• 제목/요약/키워드: tumor cell proliferation

검색결과 1,016건 처리시간 0.032초

사향과 항암제 Mitomycin C의 병용효과 (The Combined Effect of Moschus and Anti-tumor drug Mitomycin C)

  • 은재순;김대근;송정모
    • 동의생리병리학회지
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    • 제17권6호
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    • pp.1404-1408
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    • 2003
  • The combined effects of water-soluble fraction of Moschus (ME) and anti-tumor drug mitomycin C on the proliferation of human tumor cell-lines were estimated by MTT colorimetric assay. ME inhibited the proliferation of Hep G2, A540, HeLa, KHOS-NP and Balb/c 3T3 cells. Also, ME increased the cytotoxicity of mitomycin C on Hep G2, A549 and HeLa cells. In addition, ME enhanced the cell viability of murine splenocytes and human lymphocytes at the concentration of 100㎍/㎖. These results indicate that ME inhibits the proliferation of human tumor cells and increases the cytotoxicity of mitomycin C without cytoxicity on immune cells.

구강암 세포에서 혈관내피성장인자 수용체-3 억제제의 항종양 효과 (Anti-tumor Effects of Vascular Endothelial Growth Factor Receptor-3 Inhibitor on Oral Cancer Cells)

  • 김찬우;김성곤;박영욱
    • Maxillofacial Plastic and Reconstructive Surgery
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    • 제34권4호
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    • pp.239-245
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    • 2012
  • Purpose: Vascular endothelial growth factor (VEGF) plays a key role in tumor angiogenesis and lymphangiogenesis including induction of endothelial cell proliferation, migration and capillary tube formation. E7080 (S1164, Selleck chemical, Houston, TX, USA) is a muti-targeted kinase inhibitor, which targets VEGF receptor-2, 3 (VEGFR-2, 3) and inhibits survival and proliferation of tumor cell. The purpose of this study was to determine the anti-tumor effect of E7080 on oral squamous cell carcinoma. Methods: An oral squamous cell carcinoma cell line, SCC-9 was used in this study. E7080 was applied to SCC-9 cells by 3 different concentrations (1, 5, 10 ${\mu}g/mL$). Control means no application of E7080. The cellular growth was evaluated by real-time cell electronic sensing and MTT assay. The signal transduction was evaluated by Western blotting. Results: In experimental group, SCC-9 cell proliferation was decreased and the VEGFR-3 downstream pathways were inhibited compared with control. Furthermore, increasing the concentration of E7080, the ability of E7080 to disturbance of SCC-9 cell proliferation was increased. Conclusion: Proliferation of SCC-9 cells was inhibited by E7080, which was through by inhibition of VEGFR-3 downstream pathway. In vivo study with E7080 will be required to provide therapeutic benefits in oral squamous cell carcinoma.

The role of NUMB/NUMB isoforms in cancer stem cells

  • Choi, Hye Yeon;Seok, Jaekwon;Kang, Geun-Ho;Lim, Kyung Min;Cho, Ssang-Goo
    • BMB Reports
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    • 제54권7호
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    • pp.335-343
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    • 2021
  • Cancer stem cells (CSCs) are a subpopulation of cancer that can self-renew and differentiate into large tumor masses. Evidence accumulated to date shows that CSCs affect tumor proliferation, recurrence, and resistance to chemotherapy. Recent studies have shown that, like stem cells, CSCs maintain cells with self-renewal capacity by means of asymmetric division and promote cell proliferation by means of symmetric division. This cell division is regulated by fate determinants, such as the NUMB protein, which recently has also been confirmed as a tumor suppressor. Loss of NUMB expression leads to uncontrolled proliferation and amplification of the CSC pool, which promotes the Notch signaling pathway and reduces the expression of the p53 protein. NUMB genes are alternatively spliced to produce six functionally distinct isoforms. An interesting recent discovery is that the protein NUMB isoform produced by alternative splicing of NUMB plays an important role in promoting carcinogenesis. In this review, we summarize the known functions of NUMB and NUMB isoforms related to the proliferation and generation of CSCs.

Eudesmin Inhibits Tumor Necrosis Factor-$\alpha$ Production and T cell Proliferation

  • Cho, Jae-Youl;Yoo, Eun-Sook;Baik, Kyoung-Up;Park, Myung-Hwan
    • Archives of Pharmacal Research
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    • 제22권4호
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    • pp.348-353
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    • 1999
  • Possible antiinflammatory effect of eudesmin were examined by assessing the effects on tumor necrosis factor (TNF)-$\alpha$ production and lymphocyte proliferation as well as cytotoxicity against murine and human macrophages. the compound significantly inhibited TNF-$\alpha$, production by lipopolysaccaride (LPS)-stimulated murine macrophage RAW264.7 without displaying cytotoxicity suggesting that eudesmin may inhibit TNF-$\alpha$ production without any interference of normal cell function. It also significantly attenuated T cell proliferation stimulated by concanavalin A (Con A) in a dose-dependent manner.

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세포 증식 영상용 방사성의약품 (Radiopharmaceuticals for Imaging of Cellular Proliferation)

  • 오승준
    • 대한핵의학회지
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    • 제36권4호
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    • pp.209-223
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    • 2002
  • By considering the biological properties of a tumor, it should be possible to realize better results in cancer therapy. PET imaging offers the opportunity to measure tumor growth non-invasively and repeatedly as an early assessment of response to cancer therapy. Measuring cellular growth instead of energy metabolism showed offer significant advantages in evaluating therapy. Thymidine and its derivative nucleoside compounds can be changed to mono, di- and tri- phosphate compounds by thymidine kinase and then be incorporated into DNA. Their bindings are increased in highly proliferating cells due to the high DNA synthesis rate. To evaluate cell proliferation, many kinds of thymidine and uridine derivatives have been labeled with positron emitter and radioactive iodine. Compared to radiopharmaceuticals which have radioisotope labeled base ring such as pyirmidine, the radiopharmacuticals which have radioisotope labeled sugar ring are more stable in vivo and have metabolic resistance. The biological properties such as DNA incorporation ratios are highly dependent on their chemical structures and metabolic processes. This overview describes synthesis of radiopharmaceuticals and their biological properties for imaging of tumor cell proliferation.

Anti-tumor Effects of Soybeans and Fermented Soybean Paste

  • Lee, Sung-Lim;Kim, Jong-Gyu
    • 한국환경보건학회:학술대회논문집
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    • 한국환경보건학회 2004년도 International Conference Global Environmental Problems and their Health Consequences
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    • pp.182-184
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    • 2004
  • Oral cancer is the sixth most common cancer globally. The effects of several extracts from soybeans and Korean soybean paste (doen-jang) on the growth of human oral carcinoma cells in vitro were assessed. We prepared petroleum ether extract, ethyl acetate extract, chloroform extract, methanol extract, and water extract from soybeans and soybean paste. We used KB cell, which is an oral epidermoid carcinoma cell, and investigated proliferation of the tumor cells using MTT method. Each extract of soybean paste suppressed the KB cell proliferation. A dose-response relationship was observed between the level of ethyl acetate extract of soybean paste and its suppression of the cell proliferation. The effects of soybean extracts were lower than those of soybean paste extracts. The effects might be enhanced by the fermentation of soybeans. The results of this work indicate that extracts from soybeans and Korean soybean paste could have potential as anti-tumor substances.

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Ginsenoside-Rh2 Inhibits Proliferation and Induces Apoptosis of Human Gastric Cancer SGC-7901 Side Population Cells

  • Qian, Jun;Li, Jing;Jia, Jian-Guang;Jin, Xin;Yu, Da-Jun;Guo, Chen-Xu;Xie, Bo;Qian, Li-Yu
    • Asian Pacific Journal of Cancer Prevention
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    • 제17권4호
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    • pp.1817-1821
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    • 2016
  • Objectives: To observed the effects of ginsenoside -Rh2 (GS-Rh2) on proliferation and apoptosis of side population (SP) human gastric cancer SGC-7901 cells. Materials and Methods: SGC-7901 SP and Non-SP cells were sorted by flow cytometry and assessed using the cck-8 method. Expression of apoptosis-related proteins Bax and Bcl-2 of SP before and after the intervention was determined by Western-blotting. Results: It was found that the proliferation of SP was significantly faster than that of NSP (P<0.05). In addition, GS-Rh2 inhibited proliferation of gastric cancer SP cells, induced cell cycle arrest and cell apoptosis, and changed the expression of BAX/Bcl-2 proteins in a time-dependent and concentration-dependent manner (P<0.05). Conclusions: With increase of GS-Rh2 dose, GS-Rh2 gradually inhibit the proliferation of SGC-7901 SP cells, which have high proliferation rate, through G1/G0 phase arrest, followed by apoptosis which involves the up-regulation of Bax and the down-regulation of Bcl-2.

Adenine Inhibits B16-F10 Melanoma Cell Proliferation

  • Silwal, Prashanta;Park, Seung-Kiel
    • 대한의생명과학회지
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    • 제26권3호
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    • pp.179-185
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    • 2020
  • Adenine, a purine base, is a structural component of essential biomolecules such as nucleic acids and adenine nucleotides. Its physiological roles have been uncovered. Adenine suppresses IgE-mediated allergy and LPS-induced inflammation. Although adenine is known to inhibit lymphocyte proliferation, the effect of adenine to melamoma cells is not reported. Here, we investigated the growth inhibitory effects of adenine on B16-F10 mouse melanoma cells. Adenine suppressed the proliferation of B16-F10 cells in dose-dependent manner with the maximal inhibitory dose of 2 mM. Adenine treatment induced cell death molecular markers such as PARP and caspase 3 cleavages. Pan-caspase inhibitor z-VAD dramatically rescued the cell death molecular markers, cell proliferation recovered marginally. These results provide the possibility of adenine to be used as an anti-tumor agent.

MiR-454 Prompts Cell Proliferation of Human Colorectal Cancer Cells by Repressing CYLD Expression

  • Liang, Hong-Liang;Hu, Ai-Ping;Li, Sen-Lin;Xie, Jia-Ping;Ma, Qing-Zhu;Liu, Ji-Yong
    • Asian Pacific Journal of Cancer Prevention
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    • 제16권6호
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    • pp.2397-2402
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    • 2015
  • Previous studies have shown that miR-454 plays an important role in a variety of biological processes in various human cancer cells. However, the underlying mechanisms of this microRNA in colorectal cancer (CRC) cells remain largely unknown. In the present study, we investigated the miR-454 role in CRC cell proliferation. We found that miR-454 expression is markedly upregulated in CRC tissues and CRC cells compared with the matched tumor adjacent tissues and the FHC normal colonic cell line. Ectopic expression of miR-454 promoted the proliferation and anchorage-independent growth of CRC cells, whereas inhibition of miR-454 reduced this effect. Bioinformatics analysis further revealed cylindromatosis (CYLD), a putative tumor suppressor as a potential target of miR-454. Data from luciferase reporter assays showed that miR-454 directly binds to the 3'-untranslated region (3'-UTR) of CYLD mRNA and repressed expression at both transcriptional and translational levels. In functional assays, CYLD-silenced in miR-454-in-transfected SW480 cells have positive effect to promote cell proliferation, suggesting that direct CYLD downregulation is required for miR-454-induced CRC cell proliferation. In sum, our data provide compelling evidence that miR-454 functions as an onco-miRNA, playing a crucial role in the promoting cell proliferation in CRC, and its oncogenic effect is mediated chiefly through direct suppression of CYLD expression.

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.