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18 results on '"Lee, You-Soub"'

2. The TGFβ→TAK1→LATS→YAP1 Pathway Regulates the Spatiotemporal Dynamics of YAP1

Author

Kim, Min-Kyu, primary, Han, Sang-Hyun, additional, Park, Tae-Geun, additional, Song, Soo-Hyun, additional, Lee, Ja-Youl, additional, Lee, You-Soub, additional, Yoo, Seo-Yeong, additional, Chi, Xin-Zi, additional, Kim, Eung-Gook, additional, Jang, Ju-Won, additional, Lim, Dae Sik, additional, Wijnen, Andre J. van, additional, Lee, Jung-Won, additional, and Bae, Suk-Chul, additional

Published
2023
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5. K-Ras–Activated Cells Can Develop into Lung Tumors When Runx3-Mediated Tumor Suppressor Pathways Are Abrogated

Author

Lee, You-Soub, Lee, Ja-Yeol, Song, Soo-Hyun, Kim, Da-Mi, Lee, Jung-Won, Chi, Xin-Zi, Ito, Yoshiaki, and Bae, Suk-Chul

Subjects
body regions, p53, lung cancer, Runx3, cancer initiation, K-Ras, Research Article
Abstract

K-RAS is frequently mutated in human lung adenocarcinomas (ADCs), and the p53 pathway plays a central role in cellular defense against oncogenic K-RAS mutation. However, in mouse lung cancer models, oncogenic K-Ras mutation alone can induce ADCs without p53 mutation, and loss of p53 does not have a significant impact on early K-Ras–induced lung tumorigenesis. These results raise the question of how K-Ras–activated cells evade oncogene surveillance mechanisms and develop into lung ADCs. RUNX3 plays a key role at the restriction (R)-point, which governs multiple tumor suppressor pathways including the p14ARF–p53 pathway. In this study, we found that K-Ras activation in a very limited number of cells, alone or in combination with p53 inactivation, failed to induce any pathologic lesions for up to 1 year. By contrast, when Runx3 was inactivated and K-Ras was activated by the same targeting method, lung ADCs and other tumors were rapidly induced. In a urethane-induced mouse lung tumor model that recapitulates the features of K-RAS–driven human lung tumors, Runx3 was inactivated in both adenomas (ADs) and ADCs, whereas K-Ras was activated only in ADCs. Together, these results demonstrate that the R-point–associated oncogene surveillance mechanism is abrogated by Runx3 inactivation in AD cells and these cells cannot defend against K-Ras activation, resulting in the transition from AD to ADC. Therefore, K-Ras–activated lung epithelial cells do not evade oncogene surveillance mechanisms; instead, they are selected if they occur in AD cells in which Runx3 has been inactivated.

Published
2020

6. Lung Cancer Staging and Associated Genetic and Epigenetic Events

Author

Kim, Dohun, Lee, You-Soub, Kim, Duk-Hwan, and Bae, Suk-Chul

Subjects
lung cancer, adenocarcinoma, Lung Neoplasms, epigenetic alteration, Carcinogenesis, Mutation, Animals, Humans, Minireview, staging, Neoplasm Staging, Epigenesis, Genetic
Abstract

The first step in treating lung cancer is to establish the stage of the disease, which in turn determines the treatment options and prognosis of the patient. Many factors are involved in lung cancer staging, but all involve anatomical information. However, new approaches, mainly those based on the molecular biology of cancer, have recently changed the paradigm for lung cancer treatment and have not yet been incorporated into staging. In a group of patients of the same stage who receive the same treatment, some may experience unexpected recurrence or metastasis, largely because current staging methods do not reflect the findings of molecular biological studies. In this review, we provide a brief summary of the latest research on lung cancer staging and the molecular events associated with carcinogenesis. We hope that this paper will serve as a bridge between clinicians and basic researchers and aid in our understanding of lung cancer.

Published
2020

12. Runx3 Inactivation Is a Crucial Early Event in the Development of Lung Adenocarcinoma

Author

Lee, You-Soub, primary, Lee, Jung-Won, additional, Jang, Ju-Won, additional, Chi, Xin-Zi, additional, Kim, Jang-Hyun, additional, Li, Ying-Hui, additional, Kim, Min-Kyu, additional, Kim, Da-Mi, additional, Choi, Byeung-Sub, additional, Kim, Eung-Gook, additional, Chung, Jin-Haeng, additional, Lee, Ok-Jun, additional, Lee, You-Mie, additional, Suh, Joo-Won, additional, Chuang, Linda Shyue Huey, additional, Ito, Yoshiaki, additional, and Bae, Suk-Chul, additional

Published
2013
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15. Src Kinase Phosphorylates RUNX3 at Tyrosine Residues and Localizes the Protein in the Cytoplasm

Author

Goh, Yun-Mi, primary, Cinghu, Senthilkumar, additional, Hong, Eileen Tan Hwee, additional, Lee, You-Soub, additional, Kim, Jang-Hyun, additional, Jang, Ju-Won, additional, Li, Ying-Hui, additional, Chi, Xin-Zi, additional, Lee, Kyeong-Sook, additional, Wee, Heejun, additional, Ito, Yoshiaki, additional, Oh, Byung-Chul, additional, and Bae, Suk-Chul, additional

Published
2010
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17. Phosphorylation of the gastric tumor suppressor RUNX3 following H. pylori infection results in its localization to the cytoplasm.

Author

Cinghu, Senthilkumar, Goh, Yun-Mi, Oh, Byung-Chul, Lee, You-Soub, Lee, Ok-Jun, Devaraj, Halagowder, and Bae, Suk-Chul

Subjects
STOMACH cancer, HELICOBACTER pylori infections, GUT microbiome, TUMOR suppressor genes, PHOSPHORYLATION, CYTOPLASM, GENETIC regulation, GENETICS
Abstract

As H. pylori infection progresses, intestinal metaplasia (IM), a key event in gastric carcinogenesis, develops in the stomach. The mechanism by which H. pylori infection causes the trans-differentiation of gastric cells to intestinal-type cells remains an important question. In the current study, we found that RUNX3 is deregulated in all human IM specimens examined by either down regulation or mislocalization; Aberrant localization of a gastric tumor suppressor RUNX3 is observed in most human cases of IM with concurrent H. pylori infection, and RUNX3 is down-regulated in most cases of IM without H. pylori-infection. The cytoplasmic mislocalization of a RUNX3 was associated with H. pylori-induced c-Src activation and RUNX tyrosine phosphorylation. Moreover, gastric epithelial cells of Runx3 −/− mice expressed the intestinal markers Muc2 and Li-Cadherin, which suggests that the deregulation of Runx3 is a key event in the intestinalization of the gastric epithelium. Collectively, the results of the current study suggest that RUNX3 deregulation is associated with H. pylori-induced pathogenesis and the development of IM. J. Cell. Physiol. 227: 1071-1080, 2012. © 2011 Wiley Periodicals, Inc. [ABSTRACT FROM AUTHOR]

Published
2012
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18. Runx3is a crucial regulator of alveolar differentiation and lung tumorigenesis in mice

Author

Lee, Jong-Min, Shin, Jeong-Oh, Cho, Kyoung-Won, Hosoya, Akihiro, Cho, Sung-Won, Lee, You-Soub, Ryoo, Hyun-Mo, Bae, Suk-Chul, and Jung, Han-Sung

Abstract

The runt-domain transcription factor Runx3plays crucial roles during development such as regulating gene expression. It has been shown that Runx3is involved in neurogenesis, thymopoiesis and functions like a tumor suppressor. Runx3null mouse die soon after birth as a result of multiple organ defects. Runx3null mouse lung shows an abnormal phenotype and loss of Runx3induced remodeling in the lung. Interestingly, lung adenocarcinoma is observed in Runx3heterozygous mice at 18 months of age. During lung development various cellular and molecular events occur such as cell proliferation, cell death, differentiation and epithelial–mesenchymal transition (EMT). To understand the specific lethal events in Runx3null mice, we examined cellular and molecular networks involved in EMT, and EMT inducers were quantified by RT-qPCR during lung development. Excessive EMT was observed in lungs at PN1 day in Runx3null mice and PN18 months in Runx3heterozygous mice. Pharmacologic inhibition of EMT was used to curb tumor progression. In this study, U0126 was injected to pregnant mouse for inhibition of pERK signaling. After U0126 treatment, life spans of newborn mice were increased and lung hyperplasia was partially rescued by down-regulated cell proliferation and EMT. Our data suggest that Runx3is involved in crucial regulation of alveolar differentiation and tumor suppression in developing mouse lung.

Published
2011
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