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1. Data from AKT1 Inhibits Epithelial-to-Mesenchymal Transition in Breast Cancer through Phosphorylation-Dependent Twist1 Degradation

Author

Li, Chia-Wei, primary, Xia, Weiya, primary, Lim, Seung-Oe, primary, Hsu, Jennifer L., primary, Huo, Longfei, primary, Wu, Yun, primary, Li, Long-Yuan, primary, Lai, Chien-Chen, primary, Chang, Shih-Shin, primary, Hsu, Yi-Hsin, primary, Sun, Hui-Lung, primary, Kim, Jongchan, primary, Yamaguchi, Hirohito, primary, Lee, Dung-Fang, primary, Wang, Hongmei, primary, Wang, Yan, primary, Chou, Chao-Kai, primary, Hsu, Jung-Mao, primary, Lai, Yun-Ju, primary, LaBaff, Adam M., primary, Ding, Qingqing, primary, Ko, How-Wen, primary, Tsai, Fuu-Jen, primary, Tsai, Chang-Hai, primary, Hortobagyi, Gabriel N., primary, and Hung, Mien-Chie, primary

Published
2023
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3. Data from Epithelial–Mesenchymal Transition Induced by TNF-α Requires NF-κB–Mediated Transcriptional Upregulation of Twist1

Author

Li, Chia-Wei, primary, Xia, Weiya, primary, Huo, Longfei, primary, Lim, Seung-Oe, primary, Wu, Yun, primary, Hsu, Jennifer L., primary, Chao, Chi-Hong, primary, Yamaguchi, Hirohito, primary, Yang, Neng-Kai, primary, Ding, Qingqing, primary, Wang, Yan, primary, Lai, Yun-Ju, primary, LaBaff, Adam M., primary, Wu, Ting-Jung, primary, Lin, Been-Ren, primary, Yang, Muh-Hwa, primary, Hortobagyi, Gabriel N., primary, and Hung, Mien-Chie, primary

Published
2023
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4. Supplementary Figures 1-6, Tables 1-4, Methods from Epithelial–Mesenchymal Transition Induced by TNF-α Requires NF-κB–Mediated Transcriptional Upregulation of Twist1

Author

Li, Chia-Wei, primary, Xia, Weiya, primary, Huo, Longfei, primary, Lim, Seung-Oe, primary, Wu, Yun, primary, Hsu, Jennifer L., primary, Chao, Chi-Hong, primary, Yamaguchi, Hirohito, primary, Yang, Neng-Kai, primary, Ding, Qingqing, primary, Wang, Yan, primary, Lai, Yun-Ju, primary, LaBaff, Adam M., primary, Wu, Ting-Jung, primary, Lin, Been-Ren, primary, Yang, Muh-Hwa, primary, Hortobagyi, Gabriel N., primary, and Hung, Mien-Chie, primary

Published
2023
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5. Supplementary Materials and Methods from AKT1 Inhibits Epithelial-to-Mesenchymal Transition in Breast Cancer through Phosphorylation-Dependent Twist1 Degradation

Author

Li, Chia-Wei, primary, Xia, Weiya, primary, Lim, Seung-Oe, primary, Hsu, Jennifer L., primary, Huo, Longfei, primary, Wu, Yun, primary, Li, Long-Yuan, primary, Lai, Chien-Chen, primary, Chang, Shih-Shin, primary, Hsu, Yi-Hsin, primary, Sun, Hui-Lung, primary, Kim, Jongchan, primary, Yamaguchi, Hirohito, primary, Lee, Dung-Fang, primary, Wang, Hongmei, primary, Wang, Yan, primary, Chou, Chao-Kai, primary, Hsu, Jung-Mao, primary, Lai, Yun-Ju, primary, LaBaff, Adam M., primary, Ding, Qingqing, primary, Ko, How-Wen, primary, Tsai, Fuu-Jen, primary, Tsai, Chang-Hai, primary, Hortobagyi, Gabriel N., primary, and Hung, Mien-Chie, primary

Published
2023
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6. Supplementary Figure Legends from AKT1 Inhibits Epithelial-to-Mesenchymal Transition in Breast Cancer through Phosphorylation-Dependent Twist1 Degradation

Author

Li, Chia-Wei, primary, Xia, Weiya, primary, Lim, Seung-Oe, primary, Hsu, Jennifer L., primary, Huo, Longfei, primary, Wu, Yun, primary, Li, Long-Yuan, primary, Lai, Chien-Chen, primary, Chang, Shih-Shin, primary, Hsu, Yi-Hsin, primary, Sun, Hui-Lung, primary, Kim, Jongchan, primary, Yamaguchi, Hirohito, primary, Lee, Dung-Fang, primary, Wang, Hongmei, primary, Wang, Yan, primary, Chou, Chao-Kai, primary, Hsu, Jung-Mao, primary, Lai, Yun-Ju, primary, LaBaff, Adam M., primary, Ding, Qingqing, primary, Ko, How-Wen, primary, Tsai, Fuu-Jen, primary, Tsai, Chang-Hai, primary, Hortobagyi, Gabriel N., primary, and Hung, Mien-Chie, primary

Published
2023
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9. Supplementary Tables and Figures from AKT1 Inhibits Epithelial-to-Mesenchymal Transition in Breast Cancer through Phosphorylation-Dependent Twist1 Degradation

Author

Li, Chia-Wei, primary, Xia, Weiya, primary, Lim, Seung-Oe, primary, Hsu, Jennifer L., primary, Huo, Longfei, primary, Wu, Yun, primary, Li, Long-Yuan, primary, Lai, Chien-Chen, primary, Chang, Shih-Shin, primary, Hsu, Yi-Hsin, primary, Sun, Hui-Lung, primary, Kim, Jongchan, primary, Yamaguchi, Hirohito, primary, Lee, Dung-Fang, primary, Wang, Hongmei, primary, Wang, Yan, primary, Chou, Chao-Kai, primary, Hsu, Jung-Mao, primary, Lai, Yun-Ju, primary, LaBaff, Adam M., primary, Ding, Qingqing, primary, Ko, How-Wen, primary, Tsai, Fuu-Jen, primary, Tsai, Chang-Hai, primary, Hortobagyi, Gabriel N., primary, and Hung, Mien-Chie, primary

Published
2023
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11. The Crosstalk of mTOR/S6K1 and Hedgehog Pathways

Author

Wang, Yan, Ding, Qingqing, Yen, Chia-Jui, Xia, Weiya, Izzo, Julie G., Lang, Jing-Yu, Li, Chia-Wei, Hsu, Jennifer L., Miller, Stephanie A., Wang, Xuemei, Lee, Dung-Fang, Hsu, Jung-Mao, Huo, Longfei, LaBaff, Adam M., Liu, Dongping, Huang, Tzu-Hsuan, Lai, Chien-Chen, Tsai, Fuu-Jen, Chang, Wei-Chao, Chen, Chung-Hsuan, Wu, Tsung-Teh, Buttar, Navtej S., Wang, Kenneth K., Wu, Yun, Wang, Huamin, Ajani, Jaffer, and Hung, Mien-Chie

Published
2012
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12. Phosphorylation of serine 367 of FOXC2 by p38 regulates ZEB1 and breast cancer metastasis, without impacting primary tumor growth

Author

Werden, Steven, Sphyris, Nathalie, Sarkar, Tapasree Roy, Paranjape, A., LaBaff, Adam, Taube, Joseph, Hollier, Brett, other, and, Werden, Steven, Sphyris, Nathalie, Sarkar, Tapasree Roy, Paranjape, A., LaBaff, Adam, Taube, Joseph, Hollier, Brett, and other, and

Abstract

Metastatic competence is contingent upon the aberrant activation of a latent embryonic program, known as the epithelial – mesenchymal transition (EMT), which bestows stem cell properties as well as migratory and invasive capabilities upon differentiated tumor cells. We recently identified the transcription factor FOXC2 as a downstream effector of multiple EMT programs, independent of the EMT-inducing stimulus, and as a key player linking EMT, stem cell traits and metastatic competence in breast cancer. As such, FOXC2 could serve as a potential therapeutic target to attenuate metastasis. However, as FOXC2 is a transcription factor, it is difficult to target by conventional means such as small-molecule inhibitors. Herein, we identify the serine/threonine-specific kinase p38 as a druggable upstream regulator of FOXC2 stability and function that elicits phosphorylation of FOXC2 at serine 367 (S367). Using an orthotopic syngeneic mouse tumor model, we make the striking observation that inhibition of p38-FOXC2 signaling selectively attenuates metastasis without impacting primary tumor growth. In this model, circulating tumor cell numbers are significantly reduced in mice treated with the p38 inhibitor SB203580, relative to vehicle-treated counterparts. Accordingly, genetic or pharmacological inhibition of p38 decreases FOXC2 protein levels, reverts the EMT phenotype and compromises stem cell attributes in vitro. We also identify the EMT-regulator ZEB1 —known to directly repress E-cadherin/CDH1—as a downstream target of FOXC2, critically dependent on its activation by p38. Consistent with the notion that activation of the p38-FOXC2 signaling axis represents a critical juncture in the acquisition of metastatic competence, the phosphomimetic FOXC2(S367E) mutant is refractory to p38 inhibition both in vitro and in vivo , whereas the non-phosphorylatable FOXC2(S367A) mutant fails to elicit EMT and upregulate ZEB1. Collectively, our data demonstrate that FOXC2 regulates EMT, st

Published
2016

13. GSK3β inactivation promotes the oncogenic functions of EZH2 and enhances methylation of H3K27 in human breast cancers

Author

Ko, How-Wen, primary, Lee, Heng-Huan, additional, Huo, Longfei, additional, Xia, Weiya, additional, Yang, Cheng-Chieh, additional, Hsu, Jennifer L., additional, Li, Long-Yuan, additional, Lai, Chien-Chen, additional, Chan, Li-Chuan, additional, Cheng, Chien-Chia, additional, Labaff, Adam M., additional, Liao, Hsin-Wei, additional, Lim, Seung-Oe, additional, Li, Chia-Wei, additional, Wei, Yongkun, additional, Nie, Lei, additional, Yamaguchi, Hirohito, additional, and Hung, Mien-Chie, additional

Published
2016
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14. AKT1 Inhibits Epithelial-to-Mesenchymal Transition in Breast Cancer through Phosphorylation-Dependent Twist1 Degradation

Author

Li, Chia-Wei, primary, Xia, Weiya, additional, Lim, Seung-Oe, additional, Hsu, Jennifer L., additional, Huo, Longfei, additional, Wu, Yun, additional, Li, Long-Yuan, additional, Lai, Chien-Chen, additional, Chang, Shih-Shin, additional, Hsu, Yi-Hsin, additional, Sun, Hui-Lung, additional, Kim, Jongchan, additional, Yamaguchi, Hirohito, additional, Lee, Dung-Fang, additional, Wang, Hongmei, additional, Wang, Yan, additional, Chou, Chao-Kai, additional, Hsu, Jung-Mao, additional, Lai, Yun-Ju, additional, LaBaff, Adam M., additional, Ding, Qingqing, additional, Ko, How-Wen, additional, Tsai, Fuu-Jen, additional, Tsai, Chang-Hai, additional, Hortobagyi, Gabriel N., additional, and Hung, Mien-Chie, additional

Published
2016
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19. Epithelial–Mesenchymal Transition Induced by TNF-α Requires NF-κB–Mediated Transcriptional Upregulation of Twist1

Author

Li, Chia-Wei, primary, Xia, Weiya, additional, Huo, Longfei, additional, Lim, Seung-Oe, additional, Wu, Yun, additional, Hsu, Jennifer L., additional, Chao, Chi-Hong, additional, Yamaguchi, Hirohito, additional, Yang, Neng-Kai, additional, Ding, Qingqing, additional, Wang, Yan, additional, Lai, Yun-Ju, additional, LaBaff, Adam M., additional, Wu, Ting-Jung, additional, Lin, Been-Ren, additional, Yang, Muh-Hwa, additional, Hortobagyi, Gabriel N., additional, and Hung, Mien-Chie, additional

Published
2012
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21. AKT1 Inhibits Epithelial-to-Mesenchymal Transition in Breast Cancer through Phosphorylation-Dependent Twist1 Degradation.

Author

Chia-Wei Li, Weiya Xia, Seung-Oe Lim, Hsu, Jennifer L., Longfei Huo, Yun Wu, Long-Yuan Li, Chien-Chen Lai, Shih-Shin Chang, Yi-Hsin Hsu, Hui-Lung Sun, Jongchan Kim, Hirohito Yamaguchi, Dung-Fang Lee, Hongmei Wang, Yan Wang, Chao-Kai Chou, Jung-Mao Hsu, Yun-Ju Lai, and LaBaff, Adam M.

Subjects
*BREAST cancer treatment, *SERINE/THREONINE kinases, *PROTEIN kinase B, *MESENCHYMAL stem cells, *EPITHELIAL cells, *CELL transformation, *PHOSPHORYLATION, *RESVERATROL, *THERAPEUTICS
Abstract

Epithelial-to-mesenchymal transition (EMT) is an essential physiologic process that promotes cancer cell migration, invasion, and metastasis. Several lines of evidence from both cellular and genetic studies suggest that AKT1/PKBα, but not AKT2 or AKT3, serves as a negative regulator of EMT and breast cancer metastasis. However, the underlying mechanism by which AKT1 suppresses EMT remains poorly defined. Here, we demonstrate that phosphorylation of Twist1 by AKT1 is required for β-TrCP-mediated Twist1 ubiquitination and degradation. The clinically used AKT inhibitor MK-2206, which possesses higher specificity toward AKT1, stabilized Twist1 and enhanced EMT in breast cancer cells. However, we discovered that resveratrol, a naturally occurring compound, induced β-TrCP-mediated Twist1 degradation to attenuate MK-2206- induced EMT in breast cancer cells. Taken together, our findings demonstrate that resveratrol counteracts the unexpected metastatic potential induced by anti-AKT therapy and therefore suggest that the addition of resveratrol to an anti-AKT therapeutic regimen may provide extra support for limiting EMT. [ABSTRACT FROM AUTHOR]

Published
2016
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22. Epithelial-Mesenchymal Transition Induced by TNF-α Requires NF-κB-Mediated Transcriptional Upregulation of Twist1.

Author

Chia-Wei Li, Weiya Xia, Longfei Huo, Seung-Oe Lim, Yun Wu, Hsu, Jennifer L., Chi-Hong Chao, Yamaguchi, Hirohito, Neng-Kai Yang, Qingqing Ding, Yan Wang, Yun-Ju Lai, LaBaff, Adam M., Ting-Jung Wu, Been-Ren Lin, Muh-Hwa Yang, Hortobagyi, Gabriel N., and Mien-Chie Hung

Subjects
*TUMOR necrosis factor receptors, *NF-kappa B, *BREAST cancer, *CANCER cells, *EXFOLIATIVE cytology
Abstract

Proinflammatory cytokines produced in the tumor microenvironment facilitate tumor development and metastatic progression. In particular, TNF-αpromotes cancer invasion and angiogenesis associated with epithelial-mesenchymal transition (EMT); however, the mechanisms underlying its induction of EMT in cancer cells remain unclear. Here we show that EMT and cancer stemness properties induced by chronic treatment with TNF-αare mediated by the upregulation of the transcriptional repressor Twist1. Exposure to TNF-αrapidly induced Twist1 mRNA and protein expression in normal breast epithelial and breast cancer cells. Both IKK-β and NF-κB p65 were required for TNF-α-induced expression of Twist1, suggesting the involvement of canonical NF-κB signaling. In support of this likelihood, we defined a functional NF-κB -binding site in the Twist1 promoter, and overexpression of p65 was sufficient to induce transcriptional upregulation of Twist1 along with EMT in mammary epithelial cells. Conversely, suppressing Twist1 expression abrogated p65-induced cell migration, invasion, EMT, and stemness properties, establishing that Twist1 is required for NF-κB to induce these aggressive phenotypes in breast cancer cells. Taken together, our results establish a signaling axis through which the tumor microenvironment elicits Twist1 expression to promote cancer metastasis. We suggest that targeting NF-κB-mediated Twist1 upregulation may offer an effective a therapeutic strategy for breast cancer treatment. [ABSTRACT FROM AUTHOR]

Published
2012
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23. Phosphorylation of EZH2 at T416 by CDK2 contributes to the malignancy of triple negative breast cancers.

Author

Yang CC, LaBaff A, Wei Y, Nie L, Xia W, Huo L, Yamaguchi H, Hsu YH, Hsu JL, Liu D, Lang J, Du Y, Lien HC, Li LY, Deng R, Chan LC, Yao J, Kleer CG, Hortobagyi GN, and Hung MC

Abstract

Triple-negative breast cancer (TNBC), which is closely related to basal-like breast cancer, is a highly aggressive subtype of breast cancer that initially responds to chemotherapy but eventually develops resistance. This presents a major clinical challenge as there are currently no effective targeted therapies available due to its lack of HER2 and estrogen receptor expression. Here, we show that cyclin E and the enhancer of zeste 2 (EZH2) are closely co-expressed in TNBC patients, and cyclin E/CDK2 phosphorylates EZH2 at T416 (pT416-EZH2) in vivo. Phosphorylation of EZH2 at T416 enhances the ability of EZH2 to promote TNBC cell migration/invasion, tumorsphere formation, and in vivo tumor growth. In addition, high pT416-EZH2 correlates with poorer survival in TNBC patients. These findings suggest that pT416 has the potential to serve as a therapeutic biomarker for the aggressive forms of breast cancer and provide a rationale for the use of CDK2 inhibitors to treat TNBC.

Published
2015

24. Long non-coding RNAs: versatile master regulators of gene expression and crucial players in cancer.

Author

Nie L, Wu HJ, Hsu JM, Chang SS, Labaff AM, Li CW, Wang Y, Hsu JL, and Hung MC

Abstract

With rapid development of sequencing technologies such as deep sequencing and whole genome high-density tiling array, we now know that most of the "junk" genomic sequences are transcribed as non-coding RNAs (ncRNAs). A large number of long ncRNA transcripts (> 200bp) have been identified, and these long ncRNAs (LncRNAs) are found to be crucial regulators for epigenetic modulation, transcription, and translation. In this review, we briefly summarize the regulatory function of LncRNAs with a particular focus on the underlying mechanisms of LncRNAs in oncogenesis, tumor metastasis and suppression.

Published
2012

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