• 제목/요약/키워드: cancer cell proliferation

검색결과 1,864건 처리시간 0.036초

탁리익기탕(托裏益氣湯)이 항암(抗癌) 및 면역기능(免疫機能)에 미치는 작용(作用) 연구(硏究) (Study of Takliikgi-tang on the Anti-Cancer Action in Mice)

  • 박수연;김종한;최정화;문웅아
    • 한방안이비인후피부과학회지
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    • 제19권1호
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    • pp.31-42
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    • 2006
  • Objective : This Study was to investigate effects of Takliikgi-tang on the anti-cancer and proliferation of immunocytes, nitric oxide (NO) production of peritoneal macrophages. Methods : We used Takliikgi-tang extract (TLT) with freeze-dried, 8weeks-old male mice and cancer cell lines (L1210, Sarcoma-180) for this Study. The cytotoxicity and proliferation of cells were tested using a colorimetric tetrazoliun assay (MTT assay). Results : 1. TLT was significantly showed cytotoxicity on the L1210, 5-180 cell lines. 2. TLT was significantly increased proliferation of thymocytes in vitro. 3. TLT was significantly increased proliferation of thymocytes and splenocytes in normal mice. 4. TLT was significantly increased NO production from peritoneal macrophages in normal mice. 5. TLT was significantly decreased proliferation of L1210 cells in L1210 cells transplanted mice. 6. TLT was significantly increased proliferation of thymocytes and splenocytes by all-dosage in L1210 cells transplanted mice. 7. TLT was significantly increased NO production from peritoneal macrophages in L1210 cells transplanted mice. Conclusions : The present author thought that TLT had action of anti-cancer by becoming immunocytes activity (NO production, proliferation of thymocytes).

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Inhibition of Gastric Cancer Cell Cycle Progression by ${\gamma}$ -Tubulin Antisense Oligonucleotides

  • Hwang, Sun-Hee;Kim, Myung-Won;Park, Sang-Kyu;Noh, Jung-Woo;Han, In-Seob
    • Journal of Microbiology and Biotechnology
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    • 제11권5호
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    • pp.876-879
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    • 2001
  • ${\gamma}$ -Tubulin is an essential component involved in microtubule nucleation. The present work examined whether the fast proliferation of cancer cells can be retarded by the depletion of ${\gamma}$ -tubulin expression. Two different gastric cancer cell lines and one control cell line were treated with antisence oligonucleotides complementary to the messenger RNA of ${\gamma}$ -tubulin. The$[^3H]$ -thymidine incorporation in the two gastric cancer cell lines, SNU-1 and SNU-216, was dramatically reducd by treatment with the ${\gamma}$ -tubulin antisense oligonucleotides in a dosage-dependent manner. In contrast, the control cell line, NIH/3T3, showed no significant effect from the antisense oligonucleotides even at a high concentration. The ablation of ${\gamma}$ -tubulin expression in the tumor cells resulted in an altered DNA synthesis during mitosis and it decreased the cell progression. Accordingly, the use of antisense oligonucleotides may be an effective way of inhibiting the proliferation of human gastric cancers.

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Imidazole Antifungal Drugs Inhibit the Cell Proliferation and Invasion of Human Breast Cancer Cells

  • Bae, Sung Hun;Park, Ju Ho;Choi, Hyeon Gyeom;Kim, Hyesook;Kim, So Hee
    • Biomolecules & Therapeutics
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    • 제26권5호
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    • pp.494-502
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    • 2018
  • Breast cancer is currently the most prevalent cancer in women, and its incidence increases every year. Azole antifungal drugs were recently found to have antitumor efficacy in several cancer types. They contain an imidazole (clotrimazole and ketoconazole) or a triazole (fluconazole and itraconazole) ring. Using human breast adenocarcinoma cells (MCF-7 and MDA-MB-231), we evaluated the effects of azole drugs on cell proliferation, apoptosis, cell cycle, migration, and invasion, and investigated the underlying mechanisms. Clotrimazole and ketoconazole inhibited the proliferation of both cell lines while fluconazole and itraconazole did not. In addition, clotrimazole and ketoconazole inhibited the motility of MDA-MB-231 cells and induced $G_1$-phase arrest in MCF-7 and MDA-MB-231 cells, as determined by cell cycle analysis and immunoblot data. Moreover, Transwell invasion and gelatin zymography assays revealed that clotrimazole and ketoconazole suppressed invasiveness through the inhibition of matrix metalloproteinase 9 in MDA-MB-231 cells, although no significant changes in invasiveness were observed in MCF-7 cells. There were no significant changes in any of the observed parameters with fluconazole or itraconazole treatment in either breast cancer cell line. Taken together, imidazole antifungal drugs showed strong antitumor activity in breast cancer cells through induction of apoptosis and $G_1$ arrest in both MCF-7 and MDA-MB-231 cells and suppression of invasiveness via matrix metalloproteinase 9 inhibition in MDA-MB-231 cells. Imidazole drugs have well-established pharmacokinetic profiles and known toxicity, which can make these generic drugs strong candidates for repositioning as antitumor therapies.

Snail Promotes Cancer Cell Proliferation via Its Interaction with the BIRC3

  • Rho, Seung Bae;Byun, Hyun-Jung;Kim, Boh-Ram;Lee, Chang Hoon
    • Biomolecules & Therapeutics
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    • 제30권4호
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    • pp.380-388
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    • 2022
  • Snail is implicated in tumour growth and metastasis and is up-regulated in various human tumours. Although the role of Snails in epithelial-mesenchymal transition, which is particularly important in cancer metastasis, is well known, how they regulate tumour growth is poorly described. In this study, the possible molecular mechanisms of Snail in tumour growth were explored. Baculoviral inhibitor of apoptosis protein (IAP) repeat-containing protein 3 (BIRC3), a co-activator of cell proliferation during tumourigenesis, was identified as a Snail-binding protein via a yeast two-hybrid system. Since BIRC3 is important for cell survival, the effect of BIRC3 binding partner Snail on cell survival was investigated in ovarian cancer cell lines. Results revealed that Bax expression was activated, while the expression levels of anti-apoptotic proteins were markedly decreased by small interfering RNA (siRNA) specific for Snail (siSnail). siSnail, the binding partner of siBIRC3, activated the tumour suppressor function of p53 by promoting p53 protein stability. Conversely, BIRC3 could interact with Snail, for this reason, the possibility of BIRC3 involvement in EMT was investigated. BIRC3 overexpression resulted in a decreased expression of the epithelial marker and an increased expression of the mesenchymal markers. siSnail or siBIRC3 reduced the mRNA levels of matrix metalloproteinase (MMP)-2 and MMP-9. These results provide evidence that Snail promotes cell proliferation by interacting with BIRC3 and that BIRC3 might be involved in EMT via binding to Snail in ovarian cancer cells. Therefore, our results suggested the novel relevance of BIRC3, the binding partner of Snail, in ovarian cancer development.

암세포주에 대한 유근피 n-BuOH 분획과 항암제의 병용효과 (The Combined Effects of n-BuOH Fraction of Ulmi Cortex and Anticancer Drugs on Cancer Cell Lines)

  • 은재순;송원영
    • 생약학회지
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    • 제25권2호
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    • pp.144-152
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    • 1994
  • The combined effects of Ulmi Cortex and some anti-cancer drugs on the proliferation of HeLa cells, Hep G2 cells and S 180 cells were estimated by MTT calorimetric assay. The n-BuOH fraction(UBF) of Ulmi Cortex inhibited the proliferation of HeLa cell at $10^{-3}\;g/ml$, Hep G2 cell at $10^{-5}\;g/ml$ and S 180 cell at $10^{-3}\;g/ml$. The inhibitory effects of mitomycin C(MMC), cisplatin(CPT) and 5-fluorouracil (5-FU), respectively, on Hep G2 cell was increased by the UBF. The UBF did not influence the proliferation of Balb/c 3T3 cells at concentrations of $10^{-6}$ to $10^{-4}\;g/ml$, but increased the proliferation of T cells at concentrations of $10^{-5}$ to $10^{-4}\;g/ml$. The UBF did not influence the number of leukocyte, and on the thymus weight of mice. The UBF increased the number of total-peritoreal cells of mice. In conclusion, the results suggest that the UBF have anti-cancer activity without the side effect, such as leukopenia and immunosuppresion, and increase the inhibitory activity of the anti-cancer drugs on Hep G2 cells.

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Atractylochromene Is a Repressor of Wnt/β-Catenin Signaling in Colon Cancer Cells

  • Shim, Ah-Ram;Dong, Guang-Zhi;Lee, Hwa Jin;Ryu, Jae-Ha
    • Biomolecules & Therapeutics
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    • 제23권1호
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    • pp.26-30
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    • 2015
  • Wnt/${\beta}$-catenin signaling pathway was mutated in about 90% of the sporadic and hereditary colorectal cancers. The abnormally activated ${\beta}$-catenin increases the cancer cell proliferation, differentiation and metastasis through increasing the expression of its oncogenic target genes. In this study, we identified an inhibitor of ${\beta}$-catenin dependent Wnt pathway from rhizomes of Atractylodes macrocephala Koidzumi (Compositae). The active compound was purified by activity-guided purification and the structure was identified as 2,8-dimethyl-6-hydroxy-2-(4-methyl-3-pentenyl)-2H-chromene (atractylochromene, AC). AC suppressed b-catenin/Tcell factor transcriptional activity of HEK-293 reporter cells when they were stimulated by Wnt3a or inhibitor of glycogen synthase kinase-$3{\beta}$. AC down-regulated the nuclear level of ${\beta}$-catenin through the suppression of galectin-3 mediated nuclear translocation of ${\beta}$-catenin in SW-480 colon cancer cells. Furthermore, AC inhibits proliferation of colon cancer cell. Taken together, AC from A. macrocephala might be a potential chemotherapeutic agent for the prevention and treatment of human colon cancer.

Hsa-miR-181a-5p Expression and Effects on Cell Proliferation in Gastric Cancer

  • Chen, Gang;Shen, Zhi-Li;Wang, Ling;Lv, Chun-Ye;Huang, Xin-En;Zhou, Rong-Ping
    • Asian Pacific Journal of Cancer Prevention
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    • 제14권6호
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    • pp.3871-3875
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    • 2013
  • Purpose: MicroRNAs (miRNAs) are small endogenous, non-coding, single-stranded RNAs (approximately 22 nt). Accumulating evidence has shown that aberrant miRNA expression is pronounced and correlated with gastric cancer genesis and progression. Materials and Methods: Expression levels of miR-181a-5p in GC tissues and cell lines were assessed by qRT-PCR and tested for correlation with clinical features. In addition, effects of miR-181a-5p on GC cell growth were investigated. Results: Our findings indicate that miR-181a-5p is upregulated in GC, in correlation with lymph node invasion, nerve invasion and vascular invasion (P<0.05). Enforced expression of miR-181a -5p promoted cell proliferation ability. Conclusions: This study suggested that increased miR-181a-5p is related to GC progression. MiR-181a-5p may represent a potential therapeutic target for GC.

권삼(拳蔘)의 항암효과에 대한 연구 (Studies of the Anti-cancer Effects of Bistortae Rhizoma)

  • 김준범;한효상;이영종
    • 동의생리병리학회지
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    • 제23권5호
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    • pp.1139-1144
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    • 2009
  • This study was purposed to research the anti-cancer effects of Bistortae Rhizoma. A total extract of Bistortae Rhizoma decoction was prepared. By measuring the cell proliferation, apoptosis, morphology and cytokine level from the extracts, the influence on HepG2 cell, SNU-1 cell and A549 cell was compared. The Bistortae Rhizoma decoction extract did not control HepG2 cell proliferation but controlled SNU-1 cell and A549 cell proliferation. In particular, the inhibitory effect on SNU-1 cell proliferation was highest. The Bistortae Rhizoma decoction extract showed to increase the apoptosis of the HepG2 ceil, SNU-1 cell and A549 cell in a dose-dependent manner. In particular, the promotion effect of the apoptosis was highest in SNU-1 cell. Among the various fraction extracts of the Bistortae Rhizoma decoction, n-BuOH extraction showed the greatest increase of the apoptosis of the HepG2 cell. The Bistortae Rhizoma decoction extract decreased dose-dependently the secretion of the TGF-$\beta$ in the HepG2 cell, SNU-1 cell and A549 cell and increased the secretion of the TNF-$\alpha$ and the IFN-$\gamma$. These results suggest that the total extract of Bistortae Rhizoma decoction has anti-cancer effect against SNU-1 cell and A549 cell.

ALL TRANS RETINOIC ACID AND 9-cis RETINOIC ACID INHIBIT CELL PROLIFERATION ON HUMAN BREAST CANCER CELL UNE MCF-7

  • Yoon, Hyun-Jung;Gu Kong;Sheen, Yhun-Yhong
    • 한국독성학회:학술대회논문집
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    • 한국독성학회 2002년도 Current Trends in Toxicological Sciences
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    • pp.91-91
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    • 2002
  • We have examine the effect of all trans retinoic acid and 9-cis-retinoic acid on human breast cancer cell proliferation using SRB assay and cell cycle analysis. 1)In MCF-7 cells, in the presence of phenol red, either all trans retinoic acid or 9-cis-retinoic acid treatment showed the inhibition of the cell proliferation over control cells and also inhibit the estrogen stimulated cell proliferation when it was given together with estrogen.(omitted)

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Knockdown of Med19 Suppresses Proliferation and Enhances Chemo-sensitivity to Cisplatin in Non-small Cell Lung Cancer Cells

  • Wei, Ling;Wang, Xing-Wu;Sun, Ju-Jie;Lv, Li-Yan;Xie, Li;Song, Xian-Rang
    • Asian Pacific Journal of Cancer Prevention
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    • 제16권3호
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    • pp.875-880
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    • 2015
  • Mediator 19 (Med19) is a component of the mediator complex which is a coactivator for DNA-binding factors that activate transcription via RNA polymerase II. Accumulating evidence has shown that Med19 plays important roles in cancer cell proliferation and tumorigenesis. The involvement of Med19 in sensitivity to the chemotherapeutic agent cisplatin was here investigated. We employed RNA interference to reduce Med19 expression in human non-small cell lung cancer (NSCLC) cell lines and analyzed their phenotypic changes. The results showed that after Med19 siRNA transfection, expression of Med19 mRNA and protein was dramatically reduced (p<0.05). Meanwhile, impaired growth potential, arrested cell cycle at G0/G1 phase and enhanced sensitivity to cisplatin were exhibited. Apoptosis and caspase-3 activity were increased when cells were exposed to Med19 siRNA and/or cisplatin. The present findings suggest that Med19 facilitates tumorigenic properties of NSCLC cells and knockdown of Med19 may be a rational therapeutic tool for lung cancer cisplatin sensitization.