Young Chan, Chae
C
T
R
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ANCER
HERAPEUTICS
ESEARCH
AB
CANCER THERAPEUTICS RESEARCH LAB (CTRL)
Cancer cells have a different metabolism to support rapid cancer cell proliferation.
Although rapidly growing tumors are constantly exposed to unfavorable growth conditions such as nutrient deprivation, acidosis and hypoxia, they successfully reprogram their metabolism to avoid cell death and to support rapid cell growth.In addition the metabolic reprogramming of cancer is closely linked with chemo-resistance and metastatic dissemination of tumors. An important area of my ongoing research is investigating the role of mitochondrial dynamics and metabolic reprogramming in controlling cellular behaviors that drive cancer progression, particularly cancer cell proliferation, metastasis and chemo resistance. The CTRL laboratory explores the mechanisms of metabolic reprogramming to support rapid cell proliferation and survival under diverse stressful environmental condition.
Young Chan, Chae
Ulsan National Institute of Science and Technology
Office Engineering BLDG. IV RM 401-5
Lab Engineering BLDG. IV_RM 408
Tel. +82-52-217-2524
Fax. +82-52-217-5309
E-mail ychae@unist.ac.kr
Curriculum Vitae
2017
Assistant Professor,
UNIST
2013
Associate Staff Scientist,
Wistar Institute Cancer Center, USA
2010
Postdoctoral Fellow,
Wistar Institute
Cancer Center, USA
2006
Senior Researcher, POSTECH Biotech Center
Academic Credential
- 2006: Ph.D., Life Science, POSTECH
- 2001: B.S., Life Science, POSTECH
Research Publications (selected)
- Chae YC, Vaira V, Caino MC, Tang HY, Seo JH, Kossenkov AV, Ottobrini L, Martelli C, Lucignani G, Bertolini I, Locatelli M, Bryant KG, Ghosh JC, Lisanti S, Ku B, Bosari S, Languino LR, Speicher DW, and Altieri DC. “Mitochondrial Akt Regulation of Hypoxic Metabolic Reprogramming” Cancer Cell, 2016, Aug 8;30(2):257-272
- Seo JH, Rivadeneira DB, Caino MC, Chae YC, Speicher DW, Tang HY, Vaira V, Bosari S, Palleschi A, Rampini P, Kossenkov AV, Languino LR, and Altieri DC. The mitochondrial unfoldase-peptidase complex clpxp controls bioenergetics stress and metastasis.
PLOS Biology, 2016, Jul 7;14(7):e1002507.
- Caino MC, Ghosh JC, Chae YC, Vaira V, Faversani A, Rampini P, Kossenkov AV, Aird KM, Zhang R, Webster MR, Weeraratna A, Bosari S, Languino L, Altieri DC. “PI3K Therapy Reprograms Mitochondrial Trafficking to Fuel Tumor Cell Invasion” Proc Natl Acad Sci U S A. 2015 Jul 14;112(28):8638-43
- Ghosh JC , Siegelin MD, Vaira V, Faversani A, Tavecchio M, Chae YC, Lisanti S, Rampini P, Giroda M, Caino MC, Seo JH, Kossenkov AV, Michalek RD, Schultz DC, Bosari S, Languino L, Altieri DC. Adaptive Mitochondrial Reprogramming and Resistance to PI3K Therapy.
Journal of the National Cancer Institute, 2015 Feb 3;107(3).
- Chae YC, Angelin A, Lisanti S, Kossenkov AA, Speicher KD, Wang H, Powers JF, Tischler AS, Pacak K, Fliedner S, Michalek RD, Karoly ED, Wallace DC, Languino LR, Speicher DW and Altieri DC. “Landscape of the Mitochondrial HSP90 Metabolome in Tumors” Nature Communications. 2013, July 10;4, Article number: 2139
- Caino MC, Chae YC, Vaira V, Ferrero S, Nosotti M, Martin NM, Weeraratna A, O’Connell M, Jernigan D, Fatatis A, Languino LR, Bosari S and Altieri DC.
Metabolic Stress Control of Cytoskeletal Dynamics and Metastasis.
Journal of Clinical Investigation. 2013; 123(7):2907–2920
- Chae YC, Caino MC, Lisanti S, Ghosh JC, Dohi T, Danial NN, Villanueva J, Ferrero S, Vaira V, Santambrogio L, Bosari S, Languino LR, Herlyn M, Altieri DC. “Control of Tumor Bioenergetics and Survival Stress Signaling by Mitochondrial HSP90s” Cancer Cell. 2012. 22(3):331-44.
PROFESSOR
RESEARCH STRATEGY
Genetic mutations and growth signals in cancer microenvironments can dynamically alter metabolic pathways. This results in increased biosynthesis and abnormal bioenergetics which in turn promote cell proliferation, metastasis and survival and immune destruction avoidance. Furthermore, metabolic remodeling regulates tumor epigenetic alterations by regulating the activity of epigenetic modification enzymes and gene expression in cancer. Therefore, targeting of cancer metabolism may provide new effective therapies to treat cancer. To investigate role of metabolism of cancer we mainly focus on mechanism of metabolic reprograming of cancer especially in hypoxic environmental stress, oncogenic growth signaling and cancer stem cells.
RESEARCH
Research Keywords
Cancer Metabolism, Stress Response of Cancer, Mitochondria of Cancer, Tumor microenvironment
Research Interests
1. Role of Metabolic reprogramming mechanism in Cancer and Cancer Stem Cells
2. Role of Mitochondrial dynamics changes in cancer progression
3. Mechanism of tumor therapeutics resistance
Metabolic reprogramming under stress condition
One of main characteristics of cancer cell is their fast proliferation. As such, rapidly growing tumors are constantly exposed to unfavorable growth conditions on the tumor environment including nutrient deprivation, acidosis and hypoxia. Tumor cells avoid cell death through adaptive mitochondrial pathways that support rapid cell growth and buffer metabolic stress. However, We lack a comprehensive picture of the regulatory pathways at play how metabolic pathways of tumor are regulated and successfully adapt to environmental stress.
Role of Mitochondrial dynamics in Cancer
Metabolic Adaptation Anti-Apoptosis Cancer Metastasis
Alterations in Mitochondrial Dynamics
in response to cell demands and environment
Identification of metabolic pathway changed
in response to mitochondrial dynamics changes
Mitochondria are highly dynamic organelles which continually fuse and divide in response to diverse stimuli. Participation in the aforementioned processes requires a precise regulation at many levels that allows the cell to couple mitochondrial activity to nutrient availability, biosynthetic demands, proliferation rates, and external stimuli. The many functions of these organelles are intimately linked to their morphology. To investigate detail molecular role of changes in mitochondrial dynamics in cancer, our research focus on diverse molecules related to mitochondrial dynamics and its relationship to tumor progression.
MEMBERS
Yu Geon Lee, Ph.D.
> Postdoctoral Fellows
Ye Ji Nam
> Ph.D. Candidate
Hyuk Kim
> Undergraduate Student
