• 제목/요약/키워드: cancer cell proliferation

검색결과 1,868건 처리시간 0.029초

Silencing of the COPS3 Gene by siRNA Reduces Proliferation of Lung Cancer Cells Most Likely via induction of Cell Cycle Arrest and Apoptosis

  • Wang, Xue-Mei;Cui, Jiu-Wei;Li, Wei;Cai, Lu;Song, Wei;Wang, Guan-Jun
    • Asian Pacific Journal of Cancer Prevention
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    • 제13권3호
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    • pp.1043-1048
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    • 2012
  • The COPS3 gene has stimulating effect on cell proliferation and progression of osteosarcomas and related cells. However, the features of COPS3 and its potential application as a therapeutic target in other cancers has not yet been studied. In this study, therefore, the effect of COPS3 silencing via COPS3 siRNA on lung cancer cell proliferation was examined. Expression levels of COPS3 gene in COPS3 siRNA infected cells and control siRNA infected cells were compared with real time PCR and Western blot analysis. Cell proliferation levels were comprehensively analyzed by MTT, BrdU incorporationy, and colony formation assays. For mechanistic assessment the effects of COPS3 silencing on cell cycle and apoptosis were analyzed using flow cytometry. Results showed that successful silencing of the COPS3 gene at both translational and transcriptional levels significantly reduced the proliferation and colony formation by lung cancer cells (p<0.01). Flow cytometry showed cell cycle arrest in the G0/G1 phase after COPS3 silencing, and more importantly, apoptosis was induced as a result of COPS3 knockdown, which negatively affected cell survival. Therefore, these results provide another piece of important evidence that the COPS3 gene expressed in lung cancer cells may play a critical role in stimulating proliferation. Down-regulation of COPS3 could significantly inhibit lung cancer cell growth, which was most likely mediated via induction of cell cycle arrest in G0/G1 phase and apoptosis.

셀러리악 추출물의 암세포 증식 억제 효과 (Inhibitory Effect of Celeriac Extract on Cancer Cell Proliferation)

  • 이재혁;박정숙
    • 한국융합학회논문지
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    • 제12권9호
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    • pp.179-183
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    • 2021
  • 본 연구는 다양한 항암성분을 함유한 Celeriac Extract의 암세포 증식에 미치는 영향을 살펴보기 위하여 실시되었다. 실험에 사용한 암 세포주는 5종으로 폐암세포 A549, 전립샘암세포 DU-145, 자궁암세포 HeLa, 유방암세포 MCF-7, 간암세포 SNU-182 로 모두 인체 유래 암 세포주를 사용하였으며 Celeriac Extract 10ug/mL, 100ug/mL, 1000ug/mL 에 대한 암세포의 증식 억제는 CCK-8 방법을 이용하여 측정하였다. 암세포 증식 억제를 살펴본 결과 Celeriac Extract 1000ug/mL는 폐암세포 A549, 전립샘암세포 DU-145, 자궁암세포 HeLa, 간암세포 SNU-182에서 유의한 증식 억제를 보였으며 농도 의존성을 나타냈다. 그러나 유방암세포 MCF-7 에서는 농도 의존적인 감소만 보였다. 결론적으로, 다양한 인간유래 암 세포주를 이용한 Celeriac Extract의 세포 증식 억제기전들은 암 예방효과 및 치료제 개발의 잠재력을 제공한다고 볼 수 있다.

Knockdown of a Proliferation-inducing Ligand (PRIL) Suppresses the Proliferation of Gastric Cancer Cells

  • Cui, Jiu-Wei;Li, Yan;Wang, Chang;Yao, Cheng;Li, Wei
    • Asian Pacific Journal of Cancer Prevention
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    • 제13권2호
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    • pp.633-636
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    • 2012
  • Purpose: PRIL (proliferation-inducing ligand) is a newly identified member of the tumor necrosis factor (TNF) family and modulates death ligand-induced apoptosis. Here, we investigated the effect of PRIL on cellular characteristics relating to tumor progression in human gastric cancer. Method: Recombinant lentivirus containing PRIL siRNA was constructed and then infected MGC803 and SGC7901 gastric cancer cells. MTT [3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide] colony formation and cell cycle analysis were used to study the effect of PRIL knockdown on gastric cancer cell proliferation. Results: PRIL expression in lentivirus infected cells was significantly reduced as evidenced by quantitative real-time PCR. Cell viability and colony formation of MGC803 and SGC7901 cells were significantly hampered in PRIL knock-down cells. Moreover, the cell cycle was arrested at G2/M phase, elucidating the mechanism underlying the inhibitory effect of siRNA on cell proliferation. Conclusions: Our study indicated that PRIL functions in promoting cell growth, and lentivirus-mediated PRIL gene knockdown might be a promising strategy in the treatment of gastric cancer.

GPR48 Promotes Multiple Cancer Cell Proliferation via Activation of Wnt Signaling

  • Zhu, Yong-Bin;Xu, Lin;Chen, Ming;Ma, Hai-Na;Lou, Fang
    • Asian Pacific Journal of Cancer Prevention
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    • 제14권8호
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    • pp.4775-4778
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    • 2013
  • The key signaling networks regulating cancer cell proliferation remain to be defined. The leucine-rich repeat containing G-protein coupled receptor 48 (GPR48) plays an important role in multiple organ development. In the present study, we investigated whether GPR48 functions in cancer cells using MCF-7, HepG2, NCI-N87 and PC-3 cells. We found that GPR48 overexpression promotes while its knockdown using small interfering RNA oligos inhibits cell proliferation. In addition, Wnt/${\beta}$-catenin signaling was activated in cells overexpressing GPR48. Therefore, our results indicated that GPR48 activates Wnt/${\beta}$-catenin signaling to regulate cancer cell proliferation.

도파민의 위암세포증식에서의 역할 (Roles of Dopamine in Proliferation of Gastric-Cancer Cells)

  • 정희준;박기호;채현동
    • Journal of Gastric Cancer
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    • 제6권3호
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    • pp.132-138
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    • 2006
  • 목적: 도파민은 중추신경전달물질이지만 위장관에서 도파민수용체와 결합하여 점막상피세포 증식, 상피세포의 보호, 위암 세포증식과 관련이 있는 것으로 알려져 있다. 본 연구에서는 위암에서 기원한 세포주를 이용하여 도파민과 각각의 도파민 수용체가 위암 세포 증식과 억제에 작용하는 역할에 대해 알아보았다. 대상 및 방법: 위암세포기원에서 각각 유래한 세포주인 SNU601과 KCU-C2를 이용하여 RNA 추출 후 RT-PCR 시행 후 도파민수용체 D1, D2L과 D2S 각각에 대한 primer로 PCR을 시행하여 수용체 유전자의 상대적인 발현정도를 측정하였다. 도파민과 Dl 수용체의 대항제인 SCH 23390과 D2 수용체 대항제인 raclopride를 사용하여 약물처리에 따른 위암세포주에서 세포 증식에 대한 분석을 하였다. 결과: KCU-C2 세포주에서 D1과 D2L과 D2S 유전자 mRNA의 상대적인 발현정도는 모두 높은 발현을 보였지만, SNU 601 세포주에는 mRNA의 발현이 모두 낮은 수준이었으며, 특히 D2L mRNA는 발현되고 있지 않았다. 약물처리에 따른 위암세포주에서 세포증식에 대한 분석에서는 D1과 D2S 수용체를 통한 도파민의 신호는 세포의 증식을 억제하였고 D2L 수용체를 통한 도파민의 신호는 세포의 증식을 유도하였다. 결론: 본 연구를 통해 도파민이 위암의 세포증식과 억제에 관여하며, 도파민의 이러한 효과는 도파민의 신호가 어느 수용체를 통해 전달되었느냐에 따라 위암세포의 증식과 억제가 이루어짐을 알 수 있었다.

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Embryonic Stem Cell-Preconditioned Microenvironment Effects on Epidermoid Carcinoma

  • Ryoo, Zae Young;Kim, Myoung Ok
    • Reproductive and Developmental Biology
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    • 제36권4호
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    • pp.275-281
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    • 2012
  • Embryonic stem cell-preconditioned microenvironment is important for cancer cells properitities by change cell morphology and proliferation. This microenvironment induces cancer cell reprogramming and results in a change in cancer cell properties such as differentiation and migration. The cancer microenvironment affects cancer cell proliferation and growth. However, the mechanism has not been clarified yet. Using the ES-preconditioned 3-D microenvironment model, we provide evidence showing that the ES microenvironment inhibits proliferation and reduces oncogenic gene expression. But ES microenvironment has no effect on telomerase activity, cell viability, cellular senescence, and methylation on Oct4 promoter region. Furthermore, methylation of Nanog was increase on ES-preconditioned microenvironment and supports results that no difference on RNA expression levels. Taken together, these results demonstrated that in the ES-preconditioned 3-D microenvironment is a crucial role for cancer cell proliferation not senescence.

Ginkgo biloba Leaf Extract Regulates Cell Proliferation and Gastric Cancer Cell Death

  • Kim, Da Hyun;Yang, Eun Ju;Lee, JinAh;Chang, Jeong Hyun
    • 대한의생명과학회지
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    • 제28권2호
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    • pp.92-100
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    • 2022
  • Ginkgo biloba Leaf Extract (GBE) is an extract from leaves of the Ginkgo biloba tree, widely used as a health supplement. GBE can inhibit the proliferation of several types of tumor cell. Although it is known to have anti-cancer effects in breast cancer and skin cancer, research related to gastric cancer is still insufficient. Based on results showing anti-cancer effects on solid cancer, we aimed to determine whether GBE has similar effects on gastric cancer. In this study, the anti-cancer effect of GBE in gastric adenocarcinoma was investigated by confirming the cell proliferation inhibitory effect of AGS cells. We also evaluated whether GBE regulates expression of the tumor suppressor protein p53 and Rb. GBE has apoptotic effects on AGS cells that were confirmed by changes in anti-apoptosis protein Bcl-2, Bcl-xl and pro-apoptosis protein Bax levels. Wound healing and cell migration were also decreased by treatment with GBE. Furthermore, we verified the effects of GBE on mitogenic signaling by investigating AKT target gene expression levels and revealed downregulated Sod2 and Bcl6 expression. We also confirmed that expression of inflammation-related genes decreased in a time-dependent manner. These results indicate that GBE has an anti-cancer effect on human gastric cancer cell lines. Further research on the mechanism of the anti-cancer effect will serve as basic data for possible anti-cancer drug development.

The effects of human milk proteins on the proliferation of normal, cancer and cancer stem like cells

  • Kang, Nam Mi;Cho, Ssang-Goo;Dayem, Ahmed Abdal;Lee, Joohyun;Bae, Seong Phil;Hahn, Won-Ho;Lee, Jeong-Sang
    • 분석과학
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    • 제31권6호
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    • pp.232-239
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    • 2018
  • Human breast milk (HBM) provides neonates with indispensable nutrition. The present study evaluated the anti-cancer activity of diluted and pasteurized early HBM (< 6 weeks' lactation) on human breast cancer cell lines. The cell lines MCF7 and MDA-MB231 were exposed to 1 % HBM from the 1st, 3rd, and 6th weeks of lactation and exhibited reduced proliferation rates. As controls, breast cell lines (293T and MCF-10A), breast cancer cell lines (MCF-7 and MDA-MB-231), and $CD133^{hi}CXCR4^{hi}ALDH1^{hi}$ patient-derived human cancer stem-like cells (KU-CSLCs) were treated with prominent milk proteins ${\beta}$-casein, ${\kappa}$-casein, and lactoferrin at varying doses (10, 50, and $100{\mu}g$) for 24 or 48 hrs. The impact of these proteins on cell proliferation was investigated. Breast cancer cell lines treated with ${\kappa}$-casein and lactoferrin exhibited significantly reduced viability, in both a dose- and time-dependent manner. Interestingly, ${\kappa}$-casein selectively impacted only cancer (but not normal breast) cell lines, particularly the more malignant cell line. However, ${\beta}$-casein-exposed human breast cancer cell lines exhibited a significantly higher proliferation rate. Thus, ${\kappa}$-casein and lactoferrin appear to exert selective anti-cancer activities. Further studies are warranted to determine the mechanisms underlying ${\kappa}$-casein- and lactoferrin-mediated cancer cell-selective cytotoxic effects.

브로콜리 추출물의 암세포 증식 억제에 미치는 효과 (Effect of Broccoli Extract on Inhibition of Cancer Cell Proliferation)

  • 박정숙
    • 디지털정책학회지
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    • 제2권1호
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    • pp.31-35
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    • 2023
  • 본 연구는 암세포 증식에 미치는 효과를 살펴보기 위하여 Broccoli Extract를 사용하였다. 실험에 사용한 세포주는 3종으로 호흡기계에 대표적인 폐암세포 A549와 소화기계의 간암세포 SNU-182, 담도암세포 SNU-1196 로 인체 유래 암세포 주를 사용하였으며, 암세포의 증식 억제는 세포의 증식정도를 측정하는 CCK-8 방법을 이용하여 측정하였다. Broccoli Extract 1000ug/mL, 100ug/mL, 10ug/mL 에 대한 암세포 증식 억제를 살펴본 결과 Broccoli Extract은 대부분의 암세포에서 농도 의존적으로 증식을 억제하였으며, 특히 폐암세포 A549, 간암세포 SNU-182는 Broccoli Extract 1000ug/mL에서 유의한 증식 억제를 보였다. 이러한 결과 브로콜리 추출물은 세포실험을 통해서 증명된 종양억제기전들이 암 예방 및 치료제로서 잠재력을 제공한다고 볼 수 있다.

Anthocyanins from the Fruit of Vitis Coignetiae Pulliat Inhibit TNF-Augmented Cancer Proliferation, Migration, and Invasion in A549 Cells

  • Lu, Jing Nan;Panchanathan, Radha;Lee, Won Sup;Kim, Hye Jung;Kim, Dong Hoon;Choi, Yung Hyun;Kim, GonSup;Shin, Sung Chul;Hong, Soon Chan
    • Asian Pacific Journal of Cancer Prevention
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    • 제18권11호
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    • pp.2919-2923
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    • 2017
  • Objective: Anthocyanins belong to a class of flavonoids, exhibiting antioxidant and anti-inflammatory actions have been reported to have anti-cancer effects. Here, we investigated whether anthocyanins can inhibit cancer cell proliferation, invasion, and angiogenesis in human lung cancer A549 cells, which are critically involved in cancer metastasis. Methods: We used anthocyanins from fruits of Vitis coignetiae Pulliat (AIMs) which has been used in Korean folk medicine for the treatment of inflammatory diseases and cancers. We have performed cell proliferation assays, cell invasion assay, gelatin zymography, wound healing assay and western blotting to examine whether anthocyanins can inhibit cancer cell proliferation, invasion, and angiogenesis in A549 cells. Result: AIMs did not inhibit cancer cell proliferation on A549 cells. Also, AIMs suppressed cancer migration, and invasion by supressing MMP-2 and MMP-9 expression. The Immuno-blotting results also revealed that AIMs suppressed the proteins involved in cancer proliferation (COX-2, C-myc, cyclin D1), migration and invasion (MMP-2, MMP-9), anti-apoptosis (XIAP, and c-IAP2), adhesion and angiogenesis (ICAM-1, VEGF). Conclusion: This study demonstrates that the anthocyanins isolated from fruits of Vitis coignetiae Pulliat inhibit cancer proliferation, cancer migration, and invasion that is involve in cancer-metastasis. This study provides evidence that AIMs might have anti-cancer effects on human lung cancer.