Inhibition of B16 Mouse Melanoma Cell Growth and Induction of Apoptotic Cell Death with 8-Chloroadenosine-3′,5′-monophosphate and Tiazofurin

2004 ◽  
Vol 1030 (1) ◽  
pp. 384-392 ◽  
Author(s):  
LELA B. KORIĆANAC ◽  
DANIJELA V. TODOROVIĆ ◽  
NATAŠA M. POPOVIĆ ◽  
MIROSLAV A. DEMAJO ◽  
SABERA D. RUŽDIJIĆ ◽  
...  
Keyword(s):  
Cell Death ◽  
Cell Growth ◽  
Melanoma Cell ◽  
Apoptotic Cell ◽  
Apoptotic Cell Death ◽  
Mouse Melanoma ◽  
Mouse Melanoma Cell ◽  
B16 Mouse Melanoma

scholarly journals Effect of Natural Plant Water Extracts Suppressed Melanin Production in B16 Mouse Melanoma Cell

2010 ◽  
Vol 24 (S1) ◽  
Author(s):  
Tae Hyuk Kim ◽  
Mi Ja Chung ◽  
Dae Jung Kim ◽  
Jin Kyoun You ◽  
Dong Joo Seo ◽  
...  
Keyword(s):  
Melanoma Cell ◽  
Plant Water ◽  
Melanin Production ◽  
Natural Plant ◽  
Mouse Melanoma ◽  
Water Extracts ◽  
Mouse Melanoma Cell ◽  
B16 Mouse Melanoma

scholarly journals Cell cycle regulation by the Wee1 Inhibitor PD0166285, Pyrido [2,3-d] pyimidine, in the B16 mouse melanoma cell line

BMC Cancer ◽  
2006 ◽  
Vol 6 (1) ◽  
Author(s):  
Osamu Hashimoto ◽  
Masako Shinkawa ◽  
Takuji Torimura ◽  
Toru Nakamura ◽  
Karuppaiyah Selvendiran ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Cell Line ◽  
Melanoma Cell ◽  
Cell Cycle Regulation ◽  
Melanoma Cell Line ◽  
Mouse Melanoma ◽  
Mouse Melanoma Cell ◽  
B16 Mouse Melanoma ◽  
Cycle Regulation ◽  
Mouse Melanoma Cell Line

scholarly journals Expression of human full-length MUC1 inhibits the proliferation and migration of a B16 mouse melanoma cell line

2013 ◽  
Vol 30 (1) ◽  
pp. 260-268 ◽  
Author(s):  
FENGLI WANG ◽  
QIONGSHU LI ◽  
WEIHUA NI ◽  
FANG FANG ◽  
XIAXIA SUN ◽  
...  
Keyword(s):  
Cell Line ◽  
Melanoma Cell ◽  
Melanoma Cell Line ◽  
Full Length ◽  
Mouse Melanoma ◽  
Mouse Melanoma Cell ◽  
And Migration ◽  
B16 Mouse Melanoma ◽  
Mouse Melanoma Cell Line ◽  
Proliferation And Migration

Novel Therapeutic Approach to Overcome Both Bortezomib- and Lenalidomide-Resistant Multiple Myeloma By Targeting TOPK/PBK

Blood ◽  
2015 ◽  
Vol 126 (23) ◽  
pp. 1763-1763
Author(s):  
Takayuki Tabayashi ◽  
Yasuyuki Takahashi ◽  
Yuta Kimura ◽  
Tatsuki Tomikawa ◽  
Tomoe Nemoto-Anan ◽  
...  
Keyword(s):  
Multiple Myeloma ◽  
Cell Death ◽  
Protein Kinase ◽  
Cell Growth ◽  
Research Funding ◽  
Apoptotic Cell ◽  
Mapk Signaling ◽  
Apoptotic Cell Death ◽  
Dependent Manner ◽  
Dose Dependent

Abstract Multiple myeloma (MM) is a neoplasm of plasma cells that often remains fatal despite the use of high-dose chemotherapy with hematopoietic stem cell transplantation. In the clinical setting, the introduction of novel agents, such as proteasome inhibitors and immunomodulatory drugs, has improved the clinical outcomes of both patients with newly diagnosed MM and patients with advanced MM. However, most patients eventually relapse and develop drug resistance. T-LAK cell-originated protein kinase (TOPK), also known as PDZ-binding kinase (PBK), is a mitogen-activated protein kinase kinase (MAPKK)-like serine/threonine kinase that plays a critical role in many cellular functions, such as cell proliferation, apoptotic cell death, and inflammation, in normal tissues. Because the expression of TOPK is up-regulated during mitosis and is activated by the Cdk1/cyclin B1 complex, TOPK is thought to have a role in cytokinesis. While the expression of TOPK is very low in most normal human tissues except for testis and placenta, it is overexpressed in various malignant neoplasms, indicating its crucial role in tumorigenesis. Phosphorylation of TOPK leads to the activation of the MAPK signaling pathway including p38 and Ras extracellular signal-regulated kinase (ERK). Moreover, TOPK interacts with p53 tumor suppressor protein and inhibits its function. Ribosomal protein S6 kinase (RSK2) is a downstream target of the ERK/MAPK signaling cascade and it has a pivotal role in cell survival and proliferation. Recent studies suggest that RSK2 inhibition induces apoptotic cell death and sensitizes MM cells to lenalidomide. Suppression of p53 function is also involved in MM progression. Taken together, these data suggest that TOPK might be an attractive target for new therapeutic agents against this incurable hematological malignancy. HI-TOPK-032, which is a potent and specific inhibitor of TOPK, occupies the ATP-binding site of TOPK and thereby suppresses TOPK kinase activity. In the present study, we investigated the role of TOPK/PBK in MM as a potential therapeutic target by using HI-TOPK-032. MTSand trypan blue dye exclusion assays showed that HI-TOPK-032 inhibited the proliferation of various MM cell lines, including U266, RPMI8226, MM1.S, OPM-2, and KMS-11, in a dose- (0 to 10 mM) and time- (0 to 72 h) dependent manner. To examine the mechanisms behind the growth inhibition effect induced by HI-TOPK-032, assays for apoptotic cell death were performed; these assays demonstrated that HI-TOPK-032 induced both early and late apoptosis in MM cells. To investigate the molecular mechanisms of HI-TOPK-032-induced cell death in MM cells, the expression of various cell death-associated proteins and down-stream molecules of TOPK was examined. Western blotting analysis showed that HI-TOPK-032 arrested cell growth and induced apoptotic cell death in MM cells in a dose-dependent manner by reducing t he phosphorylation of ERK and RSK2, thereby reducing the expression of the target molecules of RSK2, i.e., MCL1 and c-Myc. Moreover, HI-TOPK-032 induced p53 expression in a dose-dependent manner. We next examined the effects of HI-TOPK-032 on bortezomib (BTZ)-resistant MM cells, which represent an urgent issue in clinics and for which a therapeutic solution is important. Interestingly, HI-TOPK-032 inhibited the proliferation of both BTZ-sensitive wild-type KMS cells and BTZ-resistant KMS cells, suggesting that BTZ resistance can be overcome by targeting TOPK. Because our results showed that HI-TOPK-032 reduced the phosphorylation of RSK2, and previous studies have suggested that RSK2 inhibition sensitized MM cells to lenalidomide, we next studied the effects of HI-TOPK-032 in combination with lenalidomide on MM cell growth. HI-TOPK-032 and lenalidomide synergisticallyinduced growth arrest in not only lenalidomide-sensitive MM cells, but also in lenalidomide-resistant cells. To determine whether HI-TOPK-032 can re-sensitize BTZ-resistant cells to the anti-MM activity of BTZ, the effects of the combination of HI-TOPK-032 and BTZ were tested using an MTS assay. Interestingly, HI-TOPK-032 was able to re-sensitize BTZ-resistant MM cells to BTZ. These results indicate that the inhibition of TOPK may serve as an attractive therapeutic option for both patients with BTZ- or lenalidomide-resistant MM. In conclusion, these data suggest that TOPK/PBK can be a promising molecular target for the treatment of MM. Disclosures Kizaki: Nippon Shinyaku Co., Ltd.: Research Funding; Ono Phranacutical Co., Ltd.: Consultancy; Kyowa Hakko Kirin Co., Ltd.: Research Funding; Chugai Phrarmaceutical Co., Ltd.: Research Funding.

scholarly journals Direct Induction of Autophagy by Atg1 Inhibits Cell Growth and Induces Apoptotic Cell Death

2007 ◽  
Vol 17 (1) ◽  
pp. 1-11 ◽  
Author(s):  
Ryan C. Scott ◽  
Gábor Juhász ◽  
Thomas P. Neufeld
Keyword(s):  
Cell Death ◽  
Cell Growth ◽  
Apoptotic Cell ◽  
Apoptotic Cell Death ◽  
Direct Induction

Melanogenesis inhibitory activities of diarylheptanoids fromalnus hirsuta turcz in B16 mouse melanoma cell

2002 ◽  
Vol 25 (6) ◽  
pp. 885-888 ◽  
Author(s):  
Soo Min Cho ◽  
Young Min Kwon ◽  
Jae Hee Lee ◽  
Kyu Hyeong Yon ◽  
Min Won Lee
Keyword(s):  
Melanoma Cell ◽  
Mouse Melanoma ◽  
Mouse Melanoma Cell ◽  
Inhibitory Activities ◽  
B16 Mouse Melanoma

Phenothiazines induce apoptosis in a B16 mouse melanoma cell line and attenuate in vivo melanoma tumor growth

2006 ◽  
Author(s):  
Irit Gil-Ad ◽  
Biana Shtaif ◽  
Yechiel Levkovitz ◽  
Jardena Nordenberg ◽  
Michal Taler ◽  
...  
Keyword(s):  
Tumor Growth ◽  
Cell Line ◽  
Melanoma Cell ◽  
Melanoma Cell Line ◽  
Melanoma Tumor ◽  
Mouse Melanoma ◽  
Mouse Melanoma Cell ◽  
B16 Mouse Melanoma ◽  
Mouse Melanoma Cell Line

Inhibition of cell growth and induction of apoptotic cell death by the human tumor-associated antigen RCAS1

10.1038/11383 ◽  
1999 ◽  
Vol 5 (8) ◽  
pp. 938-942 ◽  
Author(s):  
Manabu Nakashima ◽  
Kenzo Sonoda ◽  
Takeshi Watanabe
Keyword(s):  
Cell Death ◽  
Cell Growth ◽  
Apoptotic Cell ◽  
Human Tumor ◽  
Apoptotic Cell Death ◽  
Tumor Associated Antigen
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