• 제목/요약/키워드: cell growth, motility

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Conjugated Linoleic Acid (CLA)가 인체 대장암 세포주에서 Matrix Metalloproteinase (MMP) 활성과 세포이동성에 미치는 영향 (Effects of Conjugated Linoleic Acid (CLA) on Matrix Metalloproteinase (MMP) Activity and Cell Motility in Human Colon Cancer Cell Lines)

  • 설소미;방명희;최옥숙;윤정한;김우경
    • Journal of Nutrition and Health
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    • 제36권3호
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    • pp.280-286
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    • 2003
  • Conjugated linoleic acid (CLA) consists of several geometric isomers of linoleic acid. CLA is found in foods derived from ruminants and exhibits strong anticarcinogenic effects in a variety of animal models. Matrix metalloproteinases (MMPs) play a key role in cancer progression. Specifically, MMP-2 and -9, which hydrolyze the basal membrane type IV collagen, are involved in the initial breakdown of collagen and basement membrane components during tumor growth and invasion. However, the effects of CLA on cancer cell motility and MMP expression and activity are not currently well known. Therefore, the present study examined whether CLA reduces the activity of MMP and cell motility in SW480 and SW620 cells, the human colon cancer cell lines. Gelatin zymography and Western blot analysis revealed that phorbol 12-myristate 13-acetate (PMA) induced the activity and protein expression of Mr 92,000 MMP-9 in both cell lines. To examine whether CLA inhibits the MMP activity, cells were incubated with 100 ngfmL PMA in the presence of various concentrations of CLA. PMA-induced MMP-9 activity was decreased by 20 $\mu$ M CLA in SW480 cells, and by 10 $\mu$ M and 20 $\mu$ M CLA in SW620 cells. Results from the Hoyden chamber assay showed that cell motility was increased by PMA and that PMA-induced cell motility was significantly decreased by 20 $\mu$ M CLA in SW480 cells. These results indicate that CLA may reduce the motility and MMP activity in human colon cancer cells.

INVOLVEMENT OF PHOSPHATIDYLINOSITOL 3-KINASE (PI3K) PATHWAY IN H-RAS-INDUCED INVASION AND MOTILITY OF HUMAN BREAST EPITHELIAL CELLS

  • Shin, Il-Chung;Aree Moon
    • 한국독성학회:학술대회논문집
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    • 한국독성학회 2002년도 Molecular and Cellular Response to Toxic Substances
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    • pp.142-142
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    • 2002
  • Many studies have identified the phosphatidylinositol 3-kinase (PI3K) as a key regulator for various cellular functions including cell survival, growth and motility. We have previously shown that H-ras, but not N-ras, induces invasiveness and motility in human breast epithelial cells (MCF10A), while both H-ras and N-ras induce transformed phenotype.(omitted)

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Roles of Phosphatidylinositol 3-Kinase(PI3K) and Rac1

  • Shin, Il-Chung;Kim, Seon-Hoe;Moon, A-Ree
    • 대한약학회:학술대회논문집
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    • 대한약학회 2003년도 Proceedings of the Convention of the Pharmaceutical Society of Korea Vol.1
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    • pp.223.1-223.1
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    • 2003
  • Many studies have identified the phosphatidylinositol 3-kinase (PI3K) as a key regulator for various cellular functions including cell survival, growth and motility. We have previously shown that H-ras, but not N-ras. induces invasiveness and motility in human breast epithelial cells (MCF10A), while both H-ras and N-ras induce transformed phenotype. In the present study, we wished to investigate the functional role of PI3K pathway in H-ra-induced invasive phenotype and motility of MCF10A cells. (omitted)

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C-FLIP Promotes the Motility of Cancer Cells by Activating FAK and ERK, and Increasing MMP-9 Expression

  • Park, Deokbum;Shim, Eunsook;Kim, Youngmi;Kim, Young Myeong;Lee, Hansoo;Choe, Jongseon;Kang, Dongmin;Lee, Yun-Sil;Jeoung, Dooil
    • Molecules and Cells
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    • 제25권2호
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    • pp.184-195
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    • 2008
  • We examined the role of c-FLIP in the motility of HeLa cells. A small interfering RNA (siRNA) directed against c-FLIP inhibited the adhesion and motility of the cells without affecting their growth rate. The long form of c-FLIP ($c-FLIP_L$), but not the short form ($c-FLIP_S$), enhanced adhesion and motility. Downregulation of $c-FLIP_L$ with siRNA decreased phosphorylation of FAK and ERK, while overexpression of $c-FLIP_L$ increased their phosphorylation. Overexpression of FAK activated ERK, and enhanced the motility of HeLa cells. FRNK, an inhibitory fragment of FAK, inhibited ERK and decreased motility. Inhibition of ERK also significantly suppressed $c-FLIP_L$-promoted motility. Inhibition of ROCK by Y27632 suppressed the $c-FLIP_L$-promoted motility by reducing phosphorylation of FAK and ERK. Overexpression of $c-FLIP_L$ increased the expression and secretion of MMP-9, and inhibition of MMP-9 by Ilomastat reduced $c-FLIP_L$- promoted cell motility. A caspase-like domain (amino acids 222-376) was found to be necessary for the $c-FLIP_L$-promoted cell motility. We conclude that $c-FLIP_L$ promotes the motility of HeLa cells by activating FAK and ERK, and increasing MMP-9 expression.

Effects of miR-152 on Cell Growth Inhibition, Motility Suppression and Apoptosis Induction in Hepatocellular Carcinoma Cells

  • Dang, Yi-Wu;Zeng, Jing;He, Rong-Quan;Rong, Min-Hua;Luo, Dian-Zhong;Chen, Gang
    • Asian Pacific Journal of Cancer Prevention
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    • 제15권12호
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    • pp.4969-4976
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    • 2014
  • Background: miR-152 is involved in the genesis and development of several malignancies. However, its role in HCC has not been fully clarified. The aim of this study was to investigate the clinicopathological significance of miR-152 and its effect on the malignant phenotype of HCC cells. Methods: miR-152 expression was detected using real-time quantitative RT-PCR in 89 pairs of HCC formalin-fixed paraffin-embedded and their adjacent tissues. Functionally, in vitro effects and mechanisms of action of miR-152 on proliferation, viability, caspase activity, apoptosis and motility were explored in HepG2, HepB3 and SNU449 cells, as assessed by spectrophotometry, fluorimetry, fluorescence microscopy, wound-healing and Western blotting, respectively. Results: miR-152 expression in HCC was downregulated remarkably compared to that in adjacent hepatic tissues. miR-152 levels in groups of advanced clinical stage, larger tumor size and positive HBV infection, were significantly lower than in other groups. A miR-152 mimic could suppress cell growth, inhibit cell motility and increase caspase activity and apoptosis in HCC cell lines. Furthermore, Western blotting showed that the miR-152 mimic downregulated Wnt-1, DNMT1, ERK1/2, AKT and TNFRS6B signaling. Intriguingly, inverse correlation of TNFRF6B and miR-152 expression was found in HCC and bioinformatics confirmed that TNFRF6B might be a target of miR-152. Conclusions: Underexpression of miR-152 plays a vital role in hepatocarcinogenesis and lack of miR-152 is related to the progression of HCC through deregulation of cell proliferation, motility and apoptosis. miR-152 may act as a tumor suppressor miRNA by also targeting TNFRSF6B and is therefore a potential candidate biomarker for HCC diagnosis, prognosis and molecular therapy.

Anthocyanin계 성분인 Cyanidin이 인체 유방암세포 MDA-MB-231의 이동성과 침윤성에 미치는 영향 (Effect of Cyanidin on Cell Motility and Invasion in MDA-MB-231 Human Breast Cancer Cells)

  • 추수경;서은영;김우경;강남이
    • Journal of Nutrition and Health
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    • 제41권8호
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    • pp.711-717
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    • 2008
  • 본 연구는 식물의 대표적인 색소 성분인 anthocyanin계 색소 중 cyanidin이 인체 유방암 세포 MDA-MB-231에서 세포의 이동성과 침윤성에 미치는 영향을 알아보고자 실시 되었다. 실험 결과 cyanidin의 첨가량이 증가할수록 세포의 운동성, 이동성, 침윤성이 유의적으로 억제되었다. 그러나 ECM 분해 시 암세포에서 분비되는 단백질 분해 효소인 MMP-2, MMP-9의 활성과 MMP-9의 mRNA 수준은 cyanidin에 의해 영향 받지 않는 것으로 관찰되었다. 결론적으로, cyanidin은 세포 증식에 영향을 미치지 않는 범위 내에서 암세포의 전이과정 중 이동성과 침윤성을 억제할 수 있다는 가능성이 관찰되었으나, MMPs 활성에는 영향을 미치지 않는 것으로 보아 MMPs 이외의 경로를 통해 전이 과정이 이루어지는 것으로 사료된다.

Loss of βPix Causes Defects in Early Embryonic Development, and Cell Spreading and Platelet-Derived Growth Factor-Induced Chemotaxis in Mouse Embryonic Fibroblasts

  • Kang, TaeIn;Lee, Seung Joon;Kwon, Younghee;Park, Dongeun
    • Molecules and Cells
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    • 제42권8호
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    • pp.589-596
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    • 2019
  • ${\beta}Pix$ is a guanine nucleotide exchange factor for the Rho family small GTPases, Rac1 and Cdc42. It is known to regulate focal adhesion dynamics and cell migration. However, the in vivo role of ${\beta}Pix$ is currently not well understood. Here, we report the production and characterization of ${\beta}Pix$-KO mice. Loss of ${\beta}Pix$ results in embryonic lethality accompanied by abnormal developmental features, such as incomplete neural tube closure, impaired axial rotation, and failure of allantois-chorion fusion. We also generated ${\beta}Pix$-KO mouse embryonic fibroblasts (MEFs) to examine ${\beta}Pix$ function in mouse fibroblasts. ${\beta}Pix$-KO MEFs exhibit decreased Rac1 activity, and defects in cell spreading and platelet-derived growth factor (PDGF)-induced ruffle formation and chemotaxis. The average size of focal adhesions is increased in ${\beta}Pix$-KO MEFs. Interestingly, ${\beta}Pix$-KO MEFs showed increased motility in random migration and rapid wound healing with elevated levels of MLC2 phosphorylation. Taken together, our data demonstrate that ${\beta}Pix$ plays essential roles in early embryonic development, cell spreading, and cell migration in fibroblasts.

Cell Proliferation and Motility Are Inhibited by G1 Phase Arrest in 15-kDa Selenoprotein-Deficient Chang Liver Cells

  • Bang, Jeyoung;Huh, Jang Hoe;Na, Ji-Woon;Lu, Qiao;Carlson, Bradley A.;Tobe, Ryuta;Tsuji, Petra A.;Gladyshev, Vadim N.;Hatfield, Dolph L.;Lee, Byeong Jae
    • Molecules and Cells
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    • 제38권5호
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    • pp.457-465
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    • 2015
  • The 15-kDa selenoprotein (Sep15) is a selenoprotein residing in the lumen of the endoplasmic reticulum (ER) and implicated in quality control of protein folding. Herein, we established an inducible RNAi cell line that targets Sep15 mRNA in Chang liver cells. RNAi-induced Sep15 deficiency led to inhibition of cell proliferation, whereas cell growth was resumed after removal of the knockdown inducer. Sep15-deficient cells were arrested at the G1 phase by upregulating p21 and p27, and these cells were also characterized by ER stress. In addition, Sep15 deficiency led to the relocation of focal adhesions to the periphery of the cell basement and to the decrease of the migratory and invasive ability. All these changes were reversible depending on Sep15 status. Rescuing the knockdown state by expressing a silent mutant Sep15 mRNA that is resistant to siRNA also reversed the phenotypic changes. Our results suggest that SEP15 plays important roles in the regulation of the G1 phase during the cell cycle as well as in cell motility in Chang liver cells, and that this selenoprotein offers a novel functional link between the cell cycle and cell motility.

폐섬유자원의 발효공학적 이용에 관한 연구 (제8보) 섬유소자화세균의 혼합배양 (Studies on the Fermentative Utilization of Cellulosic Wastes (Part 8) Mixed Culture of Cellulose Assimilating Bacteria)

  • 윤한대;성낙계
    • 한국미생물·생명공학회지
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    • 제6권2호
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    • pp.51-57
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    • 1978
  • 섬유소 자화세균의 분리 및 이용과정에서 혼합배양하므로써 균체증식이 향상 되었는데, 이러한 혼합배양에 따른 여러 가지 영향과 보조균을 동정한 결과를 요약하면 다음과 같다. 1) Cellulomona flavigena의 단독배양에서는 O.D.가 0.26이였으나, 보조균과 혼합배양하므로써 O.D.가 0.37로 증가하였다. 2) 보조균은 gliding motility가 있었으며, microcyst가 확인되었는데 이것은 Sporocytophga 속과 일치하였다. 3) 혼합배양에서 생육최적 pH는 7.2 부근이 좋았으며, 최적온도는 3$0^{\circ}C$ 부근이었다. 4) 혼합배양에 있어서 두 균의 분포도는 10 : 1 정도로 Cellulomonas flavigena가 주로 분포되어 있었다. 5) Cellulomonas flavigena의 growth factor로서 thiamine과 biotin을 요구하였으며, Sporocytophaga sp.는 vitamin 요구성이 없었다. 6) Cellulomonas flavigena의 단독배양액에서는 추적할 만한 glucose 량이 없었으나, 혼합배양에서는 glucose가 확인되었다. 7) Cellulomonas flavigena의 균체중 필수아미노산으로 valine, leucine, arginime이 비교적 많은 편이였다

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The Synergistic Anticancer Effect of Artesunate Combined with Allicin in Osteosarcoma Cell Line in Vitro and in Vivo

  • Jiang, Wei;Huang, Yong;Wang, Jing-Peng;Yu, Xiao-Yun;Zhang, Lin-Yi
    • Asian Pacific Journal of Cancer Prevention
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    • 제14권8호
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    • pp.4615-4619
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    • 2013
  • Background: Artesunate, extracted from Artemisia annua, has been proven to have anti-cancer potential. Allicin, diallyl thiosulfinate, the main biologically active compound derived from garlic, is also of interest in cancer treatment research. This object of this report was to document synergistic effects of artesunate combined with allicin on osteosarcoma cell lines in vitro and in vivo. Methods: After treatment with artesunate and allicin at various concentrations, the viability of osteosarcoma cells was analyzed by MTT method, with assessment of invasion and motility, colony formation and apoptosis. Western Blotting was performed to determine the expression of caspase-3/9, and activity was also detected after drug treatment. Moreover, in a nude mouse model established with orthotopic xenograft tumors, tumor weight and volume were monitored after drug administration via the intraperitoneal (i.p.) route. Results: The viability of osteosarcoma cells in the combination group was significantly decreased in a concentration and time dependent manner; moreover, invasion, motility and colony formation ability were significantly suppressed and the apoptotic rate was significantly increased through caspase-3/9 expression and activity enhancement in the combination group. Furthermore, suppression of tumor growth was evident in vivo. Conclusion: Our results indicated that artesunate and allicin in combination exert synergistic effects on osteosarcoma cell proliferation and apoptosis.