scholarly journals Methoxy- and Fluoro-chalcone Derivatives Arrest Cell Cycle Progression and Induce Apoptosis in Human Melanoma Cell A375

2009 ◽  
Vol 32 (6) ◽  
pp. 1109-1113 ◽  
Author(s):  
Kayo Henmi ◽  
Yoko Hiwatashi ◽  
Eri Hikita ◽  
Naoya Toyama ◽  
Toshihiko Hirano
Keyword(s):  
Cell Cycle ◽  
Melanoma Cell ◽  
Cell Cycle Progression ◽  
Human Melanoma ◽  
Human Melanoma Cell ◽  
Cycle Progression ◽  
Chalcone Derivatives ◽  
Arrest Cell Cycle Progression

The p53/p21Cip1/ Waf1 pathway mediates the effects of SPARC on melanoma cell cycle progression

2010 ◽  
Vol 24 (1) ◽  
pp. 219-232 ◽  
Author(s):  
Nina Fenouille ◽  
Guillaume Robert ◽  
Mélanie Tichet ◽  
Alexandre Puissant ◽  
Maeva Dufies ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Melanoma Cell ◽  
Cell Cycle Progression ◽  
Cycle Progression

scholarly journals Human Cytomegalovirus UL69 Protein Induces Cells To Accumulate in G1 Phase of the Cell Cycle

1999 ◽  
Vol 73 (1) ◽  
pp. 676-683 ◽  
Author(s):  
Mansuo Lu ◽  
Thomas Shenk
Keyword(s):  
Cell Cycle ◽  
Human Cytomegalovirus ◽  
Cell Cycle Progression ◽  
Human Fibroblasts ◽  
Protein A ◽  
S Phase ◽  
Cycle Progression ◽  
Multiple Points ◽  
Cell Cycle Block ◽  
Arrest Cell Cycle Progression

ABSTRACT Earlier studies have revealed that human cytomegalovirus rapidly inhibits the growth of fibroblasts, blocking cell cycle progression at multiple points, including the G1-to-S-phase transition. The present study demonstrates that the UL69 protein, a virus-encoded constituent of the virion, is able to arrest cell cycle progression when introduced into uninfected cells. Expression of the UL69 protein causes U2 OS cells and primary human fibroblasts to accumulate within the G1 compartment of the cell cycle, and serum fails to induce the progression of quiescent human fibroblasts into the S phase when the protein is present. Therefore, the UL69 protein is at least partially responsible for the cell cycle block that is instituted after infection of permissive cells with human cytomegalovirus.

Mechanism Underlying NaF-induced Apoptosis and Cell Cycle Arrest on G361 Human Melanoma Cell Line

2011 ◽  
Vol 24 (4) ◽  
pp. 203 ◽  
Author(s):  
Do Kyun Kim ◽  
Hyeon Jin Sohn ◽  
In Ryoung Kim ◽  
Gyoo Cheon Kim ◽  
Bong Soo Park ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Cell Cycle Arrest ◽  
Cell Line ◽  
Melanoma Cell ◽  
Melanoma Cell Line ◽  
Human Melanoma ◽  
Human Melanoma Cell Line ◽  
Human Melanoma Cell ◽  
Cycle Arrest ◽  
Induced Apoptosis

scholarly journals UBTF facilitates melanoma progression via modulating MEK1/2-ERK1/2 signalling pathways by promoting GIT1 transcription

2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Jian Zhang ◽  
Jiaojiao Zhang ◽  
Wenli Liu ◽  
Rui Ge ◽  
Tianyuan Gao ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Cell Proliferation ◽  
Cell Lines ◽  
Melanoma Cell ◽  
Cell Cycle Progression ◽  
Signalling Pathways ◽  
Cell Multiplication ◽  
Cycle Progression ◽  
Qrt Pcr ◽  
Melanoma Cell Proliferation

Abstract Background UBTF is an HMGB-box DNA binding protein and a necessary Pol I/Pol II basal transcription factor. It has been found that UBTF involves in carcinogenesis and progression of a few cancers. Nevertheless, the the biological function and potential molecular mechanism of UBTF in melanoma are still not clear and need to be clarified. Methods UBTF and GIT1 expressions in melanoma specimens and cell lines were examined by quantitative real-time PCR (qRT-PCR) and Western blot. MTT and colony formation assays were used to investigate the effects of UBTF and GIT1 on melanoma cell proliferation. Cell cycle and apoptosis assays were detected by flow cytometry. Tumor formation assay was used to analyze the effect of UBTF on melanoma growth. Bioinformatics predicting, chromatin immunoprecipitation (ChIP)-qRT-PCR and reporter gene assay were fulfilled for verifing GIT1 as UBTF targeting gene. Results Here we reported that UBTF mRNA and protein expressions were upregulated in primary melanoma specimens and cell lines. UBTF overexpression facilitated melanoma cell proliferation and cell cycle progression and restrained. Silencing UBTF suppressed cell multiplication, cell cycle progression and tumor growth, and promoted apoptosis. UBTF expression was positively related with GIT1 expression in human melanoma tissues. It was verified that UBTF promoted GIT1 transcription in melanoma cells through binding to the promoter region of GIT1. Furthermore, GIT1 overexpression promoted melanoma cell growth and suppressed apoptosis. Knockdown of GIT1 inhibited cell multiplication and induced apoptosis. Overexpression of GIT1 eliminated the effects of silencing UBTF on melanoma cells. Importantly, UBTF activated MEK1/2-ERK1/2 signalling pathways by upregulating GIT1 expression. Conclusions Our study demonstrates that UBTF promotes melanoma cell proliferation and cell cycle progression by promoting GIT1 transcription, thereby activating MEK1/2-ERK1/2 signalling pathways. The findings indicate that UBTF plays a crucial function in melanoma and may be a potential therapeutic target for the treatment of this disease.

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