Jae-Hoon Jeong

Dr. Jae-Hoon Jeong


Research Focus & Metrics

Academic Career Length

17Years (2010-Present)

(Calculated once Scilit publication data is synced: current year − year of first publication + 1)

Representative Publications

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Verified
Journal Article
Open access
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SSSungho Shin
Sungho Shin
JLJeongmin Lee
Jeongmin Lee
YKYumi Kwon
Yumi Kwon
KPKang-Sik Park
Kang-Sik Park
JJJae-Hoon Jeong
Jae-Hoon Jeong
Cheolju LeeCheolju Lee
Cheolju Lee
Mesenchymal stem cells (MSCs) have the potential to be a viable therapy against various diseases due to their paracrine effects, such as secretion of immunomodulatory, trophic and protective factors. These cells are known to be distributed within various organs and tissues. Although they possess the same characteristics, MSCs from different sources are believed to have different secretion potentials and patterns, which may influence their therapeutic effects in disease environments. We characterized the protein secretome of adipose (AD), bone marrow (BM), placenta (PL), and Wharton’s jelly (WJ)-derived human MSCs by using conditioned media and analyzing the secretome by mass spectrometry and follow-up bioinformatics. Each MSC secretome profile had distinct characteristics depending on the source. However, the functional analyses of the secretome from different sources showed that they share similar characteristics, such as cell migration and negative regulation of programmed cell death, even though differences in the composition of the secretome exist. This study shows that the secretome of fetal-derived MSCs, such as PL and WJ, had a more diverse composition than that of AD and BM-derived MSCs, and it was assumed that their therapeutic potential was greater because of these properties.

7 April 2015 in PLOS ONE
Verified
Journal Article
Open access
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MKMoon-Hong Kim
Moon-Hong Kim
WKWonwoo Kim
Wonwoo Kim
MKMi Ae Kang
Mi Ae Kang
NCNicholas A. Cacalano
Nicholas A. Cacalano
SKSoon-Beom Kang
Soon-Beom Kang
JJJae-Hoon Jeong
Jae-Hoon Jeong
Suppressor of cytokine signaling (SOCS) family is an important negative regulator of cytokine signaling and deregulation of SOCS has been involved in many types of cancer. All cervical cancer cell lines tested showed lower expression of SOCS1, SOCS3, and SOCS5 than normal tissue or cell lines. The immunohistochemistry result for SOCS proteins in human cervical tissue also confirmed that normal tissue expressed higher level of SOCS proteins than neighboring tumor. Similar to the regulation of SOCS in other types of cancer, DNA methylation contributed to SOCS1 downregulation in CaSki, ME-180, and HeLa cells. However, the expression of SOCS3 or SOCS5 was not recovered by the inhibition of DNA methylation. Histone deacetylation may be another regulatory mechanism involved in SOCS1 and SOCS3 expression, however, SOCS5 expression was neither affected by DNA methylation nor histone deacetylation. Ectopic expression of SOCS1 or SOCS3 conferred radioresistance to HeLa cells, which implied SOCS signaling regulates the response to radiation in cervical cancer. In this study, we have shown that SOCS expression repressed by, in part, epigenetically and altered SOCS1 and SOCS3 expression could contribute to the radiosensitive phenotype in cervical cancer.

19 December 2012 in Cancer Biology & Therapy
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Journal Article
Open access
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YSYoung-Joo Shin
Young-Joo Shin
MKMi-Sook Kim
Mi-Sook Kim
MKMoon-Sun Kim
Moon-Sun Kim
JLJoonseok Lee
Joonseok Lee
MKMiae Kang
Miae Kang
JJJae-Hoon Jeong
Jae-Hoon Jeong
Overexpression of high-mobility group box 2 (HMGB2) is recently reported in several malignant cancers and was correlated with poor response to preoperative chemoradiotherapy of colorectal cancer patients. To enhance the chemoradiotherapy efficacy, the biological function of HMGB2 was investigated with respect to radiation response. HMGB2 gene knockdown cells were constructed by infecting shRNA expressing lentivirus and clonogenic assay was performed to count the radiosensitivity. HMGB2 knockdown sensitized HCT-116 and HT-29 colorectal cancer cells to ionizing radiation. This could be due to an increased DNA damage and an inefficient DNA damage repair in HMGB2 knockdown cells. In addition, an exposure to radiation downregulated HMGB2 expression in colorectal cancer cells with an intact TP53 gene. HMGB2 gene expression of TP53-mutant cell was not affected by irradiation. p53-mediated downregulation of HMGB2 was confirmed by direct activation of p53 using Nutlin-3 or by inducing p53 expression using Tet-On system. Luciferase reporter assay showed that HMGB2 promoter activity was inversely correlated with the amount p53 cotransfected. Our study revealed that HMGB2 is necessary to protect colorectal cancer cells from DNA damage and efficient DNA repair and p53-mediated downregulation is a critical mechanism of modulating HMGB2 expression.

7 January 2016 in Oncotarget
Verified
Journal Article
Open access
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MKMi Ae Kang
Mi Ae Kang
MKMi-Sook Kim
Mi-Sook Kim
WKWonwoo Kim
Wonwoo Kim
JUJee-Hyun Um
Jee-Hyun Um
YSYoung-Joo Shin
Young-Joo Shin
JJJae-Hoon Jeong
Jae-Hoon Jeong
Lanatoside C suppressed colorectal cancer cell growth by inducing mitochondrial dysfunction and increased radiation sensitivity by impairing DNA damage repair

31 May 2018 in International Journal of Oncology
Verified
Journal Article
Closed access
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MKMi Ae Kang
Mi Ae Kang
WKWonwoo Kim
Wonwoo Kim
HJHye-Ram Jo
Hye-Ram Jo
YSYoung-Joo Shin
Young-Joo Shin
MKMoon-Hong Kim
Moon-Hong Kim
JJJae-Hoon Jeong
Jae-Hoon Jeong
Cyclin-dependent kinases (CDK) are considered to be potential targets of anticancer drugs that can interrupt the uncontrolled division of cancer cells. In this study, we selected two selective CDK inhibitors, AT7519 and SNS-032, from current clinical trials and examined their anticancer and radiosensitizing effects in a cervical cancer model. SNS-032 was found to be more potent than AT7519, with a lower half maximal inhibitory concentration (IC50) value. Both AT7519 and SNS-032 induced the apoptosis, premature senescence and cytostasis of cervical cancer cells, which led to the attenuation of tumor growth in vivo. Moreover, using these CDK inhibitors together with radiation synergistically inhibited tumor growth in a human xenograft tumor model. The concomitant activation of the p53 tumor suppressor and the suppression of cell cycle checkpoint responses mediated by Chk1 led to the cytostasis of cervical cancer cells. Finally, AT7519 and SNS-032 inhibited cancer cell migration, invasion and angiogenesis in vitro, and suppressed lung metastases in a spontaneous metastasis model. On the whole, the findings of this study indicate that the utilization of AT7519 and SNS-032 as part of an adjuvant treatment may help control cervical cancer progression.

12 June 2013
Verified
Journal Article
Closed access
YJYoun Kyoung Jeong
Youn Kyoung Jeong
MKMi-Sook Kim
Mi-Sook Kim
JLJi Young Lee
Ji Young Lee
EKEun Ho Kim
Eun Ho Kim
WKWonwoo Kim
Wonwoo Kim
JJJae-Hoon Jeong
Jae-Hoon Jeong