scholarly journals Anti-oncogenic MicroRNA-203 Induces Senescence by Targeting E2F3 Protein in Human Melanoma Cells

2012 ◽  
Vol 287 (15) ◽  
pp. 11769-11777 ◽  
Author(s):  
Shunsuke Noguchi ◽  
Takashi Mori ◽  
Yusami Otsuka ◽  
Nami Yamada ◽  
Yuki Yasui ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Cell Growth ◽  
Malignant Melanoma ◽  
Cell Cycle Arrest ◽  
Ectopic Expression ◽  
Melanoma Cells ◽  
Microrna Target ◽  
Human Malignant Melanoma ◽  
Cycle Arrest ◽  
Tissue Specimens

MicroRNAs regulate gene expression by repressing translation or directing sequence-specific degradation of their complementary mRNA. We recently reported that miR-203 is down-regulated, and its exogenous expression inhibits cell growth in canine oral malignant melanoma tissue specimens as well as in canine and human malignant melanoma cells. A microRNA target database predicted E2F3 and ZBP-89 as putative targets of microRNA-203 (miR-203). The expression levels of E2F3a, E2F3b, and ZBP-89 were markedly up-regulated in human malignant melanoma Mewo cells compared with those in human epidermal melanocytes. miR-203 significantly suppressed the luciferase activity of reporter plasmids containing the 3′-UTR sequence of either E2F3 or ZBP-89 complementary to miR-203. The ectopic expression of miR-203 in melanoma cells reduced the levels of E2F3a, E2F3b, and ZBP-89 protein expression. At the same time, miR-203 induced cell cycle arrest and senescence phenotypes, such as elevated expression of hypophosphorylated retinoblastoma and other markers for senescence. Silencing of E2F3, but not of ZBP-89, inhibited cell growth and induced cell cycle arrest and senescence. These results demonstrate a novel role for miR-203 as a tumor suppressor acting by inducing senescence in melanoma cells.

scholarly journals Growth Suppression by Acute PromyelocyticLeukemia-Associated Protein PLZF Is Mediated by Repression ofc-mycExpression

2003 ◽  
Vol 23 (24) ◽  
pp. 9375-9388 ◽  
Author(s):  
Melanie J. McConnell ◽  
Nathalie Chevallier ◽  
Windy Berkofsky-Fessler ◽  
Jena M. Giltnane ◽  
Rupal B. Malani ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Cell Growth ◽  
Cell Cycle Arrest ◽  
Target Genes ◽  
Ectopic Expression ◽  
Growth Suppression ◽  
Quiescent State ◽  
Cycle Arrest

ABSTRACT The transcriptional repressor PLZF was identified by its translocation with retinoic acid receptor alpha in t(11;17) acute promyelocytic leukemia (APL). Ectopic expression of PLZF leads to cell cycle arrest and growth suppression, while disruption of normal PLZF function is implicated in the development of APL. To clarify the function of PLZF in cell growth and survival, we used an inducible PLZF cell line in a microarray analysis to identify the target genes repressed by PLZF. One prominent gene identified was c-myc. The array analysis demonstrated that repression of c-myc by PLZF led to a reduction in c-myc-activated transcripts and an increase in c-myc-repressed transcripts. Regulation of c-myc by PLZF was shown to be both direct and reversible. An interaction between PLZF and the c-myc promoter could be detected both in vitro and in vivo. PLZF repressed the wild-type c-myc promoter in a reporter assay, dependent on the integrity of the binding site identified in vitro. PLZF binding in vivo was coincident with a decrease in RNA polymerase occupation of the c-myc promoter, indicating that repression occurred via a reduction in the initiation of transcription. Finally, expression of c-myc reversed the cell cycle arrest induced by PLZF. These data suggest that PLZF expression maintains a cell in a quiescent state by repressing c-myc expression and preventing cell cycle progression. Loss of this repression through the translocation that occurs in t(11;17) would have serious consequences for cell growth control.

scholarly journals In Vitro Anticancer Effects of All-trans Retinoic Acid in Combination with Dacarbazine against CD117+ Melanoma Cells

Drug Research ◽  
2020 ◽  
Vol 70 (12) ◽  
pp. 563-569
Author(s):  
Bahareh Mohammadi Jobani ◽  
Elham Mohebi ◽  
Nowruz Najafzadeh
Keyword(s):  
Cell Cycle ◽  
Retinoic Acid ◽  
Malignant Melanoma ◽  
Cell Cycle Arrest ◽  
Combined Treatment ◽  
Melanoma Cells ◽  
Cycle Arrest ◽  
Trans Retinoic Acid ◽  
All Trans Retinoic Acid

Abstract Background Malignant melanoma is a common form of skin cancer that contains different cell types recognized by various cell surface markers. Dacarbazine-based combination chemotherapy is frequently used for the treatment of melanoma. Despite its potent anticancer properties, resistance to dacarbazine develops in malignant melanoma. Here, we aim to improve response to dacarbazine therapy by pretreatment with all-trans retinoic acid (ATRA) in CD117+ melanoma cells. Methods The CD117+ melanoma cells were sorted from A375 malignant melanoma cell line using magnetic-activated cell sorting (MACS). The cell viability was examined by cell proliferation assay (MTT). Apoptosis was determined by acridine orange/ ethidium bromide staining. Indeed, we performed flow cytometry to evaluate the cell cycle arrest. Results Here, the CD117+ melanoma cells were incubated with various concentrations of ATRA, dacarbazine, and their combination to determine IC50 values. We found that 20 µM ATRA treatment followed by dacarbazine was found to be more effective than dacarbazine alone. There was an indication that the combination of ATRA with dacarbazine (ATRA/dacarbazine) caused more apoptosis and necrosis in the melanoma cells (P<0.05). Furthermore, ATRA/dacarbazine treatment inhibited the cell at the G0/G1 phase, while dacarbazine alone inhibited the cells at S phase. Conclusion Collectively, combined treatment with ATRA and dacarbazine induced more apoptosis and enhanced the cell cycle arrest of CD117+ melanoma cells. These results suggested that ATRA increased the sensitivity of melanoma cells to the effect of dacarbazine.

Sodium ascorbate inhibits growth via the induction of cell cycle arrest and apoptosis in human malignant melanoma A375.S2 cells

2006 ◽  
Vol 16 (6) ◽  
pp. 509-519 ◽  
Author(s):  
Shuw-Yuan Lin ◽  
Wan-Wen Lai ◽  
Chi-Chung Chou ◽  
Hsiu-Maan Kuo ◽  
Te-Mao Li ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Malignant Melanoma ◽  
Cell Cycle Arrest ◽  
Sodium Ascorbate ◽  
S2 Cells ◽  
Human Malignant Melanoma ◽  
Cycle Arrest

scholarly journals Isothiocyanate-induced Cell Cycle Arrest in a Novel In Vitro Exposure Protocol of Human Malignant Melanoma (A375) Cells

2019 ◽  
Vol 39 (2) ◽  
pp. 591-596 ◽  
Author(s):  
THEODORA MANTSO ◽  
IOANNIS ANESTOPOULOS ◽  
ELEFTHERIA LAMPRIANIDOU ◽  
IOANNIS KOTSIANIDIS ◽  
AGLAIA PAPPA ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Malignant Melanoma ◽  
Cell Cycle Arrest ◽  
Human Malignant Melanoma ◽  
Cycle Arrest ◽  
In Vitro Exposure ◽  
A375 Cells

scholarly journals Cinobufagin Induces Cell Cycle Arrest at the G2/M Phase and Promotes Apoptosis in Malignant Melanoma Cells

2019 ◽  
Vol 9 ◽  
Author(s):  
Zhaohai Pan ◽  
Xin Zhang ◽  
Pengfei Yu ◽  
Xiaoyu Chen ◽  
Peng Lu ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Malignant Melanoma ◽  
Cell Cycle Arrest ◽  
Melanoma Cells ◽  
Cycle Arrest ◽  
M Phase
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