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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
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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: 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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Article ; Online: G protein-coupled estrogen receptor-1 agonist induces chemotherapeutic effect via ER stress signaling in gastric cancer.

Lee, Seon-Jin / Kim, Tae Woo / Park, Gyeong Lim / Hwang, Yo Sep / Cho, Hee Jun / Kim, Jong-Tae / Lee, Hee Gu

BMB reports

2019 Volume 52, Issue 11, Page(s) 647–652

Abstract: G protein-coupled estrogen receptor (GPER) is known to play an important role in hormone-associated cancers. G-1, a novel synthetic GPER agonist, has been reported to exhibit anti-carcinogenic properties. However, the chemotherapeutic mechanism of GPER ... ...

Abstract	G protein-coupled estrogen receptor (GPER) is known to play an important role in hormone-associated cancers. G-1, a novel synthetic GPER agonist, has been reported to exhibit anti-carcinogenic properties. However, the chemotherapeutic mechanism of GPER is yet unclear. Here, we evaluated GPER expression in human gastric cancer tissues and cells. We found that G-1 treatment attenuates GPER expression in gastric cancer. GPER expression increased G-1-induced antitumor effects in mouse xenograft model. We analyzed the effects of knockdown/overexpression of GPER on G-1-induced cell death in cancer cells. Increased GPER expression in human gastric cancer cells increased G-1-induced cell death via increased levels of cleaved caspase-3, -9, and cleaved poly ADP-ribose polymerase. Interestingly, during G-1-induced cell death, GPER mRNA and protein expression was attenuated and associated with ER stress-induced expression of PERK, ATF-4, GRP-78, and CHOP. Furthermore, PERK-dependent induction of ER stress activation increased G-1-induced cell death, whereas PERK silencing decreased cell death and increased drug sensitivity. Taken together, the data suggest that the induction of ER stress via GPER expression may increase G-1-induced cell death in gastric cancer cells. These results may contribute to a new paradigm shift in gastric cancer therapy. [BMB Reports 2019; 52(11): 647-652].
MeSH term(s)	Animals ; Breast Neoplasms/genetics ; Cell Line, Tumor ; Cell Proliferation/drug effects ; Cyclopentanes/metabolism ; Cyclopentanes/pharmacology ; Endoplasmic Reticulum Stress/physiology ; Estrogens/metabolism ; Female ; Gene Expression Regulation, Neoplastic/drug effects ; Humans ; MCF-7 Cells ; Mice ; Mice, Nude ; Quinolines/metabolism ; Quinolines/pharmacology ; Receptors, Estrogen/metabolism ; Receptors, G-Protein-Coupled/agonists ; Receptors, G-Protein-Coupled/metabolism ; Signal Transduction/drug effects ; Stomach Neoplasms/metabolism ; Tamoxifen/pharmacology ; Xenograft Model Antitumor Assays
Chemical Substances	1-(4-(6-bromobenzo(1,3)dioxol-5-yl)-3a,4,5,9b-tetrahydro-3H-cyclopenta(c)quinolin-8-yl)ethanone ; Cyclopentanes ; Estrogens ; GPER1 protein, human ; Quinolines ; Receptors, Estrogen ; Receptors, G-Protein-Coupled ; Tamoxifen (094ZI81Y45)
Language	English
Publishing date	2019-06-24
Publishing country	Korea (South)
Document type	News
ZDB-ID	2410389-5
ISSN	1976-670X ; 1976-6696
ISSN (online)	1976-670X
ISSN	1976-6696
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Article ; Online: KLK6/PAR1 Axis Promotes Tumor Growth and Metastasis by Regulating Cross-Talk between Tumor Cells and Macrophages.

Hwang, Yo Sep / Cho, Hee Jun / Park, Eun Sun / Lim, Jeewon / Yoon, Hyang Ran / Kim, Jong-Tae / Yoon, Suk Ran / Jung, Haiyoung / Choe, Yong-Kyung / Kim, Yong-Hoon / Lee, Chul-Ho / Kwon, Yong Tae / Kim, Bo Yeon / Lee, Hee Gu

Cells

2022 Volume 11, Issue 24

Abstract: Kallikrein-related peptidase (KLK)6 is associated with inflammatory diseases and neoplastic progression. KLK6 is aberrantly expressed in several solid tumors and regulates cancer development, metastatic progression, and drug resistance. However, the ... ...

Abstract	Kallikrein-related peptidase (KLK)6 is associated with inflammatory diseases and neoplastic progression. KLK6 is aberrantly expressed in several solid tumors and regulates cancer development, metastatic progression, and drug resistance. However, the function of KLK6 in the tumor microenvironment remains unclear. This study aimed to determine the role of KLK6 in the tumor microenvironment. Here, we uncovered the mechanism underlying KLK6-mediated cross-talk between cancer cells and macrophages. Compared with wild-type mice, KLK6-/- mice showed less tumor growth and metastasis in the B16F10 melanoma and Lewis lung carcinoma (LLC) xenograft model. Mechanistically, KLK6 promoted the secretion of tumor necrosis factor-alpha (TNF-α) from macrophages via the activation of protease-activated receptor-1 (PAR1) in an autocrine manner. TNF-α secreted from macrophages induced the release of the C-X-C motif chemokine ligand 1 (CXCL1) from melanoma and lung carcinoma cells in a paracrine manner. The introduction of recombinant KLK6 protein in KLK6-/- mice rescued the production of TNF-α and CXCL1, tumor growth, and metastasis. Inhibition of PAR1 activity suppressed these malignant phenotypes rescued by rKLK6 in vitro and in vivo. Our findings suggest that KLK6 functions as an important molecular link between macrophages and cancer cells during malignant progression, thereby providing opportunities for therapeutic intervention.
Language	English
Publishing date	2022-12-16
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2661518-6
ISSN	2073-4409 ; 2073-4409
ISSN (online)	2073-4409
ISSN	2073-4409
DOI	10.3390/cells11244101
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Article ; Online: Collapsin response mediator protein 4 enhances the radiosensitivity of colon cancer cells through calcium‑mediated cell signaling.

Park, Sang Yoon / Kim, Jong-Tae / Park, Eun Sun / Hwang, Yo Sep / Yoon, Hyang Ran / Baek, Kyoung Eun / Jung, Haiyoung / Yoon, Suk Ran / Kim, Bo Yeon / Cho, Hee Jun / Lee, Hee Gu

Oncology reports

2021 Volume 45, Issue 4

Abstract: Radiation therapy is an effective treatment against various types of cancer, but some radiation‑resistant cancer cells remain a major therapeutic obstacle; thus, understanding radiation resistance mechanisms is essential for cancer treatment. In this ... ...

Abstract	Radiation therapy is an effective treatment against various types of cancer, but some radiation‑resistant cancer cells remain a major therapeutic obstacle; thus, understanding radiation resistance mechanisms is essential for cancer treatment. In this study, we established radiation‑resistant colon cancer cell lines and examined the radiation‑induced genetic changes associated with radiation resistance. Using RNA‑sequencing analysis, collapsin response mediator protein 4 (<em>CRMP4</em>) was identified as the candidate gene associated with radiation sensitivity. When cells were exposed to radiation, intracellular Ca
MeSH term(s)	Calcium/metabolism ; Cell Death/radiation effects ; Cell Line, Tumor ; Colonic Neoplasms/genetics ; Colonic Neoplasms/metabolism ; Colonic Neoplasms/pathology ; Colonic Neoplasms/radiotherapy ; Humans ; Muscle Proteins/metabolism ; Muscle Proteins/radiation effects ; Radiation Tolerance ; Sequence Analysis, RNA ; Signal Transduction/radiation effects
Chemical Substances	DPYSL3 protein, human ; Muscle Proteins ; Calcium (SY7Q814VUP)
Language	English
Publishing date	2021-01-29
Publishing country	Greece
Document type	Journal Article
ZDB-ID	1222484-4
ISSN	1791-2431 ; 1021-335X
ISSN (online)	1791-2431
ISSN	1021-335X
DOI	10.3892/or.2021.7957
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Zs.A 4213: Show issues

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Article: Erastin Inhibits Septic Shock and Inflammatory Gene Expression via Suppression of the NF-κB Pathway.

Oh, Byung Moo / Lee, Seon-Jin / Park, Gyoung Lim / Hwang, Yo Sep / Lim, Jeewon / Park, Eun Sun / Lee, Kyung Ho / Kim, Bo Yeon / Kwon, Yong Tae / Cho, Hee Jun / Lee, Hee Gu

Journal of clinical medicine

2019 Volume 8, Issue 12

Abstract: Sepsis is a life-threatening condition that is caused by an abnormal immune response to infection and can lead to tissue damage, organ failure, and death. Erastin is a small molecule capable of initiating ferroptotic cell death in cancer cells. However, ... ...

Abstract	Sepsis is a life-threatening condition that is caused by an abnormal immune response to infection and can lead to tissue damage, organ failure, and death. Erastin is a small molecule capable of initiating ferroptotic cell death in cancer cells. However, the function of erastin in the inflammatory response during sepsis remains unknown. Here, we showed that erastin ameliorates septic shock induced by cecal ligation and puncture or lipopolysaccharides (LPS) in mice, which was associated with a reduced production of inflammatory mediators such as nitric oxide, tumor necrosis factor (TNF)-α, and interleukin (IL)-1β. Pretreatment with erastin in bone marrow-derived macrophages (BMDMs) significantly attenuated the expression of inducible nitric oxide synthase, cyclooxygenase-2, TNF-α, and IL-1β mRNA in response to LPS treatment. Furthermore, we also showed that erastin suppresses phosphorylation of IκB kinase β, phosphorylation and degradation of IκBα, and nuclear translocation of nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) in LPS-stimulated BMDMs. Our findings suggest that erastin attenuates the inflammatory response by suppressing the NF-κB signaling pathway, resulting in inhibition of sepsis development. This study provides new insights regarding the potential therapeutic properties of erastin in sepsis.
Language	English
Publishing date	2019-12-14
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2662592-1
ISSN	2077-0383
ISSN	2077-0383
DOI	10.3390/jcm8122210
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Article: DNA Replication and Sister Chromatid Cohesion 1 (DSCC1) of the Replication Factor Complex CTF18-RFC is Critical for Colon Cancer Cell Growth.

Kim, Jong-Tae / Cho, Hee Jun / Park, Sang Yoon / Oh, Byung Moo / Hwang, Yo Sep / Baek, Kyoung Eun / Lee, Young-Ha / Kim, Hee Cheol / Lee, Hee Gu

Journal of Cancer

2019 Volume 10, Issue 24, Page(s) 6142–6153

Abstract: DNA replication and sister chromatid cohesion 1 (DSCC1) combines with chromosome transmission-fidelity protein 18 (CTF18) to form a CTF18-DSCC1-CTF8 (CTF18-1-8) module, which in combination with CTF18-replication factor C (RFC) acts as a proliferating ... ...

Abstract	DNA replication and sister chromatid cohesion 1 (DSCC1) combines with chromosome transmission-fidelity protein 18 (CTF18) to form a CTF18-DSCC1-CTF8 (CTF18-1-8) module, which in combination with CTF18-replication factor C (RFC) acts as a proliferating cell nuclear antigen (PCNA) loader during DNA replication-associated processes. It was found that DSCC1 was overexpressed in tumor tissues from patients with colon cancer and that the survival probability of patients with colon cancer was lower when the expression of cytosolic DSCC1 was higher in tumor regions (P=0.047). By using DSCC1- or CTF18-knockdown cell lines (HCT116-shDSCC1 or HCT116-shCTF18, respectively), it was confirmed that DSCC1-knockdown inhibits cell proliferation and invasion, but that CTF18-knockdown does not. Tumors in mice xenografted with shDSCC1 cells were significantly smaller compared with those in mice in the mock group or those xenografted with shCTF18 cells. The shDSCC1 cells were highly sensitive to γ-irradiation and other DNA replication inhibitory treatments, resulting in low cell viability. The present results suggested that DSCC1 is the most important component in the CTF18-1-8 module for CTF18-RFC and is highly relevant to the growth and metastasis of colon cancer cells, and, therefore, it may be a potential therapeutic target for colon cancer treatment.
Language	English
Publishing date	2019-10-15
Publishing country	Australia
Document type	Journal Article
ZDB-ID	2573318-7
ISSN	1837-9664
ISSN	1837-9664
DOI	10.7150/jca.32339
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Article ; Online: Efficient Interleukin-21 Production by Optimization of Codon and Signal Peptide in Chinese Hamster Ovarian Cells.

Cho, Hee Jun / Oh, Byung Moo / Kim, Jong-Tae / Lim, Jeewon / Park, Sang Yoon / Hwang, Yo Sep / Baek, Kyoung Eun / Kim, Bo-Yeon / Choi, Inpyo / Lee, Hee Gu

Journal of microbiology and biotechnology

2018 Volume 29, Issue 2, Page(s) 304–310

Abstract: Interleukin-21 is a common γ-chain cytokine that controls the immune responses of B cells, T cells, and natural killer cells. Targeting IL-21 to strengthen the immune system is promising for the development of vaccines as well as anti-infection and anti- ... ...

Abstract	Interleukin-21 is a common γ-chain cytokine that controls the immune responses of B cells, T cells, and natural killer cells. Targeting IL-21 to strengthen the immune system is promising for the development of vaccines as well as anti-infection and anti-tumor therapies. However, the practical application of IL-21 is limited by the high production cost. In this study, we improved IL-21 production by codon optimization and selection of appropriate signal peptide in CHO-K1 cells. Codon-optimized or non-optimized human IL-21 was stably transfected into CHO-K1 cells. IL-21 expression was 10-fold higher for codon-optimized than non-optimized IL-21. We fused five different signal peptides to codon-optimized mature IL-21 and evaluated their effect on IL-21 production. The best result (a 3-fold increase) was obtained using a signal peptide derived from human azurocidin. Furthermore, codon-optimized IL-21 containing the azurocidin signal peptide promoted IFN-γ secretion and STAT3 phosphorylation in NK-92 cells similar to codon-optimized IL-21 containing original signal peptide. Collectively, these results indicate that codon optimization and azurocidin signal peptides provide an efficient approach for the high-level production of IL-21 as a biopharmaceutical.
MeSH term(s)	Animals ; Biosimilar Pharmaceuticals ; CHO Cells ; Codon/genetics ; Cricetulus ; Genetic Vectors ; Humans ; Interferon-gamma/metabolism ; Interleukins/biosynthesis ; Interleukins/genetics ; Interleukins/metabolism ; Phosphorylation ; Protein Engineering ; Protein Sorting Signals/genetics ; Recombinant Proteins/biosynthesis ; Recombinant Proteins/genetics ; STAT3 Transcription Factor/metabolism ; Transfection
Chemical Substances	Biosimilar Pharmaceuticals ; Codon ; Interleukins ; Protein Sorting Signals ; Recombinant Proteins ; STAT3 Transcription Factor ; STAT3 protein, human ; Interferon-gamma (82115-62-6) ; interleukin-21 (MKM3CA6LT1)
Language	English
Publishing date	2018-12-10
Publishing country	Korea (South)
Document type	Journal Article
ISSN	1738-8872
ISSN (online)	1738-8872
DOI	10.4014/jmb.1811.11042
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