Inhibition of metastatic potential of B16-F10 melanoma cell line in vivo and in vitro by biflorin

Life Sciences ◽  
2013 ◽  
Vol 93 (5-6) ◽  
pp. 201-207 ◽  
Author(s):  
Adriana Andrade Carvalho ◽  
Patrícia Marçal da Costa ◽  
Luciana Gregório Da Silva Souza ◽  
Telma Leda G. Lemos ◽  
Ana Paula Negreiros Nunes Alves ◽  
...  
Keyword(s):  
Cell Line ◽  
Melanoma Cell ◽  
Melanoma Cell Line ◽  
Metastatic Potential

scholarly journals An In Vitro-In Vivo Evaluation of the Antiproliferative and Antiangiogenic Effect of Flavone Apigenin against SK-MEL-24 Human Melanoma Cell Line

2021 ◽  
Vol 2021 ◽  
pp. 1-11
Author(s):  
Alexandra Ghiƫu ◽  
Ioana Zinuca Pavel ◽  
Stefana Avram ◽  
Brigitta Kis ◽  
Daliana Minda ◽  
...  
Keyword(s):  
Cell Line ◽  
Melanoma Cell ◽  
Melanoma Cell Line ◽  
Human Melanoma ◽  
Human Melanoma Cell Line ◽  
Human Melanoma Cell ◽  
Cell Growth And Migration ◽  
Vitro Effect

One of the most important class of natural compounds with successful preclinical results in the management of cancer is the flavonoids. Due to the plethora of biological activities, apigenin (4 ′ ,5,7 trihydroxyflavone) is a main representant of the flavone subclass. Although the antiproliferative and antiangiogenic effects of apigenin were studied on a significant number of human and murine melanoma cell lines, in order to complete the data existing in the literature, the aim of this study is to evaluate the in vitro effect of apigenin on SK-MEL-24 human melanoma cell line as well as in vivo on tumor angiogenesis using the aforementioned cell line on the chorioallantoic membrane assay. Results have shown that in the range of tested doses, the phytocompound presents significant antiproliferative, cytotoxic, and antimigratory potential at 30 μM, respectively, 60 μM. Moreover, the phytocompound in both tested concentrations limited melanoma cell growth and migration and induced a reduced angiogenic reaction limiting melanoma cell development.

scholarly journals Cell-cycle-controlled radiation therapy was effective for treating a murine malignant melanoma cell line in vitro and in vivo

2016 ◽  
Vol 6 (1) ◽  
Author(s):  
Keisuke Otani ◽  
Yoko Naito ◽  
Yukako Sakaguchi ◽  
Yuji Seo ◽  
Yutaka Takahashi ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Radiation Therapy ◽  
Malignant Melanoma ◽  
Cell Line ◽  
Melanoma Cell ◽  
Melanoma Cell Line ◽  
Malignant Melanoma Cell

scholarly journals In Vitro and in Vivo Anticancer Activity of Aconitine on Melanoma Cell Line B16

Molecules ◽  
2013 ◽  
Vol 18 (1) ◽  
pp. 757-767 ◽  
Author(s):  
Juan Du ◽  
Xiaonian Lu ◽  
Ziwen Long ◽  
Zhen Zhang ◽  
Xiaohua Zhu ◽  
...  
Keyword(s):  
Anticancer Activity ◽  
Cell Line ◽  
Melanoma Cell ◽  
Melanoma Cell Line

scholarly journals Establishment of a novel human CIC-DUX4 sarcoma cell line, Kitra-SRS, with autocrine IGF-1R activation and metastatic potential to the lungs

2019 ◽  
Vol 9 (1) ◽  
Author(s):  
Sho Nakai ◽  
Shutaro Yamada ◽  
Hidetatsu Outani ◽  
Takaaki Nakai ◽  
Naohiro Yasuda ◽  
...  
Keyword(s):  
Cell Line ◽  
Cell Lines ◽  
Fusion Gene ◽  
Primary Tumour ◽  
Chromosomal Rearrangements ◽  
Basic Research ◽  
Metastatic Potential ◽  
Original Tumour

Abstract Approximately 60–70% of EWSR1-negative small blue round cell sarcomas harbour a rearrangement of CIC, most commonly CIC-DUX4. CIC-DUX4 sarcoma (CDS) is an aggressive and often fatal high-grade sarcoma appearing predominantly in children and young adults. Although cell lines and their xenograft models are essential tools for basic research and development of antitumour drugs, few cell lines currently exist for CDS. We successfully established a novel human CDS cell line designated Kitra-SRS and developed orthotopic tumour xenografts in nude mice. The CIC-DUX4 fusion gene in Kitra-SRS cells was generated by t(12;19) complex chromosomal rearrangements with an insertion of a chromosome segment including a DUX4 pseudogene component. Kitra-SRS xenografts were histologically similar to the original tumour and exhibited metastatic potential to the lungs. Kitra-SRS cells displayed autocrine activation of the insulin-like growth factor 1 (IGF-1)/IGF-1 receptor (IGF-1R) pathway. Accordingly, treatment with the IGF-1R inhibitor, linsitinib, attenuated Kitra-SRS cell growth and IGF-1-induced activation of IGF-1R/AKT signalling both in vitro and in vivo. Furthermore, upon screening 1134 FDA-approved drugs, the responses of Kitra-SRS cells to anticancer drugs appeared to reflect those of the primary tumour. Our model will be a useful modality for investigating the molecular pathology and therapy of CDS.

scholarly journals A novel in vitro model of metastasis supporting passive shedding hypothesis from murine pancreatic cancer Panc-02

2019 ◽  
Vol 71 (5) ◽  
pp. 989-1002
Author(s):  
M. P. Krzykawski ◽  
R. Krzykawska ◽  
M. Paw ◽  
J. Czyz ◽  
J. Marcinkiewicz
Keyword(s):  
Pancreatic Cancer ◽  
Cell Line ◽  
Cancer Metastasis ◽  
Metastatic Potential ◽  
Blood Stream ◽  
Culture Surface ◽  
Vitro Model ◽  
In Vitro Cell Cultures

Abstract Cancer metastasis is believed to happen through active intravasation but there might be also another way to metastasize. According to passive shedding hypothesis, proposed by Munn et al., tumor cells detach from the tumor mass and passively shed to blood stream through leaky blood vessels. We propose a novel In Vitro Migrational Selection (IVMS) assay that enables the pre-selection of invasive pancreatic cancer Panc-02 cells and create a model of passive shedding. We established invasive sub-cell line of murine pancreatic cancer Panc-02 cells (refered to as Panc02-RS), which exhibited higher metastatic potential in vivo and at the same time decrease in vitro migratory skills, comparing to the initial Panc-02 cell line. In in vitro cell cultures Panc-02 spontaneously detached from the cell culture surface and later reattached and colonized new areas. We believe it can mimic the new way of metastasis, namely passive shedding. We concentrated on Panc-02 model but believe that IVMS might be used to create sub cell lines of many solid tumors to model passive shedding. Our results support the passive shedding hypothesis.

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