radiation effects, Blood Proteins physiology, Carcinoma, Squamous Cell pathology, NF-kappa B physiology, Neoplasm Proteins physiology, bcl-Associated Death Protein genetics
Abstract

BAD (BCL-2 antagonist of cell death) is a pro-apoptotic BCL-2 family protein that plays a critical role in the regulation of apoptotic response. This study presents direct evidence that AF1q increased the radiation-induced apoptosis through up-regulation of BAD in human squamous carcinoma A431 cells and the key transcription factor involved is NF-kappaB. The minimal promoter sequence of BAD was identified; the activity was increased in AF1q stable transfectants and decreased upon AF1q siRNA transfection. The NF-kappaB consensus binding sequence is detected on BAD promoter. Inactivation of NF-kappaB by NF-kappaB inhibitor Bay 11-7082 or NF-kappaB p65 siRNA suppressed the expression and promoter activity of BAD; the suppression is more obvious in AF1q stable transfectants which also have an elevated NF-kappaB level. Mutation of putative NF-kappaB motif decreased the BAD promoter activity. The binding of NF-kappaB to the BAD promoter was confirmed by chromatin-immunoprecipitation. These findings indicate that AF1q up-regulation of BAD is through its effect on NF-kappaB and this may hint of its oncogenic mechanism in cancer.

Published
2010

45. Facilitation of drug resistance development by gamma-irradiation in human cancer cells.

Author

Tsang TY, Tsang SW, Lai KP, Tsang WP, Co NN, and Kwok TT

Subjects
ATP Binding Cassette Transporter, Subfamily B, Member 1 biosynthesis, ATP Binding Cassette Transporter, Subfamily B, Member 1 genetics, Antineoplastic Agents pharmacology, Blotting, Southern, Blotting, Western, Cell Line, Tumor, Combined Modality Therapy adverse effects, Doxorubicin pharmacology, Drug Resistance, Neoplasm drug effects, Drug Resistance, Neoplasm genetics, Humans, Radiotherapy adverse effects, Reverse Transcriptase Polymerase Chain Reaction, Drug Resistance, Neoplasm radiation effects, Gamma Rays adverse effects, Gene Expression radiation effects
Abstract

Hepatocellular carcinoma HepG2 cells (G cells) were subjected to selection first with gamma-radiation and then doxorubicin (Dox). The radiation treatment consisted of 2 Gy for 10 days (G2) or 10 Gy for 2 days (G10) and the Dox treatment was continuous exposure for up to 10 microM. Compared with respective parental G, G2, G10 cells, the Dox-selected cells showed mdr1 amplification/P-glycoprotein overexpression, Dox resistance and also less intracellular Dox accumulation. Verapamil reversed the drug resistance and increased the Dox accumulation in all cells. Decay in drug resistance and reduction in mdr1 amplification/P-glycoprotein overexpression were observed in the Dox-selected cells culturing in Dox-free condition. Among the Dox-selected cells, G2R cells showed the highest levels of drug resistance, mdr1 amplification, but the least resistance decay. Results from the study indicate the possible influence of radiation treatment on the development of drug resistance in cancer cells and it may even lead to a highly resistant phenotype.

Published
2009
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