Kidong Kim

Dr. Kidong Kim

orcid

Research Focus & Metrics

Academic Career Length

19Years (2008-Present)

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

Representative Publications

View All Publications
1 October 2019 in Gynecologic Oncology
Verified
Journal Article
Closed access
SKSe Ik Kim
Se Ik Kim
MLMaria Lee
Maria Lee
SLSungyoung Lee
Sungyoung Lee
DSDong Hoon Suh
Dong Hoon Suh
HKHee Seung Kim
Hee Seung Kim
YKYong Beom Kim
Yong Beom Kim

1 January 2022 in Journal of Gynecologic Oncology
Verified
Journal Article
Open access
PDF file
GKGilhyang Kim
Gilhyang Kim
SLSong Kook Lee
Song Kook Lee
DSDong Hoon Suh
Dong Hoon Suh
KKKidong Kim
Kidong Kim
JNJae Hong No
Jae Hong No
HKHyojin Kim
Hyojin Kim
Kim G, et al. J Gynecol Oncol. 2021 Dec;33(2):e15. https://doi.org/10.3802/jgo.2022.33.e15

1 November 2015 in European Journal of Obstetrics & Gynecology and Reproductive Biology
Verified
Journal Article
Closed access
BLbanghyun Lee.
banghyun Lee.
SHSeung Hwa Hong
Seung Hwa Hong
KKKidong Kim
Kidong Kim
WKWee Chang Kang
Wee Chang Kang
JNJae Hong No
Jae Hong No
YKYong Beom Kim
Yong Beom Kim

1 January 2020 in Journal of Gynecologic Oncology
Verified
Journal Article
Open access
PDF file
SKSe Ik Kim
Se Ik Kim
SKSe Jeong Kim
Se Jeong Kim
DSDong Hoon Suh
Dong Hoon Suh
KKKidong Kim
Kidong Kim
JNJae Hong No
Jae Hong No
YKYong Beom Kim
Yong Beom Kim
Kim SI, et al. J Gynecol Oncol. 2019 Jun;31:e13. https://doi.org/10.3802/jgo.2020.31.e13

1 December 2018 in Biomedicine & Pharmacotherapy
Verified
Journal Article
Open access
MKMiseon Kim
Miseon Kim
SLSeul Lee
Seul Lee
WPWook Ha Park
Wook Ha Park
DSDong Hoon Suh
Dong Hoon Suh
KKKidong Kim
Kidong Kim
JNJae Hong No
Jae Hong No
Bmi1, a polycomb group gene, is essential for self-renewal of stem cells and is frequently upregulated in various cancer cells. We aimed to investigate the effect of Bmi1 silencing on cancer stemness and chemosensitivity in endometrial cancer using targeted siRNA approach in HEC1A and Ishikawa cells. Cell viability after treatment with Bmi1 siRNA was assessed using the MTT assay, and cell apoptosis was visualized using the TdT-mediated dUTP nick-end labeling (TUNEL) method. Western blotting, migration assays and invasion assays were performed to detect changes in the stem-like properties of cancer cells. To evaluate the anticancer effect of Bmi1 silencing, HEC1A and Ishikawa cells were treated with 100 nM Bmi1 siRNA and/or 40 μM cisplatin. In the MTT assay, compared to control, viability of HEC1A and Ishikawa cells significantly decreased after Bmi1 siRNA treatment in a dose-dependent manner. Bmi1 silencing using siRNA increased the expression of cleaved caspase-3 and cleaved poly adenosine diphosphate-ribose polymerase polymerase (PARP) as observed in the western blot analysis. Apoptosis significantly increased in the HEC1A and Ishikawa cells treated with 100 nM Bmi1 siRNA for 48 h than in the control cells in TUNEL assay. SOX2 and Oct4 expression decreased in the HEC1A and Ishikawa cells treated with Bmi1 siRNA, while E-cadherin expression increased. Further, migratory and invasive properties were significantly inhibited by Bmi1 siRNA treatment in both cell lines. Notably, viability of HEC1A and Ishikawa cells decreased more when they were concurrently treated with Bmi1 siRNA and cisplatin compared to when they were treated with Bmi1 siRNA or cisplatin alone. Bmi1 silencing suppresses cancer stemness in HEC1A and Ishikawa cells. Concurrent treatment with Bmi1 siRNA and cisplatin resulted in additive anticancer effect with a cell line-specific pattern, which was higher than that shown by cisplatin treatment alone.

1 January 2017 in Journal of Gynecologic Oncology
Verified
Journal Article
Open access
PDF file
DSDong Hoon Suh
Dong Hoon Suh
MKMiseon Kim
Miseon Kim
KKKidong Kim
Kidong Kim
HKHak Jae Kim
Hak Jae Kim
KLKyung-Hun Lee
Kyung-Hun Lee
HKHak Jae Kim
Hak Jae Kim
Suh DH, et al. J Gynecol Oncol. 2017 Mar;28(3):e45. https://doi.org/10.3802/jgo.2017.28.e45