• Title, Summary, Keyword: cancer cell lines

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Effects of Aloe vera on the Cytotoxicity of Anticancer Drugs in Vitro (Aloe vera가 항암제의 세포독성에 미치는 영향)

  • 표명윤;윤지현
    • YAKHAK HOEJI
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    • v.43 no.1
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    • pp.104-110
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    • 1999
  • We investigated effects of methanol extract of Aloe vera on anticancer drugs(cisplatin, mitomycin C, 5-fluorouracil)-induced growth inhibition in p388, L1210, HCT-15, SK-HepG-1 as cancer cell lines and mouse splenocytes as a normal cell by MTT assay, respectively. We also examined the effects of aloe extract and mitomycin C on the mitogen(Con, A, LPS)-induced splenocyte proliferation. Aloe extract(0.25 mg/m , 1.25 mg/m , 2.5 mg/m , 5.0 mg/m ) showed dose-dependently selective cytotoxicity against the cancer cell lines. In contrast, Aloe extract increased the growth and proliferation of the normal mouse splenocytes. The combination of aloe extract with anticancer drugs showed an additive effect for the cytotoxicity against cancer cell lines. However, that combination reduced clealy the anticancer drugs-induced toxicity against the normal mouse splenocytes.

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Induction of Apoptosis by IGFBP3 Overexpression in Hepatocellular Carcinoma Cells

  • Han, Jian-Jun;Xue, De-Wen;Han, Qiu-Rong;Liang, Xiao-Hong;Xie, Li;Li, Sheng;Wu, Hui-Yong;Song, Bao
    • Asian Pacific Journal of Cancer Prevention
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    • v.15 no.23
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    • pp.10085-10089
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    • 2015
  • Background: The insulin-like growth factor (IGF) system comprises a group of proteins that play key roles in regulating cell growth, differentiation, and apoptosis in a variety of cellular systems. The aim of this study was to investigate the role of insulin-like growth factor binding protein 3 (IGFBP3) in hepatocellular carcinoma. Materials and Methods: Expression of IGF2, IGFBP3, and PTEN was analyzed by qRT-PCR. Lentivirus vectors were used to overexpress IGFBP3 in hepatocellular carcinoma cell (HCC) lines. The effect of IGFBP3 on proliferation was investigated by MTT and colony formation assays. Results: Expression of IGF2, IGFBP3, and PTEN in several HCC cell lines was lower than in normal cell lines. After 5-aza-2'-deoxycytidine/trichostatin A treatment, significant demethylation of the promoter region of IGFBP3 was observed in HCC cells. Overexpression of IGFBP3 induced apoptosis and reduced colony formation in HUH7 cells. Conclusions: Expression of IGF2, IGFBP3, and PTEN in several HCC cell lines was lower than in normal cell lines. After 5-aza-2'-deoxycytidine/trichostatin A treatment, significant demethylation of the promoter region of IGFBP3 was observed in HCC cells. Overexpression of IGFBP3 induced apoptosis and reduced colony formation in HUH7 cells.

The influence of p53 mutation status on the anti-cancer effect of cisplatin in oral squamous cell carcinoma cell lines

  • Jo, Deuk-Won;Kim, Young-Kyun;Yun, Pil-Young
    • Journal of the Korean Association of Oral and Maxillofacial Surgeons
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    • v.42 no.6
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    • pp.337-344
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    • 2016
  • Objectives: The purpose of this study was to evaluate the anti-cancer activity of cisplatin by studying its effects on cell viability and identifying the mechanisms underlying the induction of cell cycle arrest and apoptosis on oral squamous cell carcinoma (OSCC) cell lines with varying p53 mutation status. Materials and Methods: Three OSCC cell lines, YD-8 (p53 point mutation), YD-9 (p53 wild type), and YD-38 (p53 deletion) were used. To determine the cytotoxic effect of cisplatin, MTS assay was performed. The cell cycle alteration and apoptosis were analyzed using flow cytometry. Western blot analysis was used to detect the expression of cell cycle alteration- or apoptosis-related proteins as well as p53. Results: Cisplatin showed a time- and dose-dependent anti-proliferative effect in all cell lines. Cisplatin induced G2/M cell accumulation in the three cell lines after treatment with 0.5 and $1.0{\mu}g/mL$ of cisplatin for 48 hours. The proportion of annexin V-FITC-stained cells increased following treatment with cisplatin. The apoptotic proportion was lower in the YD-38 cell line than in the YD-9 or YD-8 cell lines. Also, immunoblotting analysis indicated that p53 and p21 were detected only in YD-8 and YD-9 cell lines after cisplatin treatment. Conclusion: In this study, cisplatin showed anti-cancer effects via G2/M phase arrest and apoptosis, with some difference among OSCC cell lines. The mutation status of p53 might have influenced the difference observed among cell lines. Further studies on p53 mutation status are needed to understand the biological behavior and characteristics of OSCCs and to establish appropriate treatment.

Combination Effect of Nimotuzumab with Radiation in Colorectal Cancer Cells (대장암 세포에서 EGFR 저해제 Nimotuzumab의 방사선 병합 효과)

  • Shin, Hye-Kyung;Kim, Mi-Sook;Jeong, Jae-Hoon
    • Radiation Oncology Journal
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    • v.28 no.3
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    • pp.147-154
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    • 2010
  • Purpose: To investigate the radiosensitizing effect of the selective epidermal growth factor receptor (EGFR) inhibitor nimotuzumab in human colorectal cancer cell lines. Materials and Methods: Four human colorectal cancer cell lines, HCT-8, LoVo, WiDr, and HCT-116 were treated with nimotuzumab and/or radiation. The effects on cell proliferation, viability, and cell cycle progression were measured by MTT, clonogenic survival assay, flow cytometry, and Western blot. Results: An immunoblot analysis revealed that EGFR phosphorylation was inhibited by nimotuzumab in colorectal cancer cell lines. Under these experimental conditions, pre-treatment with nimotuzumab increased radiosensitivity of colorectal cancer cell lines, except for cell line HCT-116. However, cell proliferation or cell cycle progression was not affected by the addition of nimotuzumab, irrespective of irradiation. Conclusion: Nimotuzumab enhanced the radiosensitivity of colorectal cancer cells in vitro by inhibiting EGFR-mediated cell survival signaling. This study provided a rationale for the clinical application of the selective EGFR inhibitor, nimotuzumab in combination with radiation in colorectal cancer cells.

Antiproliferative Effect of the Salviae miltiorrhizae Radix Extracts on the Cancer Cell Lines (단삼 추출물이 암세포주에 미치는 세포증식 억제 효과)

  • Yang, Weo-Ho;Jung, Tae-San;Choi, Chang-Won
    • Herbal Formula Science
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    • v.22 no.2
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    • pp.35-43
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    • 2014
  • Objectives : The purpose of this study was to identify antiproliferative effects of Salviae miltiorrhizae Radix(SM) extracts against cancer cell lines. Methods : We used 2 kinds of cancer cell lines such as colon cancer cells(HT-29), human oral epitheloid carcinoma cells(KB). MTT assay was performed to examine the efficacy of SM extracts on the cytostaticity of cancer cells in proportion to time and doses. Apoptosis was evaluated by DNA laddering and DAPI nuclei staining. Results : The MTT absorbances against HT-29 and KB of SM extracts were significantly decresed. DNA ladders could be identified in KB of SM extracts. The morphological change were observed and number of cells were decreased by SM extracts. Conclusions : SM extracts is considered to be effective to induce apoptosis and inhibit cancer cell proliferation.

Enhanced proliferation of SNU-407 human colon cancer cells by muscarinic acetylcholine receptors

  • Park, Yang-Seo;Cho, Nam-Jeong
    • BMB Reports
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    • v.41 no.11
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    • pp.803-807
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    • 2008
  • We investigated the expression of muscarinic acetylcholine receptors (mAChRs) and their possible involvement in the regulation of cell proliferation in four colon cancer cell lines (SNU-61, SNU-81, SNU-407, and SNU-1033) derived from Korean colon carcinoma patients. A ligand binding assay showed that all four cell lines expressed mAChRs. Treatment of the four cell lines with the cholinergic agonist carbachol led to the activation of extracellular signal-regulated kinases 1 and 2 (ERK1/2). In SNU-407 cells, carbachol significantly stimulated cell proliferation, which could be abolished by the muscarinic antagonist atropine and the ERK1/2 kinase inhibitor PD98059. These results indicate that mAChRs specifically mediate the proliferation of SNU-407 colon cancer cells via the ERK1/2 pathway.

miR-335 Targets SIAH2 and Confers Sensitivity to Anti-Cancer Drugs by Increasing the Expression of HDAC3

  • Kim, Youngmi;Kim, Hyuna;Park, Deokbum;Jeoung, Dooil
    • Molecules and Cells
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    • v.38 no.6
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    • pp.562-572
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    • 2015
  • We previously reported the role of histone deacetylase 3 (HDAC3) in response to anti-cancer drugs. The decreased expression of HDAC3 in anti-cancer drug-resistant cancer cell line is responsible for the resistance to anti-cancer drugs. In this study, we investigated molecular mechanisms associated with regulation of HDAC3 expression. MG132, an inhibitor of proteasomal degradation, induced the expression of HDAC3 in various anti-cancer drug-resistant cancer cell lines. Ubiquitination of HDAC3 was observed in various anti-cancer drug-resistant cancer cell lines. HDAC3 showed an interaction with SIAH2, an ubiquitin E3 ligase, that has increased expression in various anti-cancer drug-resistant cancer cell lines. miRNA array analysis showed the decreased expression of miR-335 in these cells. Targetscan analysis predicted the binding of miR-335 to the 3'-UTR of SIAH2. miR-335-mediated increased sensitivity to anti-cancer drugs was associated with its effect on HDAC3 and SIAH2 expression. miR-335 exerted apoptotic effects and inhibited ubiquitination of HDAC3 in anti-cancer drug-resistant cancer cell lines. miR-335 negatively regulated the invasion, migration, and growth rate of cancer cells. The mouse xenograft model showed that miR-335 negatively regulated the tumorigenic potential of cancer cells. The down-regulation of SIAH2 conferred sensitivity to anti-cancer drugs. The results of the study indicated that the miR-335/SIAH2/HDAC3 axis regulates the response to anti-cancer drugs.

Somatic mutation patterns and compound response in cancers

  • He, Ningning;Kim, Nayoung;Yoon, Sukjoon
    • BMB Reports
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    • v.46 no.2
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    • pp.97-102
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    • 2013
  • The use of various cancer cell lines can recapitulate known tumor-associated mutations and genetically define cancer subsets. This approach also enables comparative surveys of associations between cancer mutations and drug responses. Here, we analyzed the effects of ~40,000 compounds on cancer cell lines that showed diverse mutation-dependent sensitivity profiles. Over 1,000 compounds exhibited unique sensitivity on cell lines with specific mutational genotypes, and these compounds were clustered into six different classes of mutation-oriented sensitivity. The present analysis provides new insights into the relationship between somatic mutations and selectivity response of chemicals, and these results should have applications related to predicting and optimizing thera-peutic windows for anti-cancer agents.

Chalcones-Sulphonamide Hybrids: Synthesis, Characterization and Anticancer Evaluation

  • Khanusiya, Mahammadali;Gadhawala, Zakirhusen
    • Journal of the Korean Chemical Society
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    • v.63 no.2
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    • pp.85-93
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    • 2019
  • A panel of chalcone-sulphonamide hybrids has been designed by tethering appropriate sulphonamide scaffold with substituted chalcones as a multi-target drug for anticancer screening. Chalcones were prepared by Claisen-Schmidt condensation reaction of a substituted aldehyde with para aminoacetophenone. All the synthesized compounds were evaluated against selected five cancer cell lines, MCF-7 (Breast cancer), DU-145 (Human prostate Carcinoma), HCT-15 (Colon cancer), NCIH-522 (stage 2, adenocarcinoma; non-small cell lung cancer) and HT-3 (Human cervical cancer). Most of the synthesized chalcone-sulphonamide hybrids showed amended cytotoxic activity against various cancer cell lines which may be attributed to the linkage of sulphonamide with chalcone skeleton. The synthesized compounds were characterized by FT-IR, $^1H$ NMR, $^{13}C$ NMR and HR-LCMS and spectral study assert the structures of synthesized sulphonamide-chalcone hybrids.

Novel Hydrophilic Taxane Analogues inhibit Growth of Cancer Cells

  • Fauzee, Nilufer Jasmine Selimah;Wang, Ya-Lan;Dong, Zhi;Li, Qian-Ge;Wang, Tao;Mandarry, Muhammad Tasleem;Lu, Xu;Juan, Pan
    • Asian Pacific Journal of Cancer Prevention
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    • v.13 no.2
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    • pp.563-567
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    • 2012
  • In our era there has been several anti-cancer drugs which have undergone both experimental and clinical trials; however, due to their poor solubilities, numerous side effects, insufficient bioavailability and poor compliance, many have resulted into poor outcomes. Therefore, our aim was to investigate the effects of novel hydrophilic taxanes analogues CQMU-0517 and CQMU-0519 on growth of A549 lung, SKVO3 ovary and MCF7 breast carcinoma cell lines. Different concentrations of original paclitaxel, CQMU-0517, original docetaxel and CQMU-0519 were utilized on three cell lines, where cell growth was assessed using cell culture kit-8 and flow cytometry analysis. The results unveiled that CQMU-0517 and CQMU-0519 suppressed cell growth in the three particular cell lines, cell cycle arrest being evident in the G2/M phase. Hence, the results showed that these new taxane analogues have potential and warrant future clinical trials.