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Article: PLK1 phosphorylates RhoGDI1 and promotes cancer cell migration and invasion.

Lim, Jeewon / Hwang, Yo Sep / Yoon, Hyang Ran / Yoo, Jiyun / Yoon, Suk Ran / Jung, Haiyoung / Cho, Hee Jun / Lee, Hee Gu

Cancer cell international

2024 Volume 24, Issue 1, Page(s) 73

Abstract: Background: Rho guanine nucleotide dissociation inhibitor 1 (RhoGDI1) plays an important role in diverse cellular processes by regulating Rho guanosine triphosphate (GTP)ases activity. RhoGDI1 phosphorylation regulates the spatiotemporal activation of ... ...

Abstract	Background: Rho guanine nucleotide dissociation inhibitor 1 (RhoGDI1) plays an important role in diverse cellular processes by regulating Rho guanosine triphosphate (GTP)ases activity. RhoGDI1 phosphorylation regulates the spatiotemporal activation of Rho GTPases during cell migration. In this study, we identified polo-like kinase 1 (PLK1) as a novel kinase of RhoGDI1 and investigated the molecular mechanism by which the interaction between RhoGDI1 and PLK1 regulates cancer cell migration. Methods: Immunoprecipitation, GST pull-down assay, and proximity ligation assay (PLA) were performed to analyze the interaction between RhoGDI1 and PLK1. In vitro kinase assay and immunoprecipitation were performed with Phospho-(Ser/Thr) antibody. We evaluated RhoA activation using RhoGTPases activity assay. Cell migration and invasion were analyzed by transwell assays. Results: GST pull-down assays and PLA showed that PLK1 directly interacted with RhoGDI1 in vitro and in vivo. Truncation mutagenesis revealed that aa 90-111 of RhoGDI1 are critical for interacting with PLK1. We also showed that PLK1 phosphorylated RhoGDI1 at Thr7 and Thr91, which induces cell motility. Overexpression of the GFP-tagged RhoGDI1 truncated mutant (aa 90-111) inhibited the interaction of PLK1 with RhoGDI1 and attenuated RhoA activation by PLK1. Furthermore, the overexpression of the RhoGDI1 truncated mutant reduced cancer cell migration and invasion in vitro and suppressed lung metastasis in vivo. Conclusions: Collectively, we demonstrate that the phosphorylation of RhoGDI1 by PLK1 promotes cancer cell migration and invasion through RhoA activation. This study connects the interaction between PLK1 and RhoGDI1 to the promotion of cancer cell behavior associated with malignant progression, thereby providing opportunities for cancer therapeutic interventions.
Language	English
Publishing date	2024-02-14
Publishing country	England
Document type	Journal Article
ZDB-ID	2091573-1
ISSN	1475-2867
ISSN	1475-2867
DOI	10.1186/s12935-024-03254-z
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: Astragalus Complanatus Ethanol Attenuates Septic Shock by Exerting Anti-Inflammatory Effects on Macrophages.

Hwang, Yo Sep / Lim, Jeewon / Yoon, Hyang Ran / Park, Seong-Hoon / Kim, Aeyung / Jang, Jun-Pil / Cho, Hee Jun / Lee, Hee Gu

International journal of molecular sciences

2023 Volume 25, Issue 1

Abstract: Sepsis is a systemic inflammatory syndrome that results in multiple-organ failure caused by a dysregulated host immune response to microbial infection. Astragali complanati semen extract (ACSE) exhibits pharmacological activities, including antioxidant, ... ...

Abstract	Sepsis is a systemic inflammatory syndrome that results in multiple-organ failure caused by a dysregulated host immune response to microbial infection. Astragali complanati semen extract (ACSE) exhibits pharmacological activities, including antioxidant, anticancer, antiaging, and anti-diabetes effects. It is widely used in traditional medicine to treat liver and kidney diseases; however, the protective effect of ACSE on sepsis and its mechanisms are unknown. In the present study, we investigated the anti-inflammatory effects and potential mechanisms of the action of ACSE on sepsis. We show that ACSE improved survival rates in mouse models of acute sepsis induced by CLP (cecal ligation and puncture) and LPS stimulation. ACSE administration decreased aspartate aminotransferase (AST) and alanine aminotransferase (ALT) in sepsis-induced mice. Furthermore, ACSE reduced the levels of nitric oxide (NO), tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), and interleukin-6 (IL-6) in the serum of septic mice. ACSE treatment inhibited the expression of these proinflammatory genes in LPS-stimulated J774 macrophages. Moreover, ACSE inhibited the phosphorylation of the IκB kinase (IKK) and the nuclear translocation of p65 NF-κB by LPS stimulation in macrophages. These results reveal the mechanism underlying the protective effect of ACSE against sepsis by inhibiting NF-κB activation and suggest that ACSE could be a potential therapeutic candidate to treat acute inflammatory diseases.
MeSH term(s)	Animals ; Mice ; Shock, Septic ; Lipopolysaccharides/toxicity ; NF-kappa B ; Sepsis/complications ; Sepsis/drug therapy ; Astragalus Plant ; Ethanol ; Anti-Inflammatory Agents/pharmacology ; Anti-Inflammatory Agents/therapeutic use
Chemical Substances	Lipopolysaccharides ; NF-kappa B ; Ethanol (3K9958V90M) ; Anti-Inflammatory Agents
Language	English
Publishing date	2023-12-27
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2019364-6
ISSN	1422-0067 ; 1422-0067 ; 1661-6596
ISSN (online)	1422-0067
ISSN	1422-0067 ; 1661-6596
DOI	10.3390/ijms25010384
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Article: miR-302 Suppresses the Proliferation, Migration, and Invasion of Breast Cancer Cells by Downregulating ATAD2.

Hwang, Yo Sep / Park, Eun Sun / Oh, Byung Moo / Uhm, Tae Gi / Yoon, Suk Ran / Park, Jong-Lyul / Cho, Hee Jun / Lee, Hee Gu

Cancers

2022 Volume 14, Issue 18

Abstract: Breast cancer is the most common malignant tumor in women. The ATPase family AAA domain-containing protein 2 (ATAD2) contains an ATPase domain and a bromodomain, and is abnormally expressed in various human cancers, including breast cancer. However, the ... ...

Abstract	Breast cancer is the most common malignant tumor in women. The ATPase family AAA domain-containing protein 2 (ATAD2) contains an ATPase domain and a bromodomain, and is abnormally expressed in various human cancers, including breast cancer. However, the molecular mechanisms underlying the regulation of ATAD2 expression in breast cancer remain unclear. This study aimed to investigate the expression and function of ATAD2 in breast cancer. We found that ATAD2 was highly expressed in human breast cancer tissues and cell lines. ATAD2 depletion via RNA interference inhibited the proliferation, migration, and invasive ability of the SKBR3 and T47D breast cancer cell lines. Furthermore, Western blot analysis and luciferase assay results revealed that ATAD2 is a putative target of miR-302. Transfection with miR-302 mimics markedly reduced cell migration and invasion. These inhibitory effects of miR-302 were restored by ATAD2 overexpression. Moreover, miR-302 overexpression in SKBR3 and T47D cells suppressed tumor growth in the xenograft mouse model. However, ATAD2 overexpression rescued the decreased tumor growth seen after miR-302 overexpression. Our findings indicate that miR-302 plays a prominent role in inhibiting the cancer cell behavior associated with tumor progression by targeting ATAD2, and could thus be a valuable target for breast cancer therapy.
Language	English
Publishing date	2022-09-06
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2527080-1
ISSN	2072-6694
ISSN	2072-6694
DOI	10.3390/cancers14184345
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Article ; Online: Cisplatin Induces Kidney Cell Death

Zhang, Hui-Na / Xiao, Wan-Qiu / Lee, Dong Hun / Li, Nan / Feng, Yao-Yuan / Su, Ting / Gu, Han-Yu / Yoon, Ijoo / Jung, Haiyoung / Lee, Kyung Ho / Cho, Hee Jun / Han, Ying-Hao / Sun, Hu-Nan / Kwon, Taeho

In vivo (Athens, Greece)

2024 Volume 38, Issue 2, Page(s) 630–639

Abstract: Background/aim: Cisplatin [cis-diamminedichloroplatinum(II), CDDP] is a widely used and effective antitumor drug in clinical settings, notorious for its nephrotoxic side effects. This study investigated the mechanisms of CDDP-induced damage in African ... ...

Abstract	Background/aim: Cisplatin [cis-diamminedichloroplatinum(II), CDDP] is a widely used and effective antitumor drug in clinical settings, notorious for its nephrotoxic side effects. This study investigated the mechanisms of CDDP-induced damage in African green monkey kidney (Vero) cells, with a focus on the role of Peroxiredoxin I (Prx I) and Peroxiredoxin II (Prx II) of the peroxiredoxin (Prx) family, which scavenge reactive oxygen species (ROS). Materials and methods: We utilized the Vero cell line derived from African green monkey kidneys and exposed these cells to various concentrations of CDDP. Cell viability, apoptosis, ROS levels, and mitochondrial membrane potential were assessed. Results: CDDP significantly compromised Vero cell viability by elevating both cellular and mitochondrial ROS, which led to increased apoptosis. Pretreatment with the ROS scavenger N-acetyl-L-cysteine (NAC) effectively reduced CDDP-induced ROS accumulation and subsequent cell apoptosis. Furthermore, CDDP reduced Prx I and Prx II levels in a dose- and time-dependent manner. The inhibition of Prx I and II exacerbated cell death, implicating their role in CDDP-induced accumulation of cellular ROS. Additionally, CDDP enhanced the phosphorylation of MAPKs (p38, ERK, and JNK) without affecting AKT. The inhibition of these pathways significantly attenuated CDDP-induced apoptosis. Conclusion: The study highlights the involvement of Prx proteins in CDDP-induced nephrotoxicity and emphasizes the central role of ROS in cell death mediation. These insights offer promising avenues for developing clinical interventions to mitigate the nephrotoxic effects of CDDP.
MeSH term(s)	Animals ; Chlorocebus aethiops ; Cisplatin/pharmacology ; Reactive Oxygen Species/metabolism ; Peroxiredoxins/metabolism ; Signal Transduction ; Apoptosis ; Kidney/metabolism
Chemical Substances	Cisplatin (Q20Q21Q62J) ; Reactive Oxygen Species ; Peroxiredoxins (EC 1.11.1.15)
Language	English
Publishing date	2024-02-27
Publishing country	Greece
Document type	Journal Article
ZDB-ID	807031-3
ISSN	1791-7549 ; 0258-851X
ISSN (online)	1791-7549
ISSN	0258-851X
DOI	10.21873/invivo.13482
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Article: IL-17A and Th17 Cells Contribute to Endometrial Cell Survival by Inhibiting Apoptosis and NK Cell Mediated Cytotoxicity of Endometrial Cells via ERK1/2 Pathway.

Kang, Young-Ju / Cho, Hee Jun / Lee, Yunhee / Park, Arum / Kim, Mi Jeong / Jeung, In Cheul / Jung, Yong-Wook / Jung, Haiyoung / Choi, Inpyo / Lee, Hee Gu / Yoon, Suk Ran

Immune network

2023 Volume 23, Issue 2, Page(s) e14

Abstract: Immune status including the immune cells and cytokine profiles has been implicated in the development of endometriosis. In this study, we analyzed Th17 cells and IL-17A in peritoneal fluid (PF) and endometrial tissues of patients with (n=10) and without ( ...

Abstract	Immune status including the immune cells and cytokine profiles has been implicated in the development of endometriosis. In this study, we analyzed Th17 cells and IL-17A in peritoneal fluid (PF) and endometrial tissues of patients with (n=10) and without (n=26) endometriosis. Our study has shown increased Th17 cell population and IL-17A level in PF with endometriosis patients. To determine the roles of IL-17A and Th17 cells in the development of endometriosis, the effect of IL-17A, major cytokine of Th17, on endometrial cells isolated from endometriotic tissues was examined. Recombinant IL-17A promoted survival of endometrial cells accompanied by increased expression of anti-apoptotic genes, including Bcl-2 and MCL1, and the activation of ERK1/2 signaling. In addition, treatment of IL-17A to endometrial cells inhibited NK cell mediated cytotoxicity and induced HLA-G expression on endometrial cells. IL-17A also promoted migration of endometrial cells. Our data suggest that Th17 cells and IL-17A play critical roles in the development of endometriosis by promoting endometrial cell survival and conferring a resistance to NK cell cytotoxicity through the activation of ERK1/2 signaling. Targeting IL-17A has potential as a new strategy for the treatment of endometriosis.
Language	English
Publishing date	2023-01-30
Publishing country	Korea (South)
Document type	Journal Article
ZDB-ID	2536191-0
ISSN	2092-6685 ; 1598-2629
ISSN (online)	2092-6685
ISSN	1598-2629
DOI	10.4110/in.2023.23.e14
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Article ; Online: Peroxiredoxin II regulates exosome secretion from dermal mesenchymal stem cells through the ISGylation signaling pathway.

Han, Ying-Hao / Mao, Ying-Ying / Lee, Kyung Ho / Cho, Hee Jun / Yu, Nan-Nan / Xing, Xiao-Ya / Wang, Ai-Guo / Jin, Mei-Hua / Hong, Kwan Soo / Sun, Hu-Nan / Kwon, Taeho

Cell communication and signaling : CCS

2023 Volume 21, Issue 1, Page(s) 296

Abstract: Background: Exosomes are small extracellular vesicles that play important roles in intercellular communication and have potential therapeutic applications in regenerative medicine. Dermal mesenchymal stem cells (DMSCs) are a promising source of exosomes ...

Abstract	Background: Exosomes are small extracellular vesicles that play important roles in intercellular communication and have potential therapeutic applications in regenerative medicine. Dermal mesenchymal stem cells (DMSCs) are a promising source of exosomes due to their regenerative and immunomodulatory properties. However, the molecular mechanisms regulating exosome secretion from DMSCs are not fully understood. Results: In this study, the role of peroxiredoxin II (Prx II) in regulating exosome secretion from DMSCs and the underlying molecular mechanisms were investigated. It was discovered that depletion of Prx II led to a significant reduction in exosome secretion from DMSCs and an increase in the number of intracellular multivesicular bodies (MVBs), which serve as precursors of exosomes. Mechanistically, Prx II regulates the ISGylation switch that controls MVB degradation and impairs exosome secretion. Specifically, Prx II depletion decreased JNK activity, reduced the expression of the transcription inhibitor Foxo1, and promoted miR-221 expression. Increased miR-221 expression inhibited the STAT signaling pathway, thus downregulating the expression of ISGylation-related genes involved in MVB degradation. Together, these results identify Prx II as a critical regulator of exosome secretion from DMSCs through the ISGylation signaling pathway. Conclusions: Our findings provide important insights into the molecular mechanisms regulating exosome secretion from DMSCs and highlight the critical role of Prx II in controlling the ISGylation switch that regulates DMSC-exosome secretion. This study has significant implications for developing new therapeutic strategies in regenerative medicine. Video Abstract.
MeSH term(s)	Exosomes/metabolism ; Peroxiredoxins/metabolism ; Signal Transduction ; Mesenchymal Stem Cells/metabolism ; MicroRNAs/metabolism
Chemical Substances	Peroxiredoxins (EC 1.11.1.15) ; MicroRNAs
Language	English
Publishing date	2023-10-20
Publishing country	England
Document type	Video-Audio Media ; Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2126315-2
ISSN	1478-811X ; 1478-811X
ISSN (online)	1478-811X
ISSN	1478-811X
DOI	10.1186/s12964-023-01331-w
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Article ; Online: Regulation of Hematopoietic Stem Cell Fate and Malignancy.

Cho, Hee Jun / Lee, Jungwoon / Yoon, Suk Ran / Lee, Hee Gu / Jung, Haiyoung

International journal of molecular sciences

2020 Volume 21, Issue 13

Abstract: The regulation of hematopoietic stem cell (HSC) fate decision, whether they keep quiescence, self-renew, or differentiate into blood lineage cells, is critical for maintaining the immune system throughout one's lifetime. As HSCs are exposed to age- ... ...

Abstract	The regulation of hematopoietic stem cell (HSC) fate decision, whether they keep quiescence, self-renew, or differentiate into blood lineage cells, is critical for maintaining the immune system throughout one's lifetime. As HSCs are exposed to age-related stress, they gradually lose their self-renewal and regenerative capacity. Recently, many reports have implicated signaling pathways in the regulation of HSC fate determination and malignancies under aging stress or pathophysiological conditions. In this review, we focus on the current understanding of signaling pathways that regulate HSC fate including quiescence, self-renewal, and differentiation during aging, and additionally introduce pharmacological approaches to rescue defects of HSC fate determination or hematopoietic malignancies by kinase signaling pathways.
MeSH term(s)	Aging ; Animals ; Cell Differentiation ; Cell Self Renewal ; Hematologic Neoplasms/genetics ; Hematologic Neoplasms/metabolism ; Hematologic Neoplasms/pathology ; Hematopoietic Stem Cells/metabolism ; Humans ; Signal Transduction
Language	English
Publishing date	2020-07-06
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2019364-6
ISSN	1422-0067 ; 1422-0067 ; 1661-6596
ISSN (online)	1422-0067
ISSN	1422-0067 ; 1661-6596
DOI	10.3390/ijms21134780
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Article: Dysregulation of Rho GTPases in Human Cancers.

Jung, Haiyoung / Yoon, Suk Ran / Lim, Jeewon / Cho, Hee Jun / Lee, Hee Gu

Cancers

2020 Volume 12, Issue 5

Abstract: Rho GTPases play central roles in numerous cellular processes, including cell motility, cell polarity, and cell cycle progression, by regulating actin cytoskeletal dynamics and cell adhesion. Dysregulation of Rho GTPase signaling is observed in a broad ... ...

Abstract	Rho GTPases play central roles in numerous cellular processes, including cell motility, cell polarity, and cell cycle progression, by regulating actin cytoskeletal dynamics and cell adhesion. Dysregulation of Rho GTPase signaling is observed in a broad range of human cancers, and is associated with cancer development and malignant phenotypes, including metastasis and chemoresistance. Rho GTPase activity is precisely controlled by guanine nucleotide exchange factors, GTPase-activating proteins, and guanine nucleotide dissociation inhibitors. Recent evidence demonstrates that it is also regulated by post-translational modifications, such as phosphorylation, ubiquitination, and sumoylation. Here, we review the current knowledge on the role of Rho GTPases, and the precise mechanisms controlling their activity in the regulation of cancer progression. In addition, we discuss targeting strategies for the development of new drugs to improve cancer therapy.
Language	English
Publishing date	2020-05-07
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2527080-1
ISSN	2072-6694
ISSN	2072-6694
DOI	10.3390/cancers12051179
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Article ; Online: Regulation of Rho GTPases by RhoGDIs in Human Cancers.

Cho, Hee Jun / Kim, Jong-Tae / Baek, Kyoung Eun / Kim, Bo-Yeon / Lee, Hee Gu

Cells

2019 Volume 8, Issue 9

Abstract: Rho GDP dissociation inhibitors (RhoGDIs) play important roles in various cellular processes, including cell migration, adhesion, and proliferation, by regulating the functions of the Rho GTPase family. Dissociation of Rho GTPases from RhoGDIs is ... ...

Abstract	Rho GDP dissociation inhibitors (RhoGDIs) play important roles in various cellular processes, including cell migration, adhesion, and proliferation, by regulating the functions of the Rho GTPase family. Dissociation of Rho GTPases from RhoGDIs is necessary for their spatiotemporal activation and is dynamically regulated by several mechanisms, such as phosphorylation, sumoylation, and protein interaction. The expression of RhoGDIs has changed in many human cancers and become associated with the malignant phenotype, including migration, invasion, metastasis, and resistance to anticancer agents. Here, we review how RhoGDIs control the function of Rho GTPases by regulating their spatiotemporal activity and describe the regulatory mechanisms of the dissociation of Rho GTPases from RhoGDIs. We also discuss the role of RhoGDIs in cancer progression and their potential uses for therapeutic intervention.
MeSH term(s)	Humans ; Neoplasms/metabolism ; Protein Binding ; Protein Processing, Post-Translational ; rho GTP-Binding Proteins/metabolism ; rho-Specific Guanine Nucleotide Dissociation Inhibitors/metabolism
Chemical Substances	rho-Specific Guanine Nucleotide Dissociation Inhibitors ; rho GTP-Binding Proteins (EC 3.6.5.2)
Language	English
Publishing date	2019-09-05
Publishing country	Switzerland
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2661518-6
ISSN	2073-4409 ; 2073-4409
ISSN (online)	2073-4409
ISSN	2073-4409
DOI	10.3390/cells8091037
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Article: Ponciri Fructus Immaturus

Hwang, Yo Sep / Jang, Jun-Pil / Park, Seong-Hoon / Kim, Aeyung / Jang, Jae-Hyuk / Yoon, Hyang Ran / Yoon, Suk Ran / Park, Jun Hong / Cho, Hee Jun / Lee, Hee Gu

Frontiers in nutrition

2022 Volume 9, Page(s) 988309

Abstract: Sepsis is a systemic inflammatory disease to infections and results in tissue damage and multiple organ failure. ...

Abstract	Sepsis is a systemic inflammatory disease to infections and results in tissue damage and multiple organ failure.
Language	English
Publishing date	2022-09-15
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2776676-7
ISSN	2296-861X
ISSN	2296-861X
DOI	10.3389/fnut.2022.988309
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