scholarly journals Viability of Airborne Tumor Cells during Excision by Ultrasonic Device

2017 ◽  
Vol 2017 ◽  
pp. 1-5
Author(s):  
Masakazu Hashimoto ◽  
Tsuyoshi Kobayashi ◽  
Hirotaka Tashiro ◽  
Shintaro Kuroda ◽  
Yoshihiro Mikuriya ◽  
...  
Keyword(s):  
Laparoscopic Surgery ◽  
Cancer Cells ◽  
Flow Cytometric Analysis ◽  
Cell Counting ◽  
Trypan Blue Exclusion ◽  
Flow Cytometric ◽  
Viable Cells ◽  
Bipolar Scissors ◽  
Cellular Debris ◽  
Power Mode

Background. Laparoscopic surgery has become more widely used, but peritoneal dissemination and port-site metastasis have been reported to occur in these surgeries. One reason for these problems is the ultrasonically activated scalpel (UAS) used for laparoscopic surgery. This study aimed to investigate the viability of airborne cells released during cancer dissection using a UAS. Methods. Flank tumors measuring about 2 cm were induced in male NOD-Cg-Rag1tm1MomIL2rgtm1wjl/SzJ mice by subcutaneous injection of 1 × 106 HepG2 cells. Dissection was performed with UAS (in high or low power modes) and PowerStar bipolar scissors. The mist of released tissue was collected in cell culture medium. The viability of the cellular material was assessed with trypan blue exclusion cell counting, counting after immunofluorescence staining, and flow cytometric analysis. Results. Large quantities of cellular debris were trapped in the tissue dispersed by both devices. In all experiments, there were significantly more viable cells produced by the UAS in high power mode. By using suction at the excision site, the number of viable cancer cells was reduced. Conclusions. This study demonstrates that viable cancer cells can be released into the nearby environment during tumor ablation with a UAS.

Flow cytometric analysis of the expression of 9A3 antigen, E-cadherin and EGF receptor in TMK-1 stomach cancer cells

2007 ◽  
Vol 48 (1) ◽  
pp. 81-84 ◽  
Author(s):  
Ryuichi Fukuyama ◽  
Shinsei Minoshima ◽  
Atsushi Ochiai ◽  
Eiichi Tahara ◽  
Nobuyoshi Shimizu
Keyword(s):  
Cancer Cells ◽  
Stomach Cancer ◽  
Egf Receptor ◽  
Flow Cytometric Analysis ◽  
Flow Cytometric ◽  
E Cadherin

Flow-cytometric analysis of reactive oxygen species in cancer cells under treatment with brassinosteroids

Steroids ◽  
2017 ◽  
Vol 117 ◽  
pp. 11-15 ◽  
Author(s):  
Pyotr A. Kisselev ◽  
Olesya V. Panibrat ◽  
Aliaksei R. Sysa ◽  
Marina V. Anisovich ◽  
Vladimir N. Zhabinskii ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Cancer Cells ◽  
Flow Cytometric Analysis ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Flow Cytometric

scholarly journals Coix lacryma-jobi var. ma-yuen Stapf sprout extract induces cell cycle arrest and apoptosis in human cervical carcinoma cells

2019 ◽  
Vol 19 (1) ◽  
Author(s):  
Eun Suk Son ◽  
Se-Hee Kim ◽  
Young Ock Kim ◽  
Young Eun Lee ◽  
Sun Young Kyung ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Cervical Cancer ◽  
Cell Proliferation ◽  
Cell Cycle Arrest ◽  
Hela Cells ◽  
Flow Cytometric Analysis ◽  
B Cell Lymphoma ◽  
Cell Counting ◽  
Cycle Arrest ◽  
Flow Cytometric

Abstract Background Cervical cancer is the second-leading cause of cancer-related mortality in females. Coix lacryma-jobi L. var. ma-yuen (Rom.Caill.) Stapf ex Hook. f. is the most widely recognized medicinal herb for its remedial effects against inflammation, endocrine system dysfunctions, warts, chapped skin, rheumatism, and neuralgia and is also a nourishing food. Methods To investigate the activity of Coix lacryma-jobi sprout extract (CLSE) on cell proliferation in human cervical cancer HeLa cells, we conducted a Cell Counting Kit-8 (CCK-8) assay. Flow-cytometric analysis and western blot analysis were performed to verify the effect of CLSE on the regulation of the cell cycle and apoptosis in HeLa cells. Results We observed that CLSE significantly inhibited cell proliferation. Furthermore, CLSE dose-dependently promoted cell cycle arrest at the sub-G1/ S phase in HeLa cells, as detected by bromodeoxyuridine (BrdU) staining. The cell-cycle-arrest effects of CLSE in HeLa cells were associated with downregulation of cyclin D1 and cyclin-dependent kinases (CDKs) 2, 4, and 6. Moreover, CLSE induced apoptosis, as determined by flow-cytometric analysis and nuclear DNA fragmentation with Annexin V/propidium iodide (PI) and 4′6′-diamidino-2-phenylindole (DAPI) staining. Induction of apoptosis by CLSE was involved in inhibition of the antiapoptotic protein B-cell lymphoma 2 (Bcl-2) and upregulation of the apoptotic proteins p53, cleaved poly (ADP-ribose) polymerase (PARP), cleaved caspase-3, and cleaved caspase-8. Finally, we observed that CLSE inactivated the phosphoinositide 3-kinase (PI3K) and protein kinase B (AKT) pathways. Conclusions CLSE causes cell cycle arrest and apoptotic cell death through inactivation of the PI3K/AKT pathway in HeLa cells, suggesting it is a viable therapeutic agent for cervical cancer owing to its anticancer effects.

scholarly journals Actinobacillus actinomycetemcomitansLeukotoxin Induces Apoptosis in HL-60 Cells

1998 ◽  
Vol 66 (9) ◽  
pp. 4474-4483 ◽  
Author(s):  
Jonathan Korostoff ◽  
Jian Fei Wang ◽  
Irene Kieba ◽  
Mark Miller ◽  
Bruce J. Shenker ◽  
...  
Keyword(s):  
Apoptotic Cell ◽  
Critical Role ◽  
Flow Cytometric Analysis ◽  
Inflammatory Cells ◽  
Target Cells ◽  
Light Scatter ◽  
Flow Cytometric ◽  
Final Population ◽  
Cellular Debris ◽  
Phosphatidylserine Translocation

ABSTRACT Actinobacillus actinomycetemcomitans leukotoxin (Ltx) is a member of the repeats-in-toxin (RTX) family of pore-forming toxins and kills human immune cells. Currently, it remains unclear whether toxin-mediated killing of target cells involves the induction of necrosis or apoptosis. Therefore, the goal of this investigation was to determine whether Ltx is capable of causing apoptotic cell death in toxin-sensitive promyelocytic HL-60 cells. Multiparameter flow cytometric analysis of toxin-treated cells stained with Hoechst 33258 (or 33342) and 7-aminoactinomycin D allowed us to identify four populations: viable cells, early apoptotic cells, late apoptotic and/or secondarily necrotic cells, and a final population that was composed of cellular debris. Compared with control cells, HL-60 cells treated with Ltx exhibited a gradual decrease in forward light scatter with a coincident increase in side light scatter, indicative of a decrease in cell size and organelle condensation, respectively. Additional experiments demonstrated that Ltx-treated cells showed evidence of internucleosomal DNA fragmentation and phosphatidylserine translocation. The results of our studies clearly demonstrate that Ltx can kill HL-60 cells by inducing apoptosis. We hypothesize that elimination of acute inflammatory cells via this mechanism plays a critical role in the pathogenesis of diseases caused by A. actinomycetemeomitans.

Insights into Nano-Photo-Thermal Therapy of Cancer: The Kinetics of Cell Death and Effect on Cell Cycle

2020 ◽  
Vol 20 (5) ◽  
pp. 612-621
Author(s):  
Mousa Tabei ◽  
Elham Zeinizade ◽  
Jaber Beik ◽  
S. Kamran Kamrava ◽  
Zahra Nasiri ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Cell Death ◽  
Cancer Cells ◽  
Signaling Pathway ◽  
Flow Cytometric Analysis ◽  
Thermal Therapy ◽  
Normal Fibroblast ◽  
Cycle Phase ◽  
Flow Cytometric ◽  
Kinetics Of

Background: Despite considerable advances in nano-photo-thermal therapy (NPTT), there have been a few studies reporting in-depth kinetics of cell death triggered by such a new modality of cancer treatment. Objective: In this study, we aimed to (1) investigate the cell death pathways regulating the apoptotic responses to NPTT; and (2) ascertain the effect of NPTT on cell cycle progression. Methods: Folate conjugated gold nanoparticle (F-AuNP) was firstly synthesized, characterized and then assessed to determine its potentials in targeted NPTT. The experiments were conducted on KB nasopharyngeal cancer cells overexpressing folate receptors (FRs), as the model, and L929 normal fibroblast cells with a low level of FRs, as the control. Cytotoxicity was evaluated by MTT assay and the cell death mode (i.e., necrosis or apoptosis) was determined through AnnexinV/FITC-propidium iodide staining. Next, the gene expression profiles of some key apoptotic factors involved in the mitochondrial signaling pathway were investigated using RT-qPCR. Finally, cell cycle phase distribution was investigated at different time points post NPTT using flow cytometric analysis. Results: The obtained results showed that KB cell death following targeted NPTT was greater than that observed for L929 cells. The majority of KB cell death following NPTT was related to apoptosis. RT-qPCR analysis indicated that the elevated expression of Bax along with the depressed expression of Bcl-xL, Survivin and XIAP may involve in the regulation of apoptosis in response to NPTT. Flow cytometric analysis manifested that 16-24 hours after NPTT, the major proportion of KB cells was in the most radiosensitive phases of the cell cycle (G2/M). Conclusion: This study extended the understanding of the signaling pathway involved in the apoptotic response to NPTT. Moreover, the potential effect of NPTT on sensitizing cancer cells to subsequent radiation therapy was highlighted.

Flow cytometric analysis of the kinetic effects of cisplatin on lung cancer cells

Cytometry ◽  
1989 ◽  
Vol 10 (6) ◽  
pp. 788-795 ◽  
Author(s):  
Toshiaki Fujikane ◽  
Tetsuo Shimizu ◽  
Tadakatsu Tsuji ◽  
Sakae Ishida ◽  
Yoshinobu Ohsaki ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Cancer Cells ◽  
Flow Cytometric Analysis ◽  
Lung Cancer Cells ◽  
Flow Cytometric ◽  
Kinetic Effects

scholarly journals Long intergenic non-coding RNA 1939 inhibits proliferation and migration of human renal cell carcinoma (RCC) cells by down-regulation of miR-154

2019 ◽  
Author(s):  
Rongyuan Zhang ◽  
Yuhua Huang ◽  
Baocai Xu ◽  
Chuan Lv ◽  
Jianquan Hou ◽  
...  
Keyword(s):  
Flow Cytometric Analysis ◽  
Cell Counting ◽  
Regulation Mechanism ◽  
Human Renal Cell Carcinoma ◽  
Flow Cytometric ◽  
Non Coding Rna ◽  
And Migration ◽  
Induced Apoptosis ◽  
Proliferation And Migration

Abstract Background: Renal carcinoma (RCC) is widely accepted as a malignant tumor of urinary system. Long intergenic non-coding RNA 1939 (LINC01939) is a novel lncRNA which was found to be down-regulated in RCC. Thus, we set out to explore the effect and regulation mechanism of LINC01939 in RCC. Methods: LINC01939 and miR-154 in RCC tissues and cell lines were detected using qRT-PCR assay. Cell counting kit-8 (CCK-8) assays was exploited to examine cell viability. Flow cytometric analysis was conducted to examine apoptosis. Cell mobility was valued through wound healing assays. Western blotting was applied for examination of proteins related to proliferation, apoptosis, migration and Wnt/β-catenin/Notch. Results: LINC01939 was down-regulated in RCC tissues. LINC01939 overexpression impeded proliferation and migration, and induced apoptosis. Further study found that the overexpression of LINC01939 strongly suppressed miR-154 expression. Then, the inhibiting effect of overexpressed LINC01939 on proliferation and mobility and the promoting role of LINC01939 in apoptosis were abolished by the combination of miR-154 mimic. Finally, we found that the overexpressed LINC01939 inactivated Wnt/β-catenin and Notch through suppressing miR-154. Conclusion: The up-regulation of LINC01939 inhibited proliferation and migration of RCC cells by down-regulating miR-154.

scholarly journals Naringenin inhibits human breast cancer cells (MDA-MB-231) by inducing programmed cell death, caspase stimulation, G2/M phase cell cycle arrest and suppresses cancer metastasis

2021 ◽  
Vol 67 (2) ◽  
pp. 8-13
Author(s):  
Zhaozhen Qi ◽  
Shuangxi Kong ◽  
Shunyu Zhao ◽  
Qiu Tang
Keyword(s):  
Breast Cancer ◽  
Cell Cycle ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Apoptotic Cell ◽  
Flow Cytometric Analysis ◽  
Annexin V ◽  
Cycle Arrest ◽  
Flow Cytometric ◽  
M Phase

The current study was designed to unveil the anticancer effects of naringenin against breast cancer MDA-MB-231 cells. Cytotoxic effects were estimated via MTT viability assay. Clonogenic assay was performed to assess clonogenic potential of MDA-MB-231 cells. Apoptosis was examined via AO/EB staining, quantified via annexin V/PI staining and western blotting was performed to monitor apoptosis allied protein expressions. Cell cycle was analyzed through flow cytometric analysis. Transwell chambers assay was executed for determination of cell migration and cell invasion tendency of MDA-MB-231 breast cancer cells. Results indicated significant anticancer potential of naringenin drug against MDA-MB-231 cells. On evaluation of cell proliferation rate of breast cancer cells by MTT assay, it was observed that naringenin inhibited proliferation rate in dose as well as time dependent manner. AO/EB staining assay revealed potential morphological changes indicating apoptotic cell death. Annexin V/PI staining assay revealed increased apoptotic cell percentage with increased drug doses. The apoptosis inducing potential of naringenin drug was observed to be mediated via caspase activation. Flow cytometric analysis predicted cell cycle arrest at G2/M phase of cell cycle. Further cell migration as well as cell invasion tendency of MDA-MB-231 cells was reduced to minimum upon application of naringenin drug.

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