Four-and-a-half-LIM protein 1 down-regulates estrogen receptor α activity through repression of AKT phosphorylation in human breast cancer cell

Zhang, Fan; Feng, Fan; Yang, Pingxun; Li, Zijian; You, Jie; Xie, Wenxiu; Gao, Xudong; Yang, Junlan

doi:10.1016/j.biocel.2011.11.002

Cited by 34 publications

(33 citation statements)

References 23 publications

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“…This was consistent with our previous studies, and established a clear molecular mechanism for previous results. The mechanisms of co-regulation of the transcription factor were evident in four aspects (Choi et al, 2009;Ding et al, 2009;Zhang et al, 2012): a) physical interaction, b) promoting the recruitment of transcription factor with their DNA binding elements, c) modulating the cytoplasmic/nucleus translocation of the transcription factor, and d) recruiting other co-regulators to the promoter of the downstream gene. This study demonstrated that LINE-1 ORF-1p increased ETS-1 transcriptional activity through physical interactions, but whether LINE-1 ORF-1p might function through other mechanisms remains unknown.…”

Section: Discussionmentioning

confidence: 99%

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Long interspersed nucleotide acid element-1 ORF-1 protein promotes proliferation and invasion of human colorectal cancer LoVo cells through enhancing ETS-1 activity

Li¹,

Zhu²,

Feng³

et al. 2014

Genet. Mol. Res.

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ABSTRACT. The human proto-oncogene long interspersed nucleotide acid element-1 (LINE-1) open reading frame-1 protein (ORF-1p) is involved in the progress of several cancers. The transcription factor ETS-1 can mediate the transcription of some downstream genes that play specific roles in the regulation of cancerous cell invasion and metastasis. In this study, the effects of LINE-1 ORF-1p on ETS-1 activity and on the proliferation and invasion of human colorectal cancer LoVo cells were investigated. Results showed that the overexpression of LINE-1 ORF1p enhanced the transcription of ETS-1 downstream genes and increased their protein levels, and downregulation of the LINE-1 ORF-1p level by small interfering RNA (siRNA) reduced the transcriptional activation of ETS-1. In addition, overexpression of LINE-1 ORF-1p promoted LoVo cell proliferation and anchor-independent growth, and a knockdown of the LINE-1 protein level by siRNA reduced the proliferation and anchorindependent growth ability of LoVo cells. In vivo data revealed that LINE-1 ORF-1p overexpression increased LoVo tumor growth in nude mice, whereas the siRNA knockdown of endogenous LINE-1 ORF-1p expression decreased LoVo cell growth in nude mice. Therefore, LINE-1 ORF-1p could promote LoVo cell proliferation and invasion both in vitro and in vivo, indicating that it might be a useful molecular target for the treatment of human colorectal cancer.

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Section: Discussionmentioning

confidence: 99%

“…Then, 500 cells per well were plated on a 6-well plate, with a bottom layer of 0.7% low melting temperature agar in DMEM and a top layer of 0.25% agar in DMEM. Colonies were scored after 3-4 weeks of growth (Reid et al, 2003;Chen et al, 2005;Hu et al, 2010;Zhang et al, 2012).…”

Section: Soft Agar Colony Analysismentioning

confidence: 99%

Long interspersed nucleotide acid element-1 ORF-1 protein promotes proliferation and invasion of human colorectal cancer LoVo cells through enhancing ETS-1 activity

Li¹,

Zhu²,

Feng³

et al. 2014

Genet. Mol. Res.

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“…For measuring proliferation, Caki-1 or 786-O cells, which were infected with Ad-control or Ad-MEIS1, were seeded in 96-well plates (Corning, NY, USA), incubated for 1, 2, 3 and 4 days, and the cells were analyzed for MTT assays [22]. HKC cells were transfected with siRNA of MEIS1 and then harvested for MTT analysis.…”

Section: Methodsmentioning

confidence: 99%

MEIS1 inhibits clear cell renal cell carcinoma cells proliferation and in vitro invasion or migration

Zhu

Cui

et al. 2017

BMC Cancer

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BackgroundMyeloid ecotropic viral integration site 1 (MEIS1) protein plays a synergistic causative role in acute myeloid leukemia (AML). However, MEIS1 has also shown to be a potential tumor suppressor in some other cancers, such as non-small-cell lung cancer (NSCLC) and prostate cancer. Although multiple roles of MEIS1 in cancer development and progression have been identified, there is an urgent demand to discover more functions of this molecule for further therapeutic design.MethodsMEIS1 was overexpressed via adenovirus vector in clear cell renal cell carcinoma (ccRCC) cells. Western blot and real-time qPCR (quantitative Polymerase Chain Reaction) was performed to examine the protein and mRNA levels of MEIS1. Cell proliferation, survival, in vitro migration and invasion were tested by MTT, colony formation, soft-agar, transwell (in vitro invasion/migration) assays, and tumor in vivo growthwas measured on nude mice model. In addition, flow-cytometry analysis was used to detect cell cycle arrest or non-apoptotic cell death of ccRCC cells induced by MEIS1.ResultsMEIS1 exhibits a decreased expression in ccRCC cell lines than that in non-tumor cell lines. MEIS1 overexpression inhibits ccRCC cells proliferation and induces G1/S arrest concomitant with marked reduction of G1/S transition regulators, Cyclin D1 and Cyclin A. Moreover, MEIS1-1 overexpression also induces non-apoptotic cell death of ccRCC cells via decreasing the levels of pro-survival regulators Survivin and BCL-2. Transwell migration assay (TMA) shows that MEIS1 attenuates in vitro invasion and migration of ccRCC cells with down-regulated epithelial-mesenchymal transition (EMT) process. Further, in nude mice model, MEIS1 inhibits the in vivo growth of Caki-1 cells.ConclusionsBy investigating the role of MEIS1 in ccRCC cells’ survival, proliferation, anchorage-independent growth, cell cycle progress, apoptosis and metastasis, in the present work, we propose that MEIS1 may play an important role in clear cell renal cell carcinoma (ccRCC) development.

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“…Transfections were performed by the Lipofectamine 2000 agent (Invitrogen, Carlsbad, CA). Cells were co-transfected with Luciferase reporters and harvested for the luciferase and β-galactosidase activities analysis [18], [19]. The luciferase assays were performed for three independent times with similar results.…”

Section: Methodsmentioning

confidence: 99%

“…Then, cells (500 per well) were plated on 6-well plates (corning, NY, USA), with a bottom layer of 0.7% low-melting-temperature agar in DMEM and a top layer of 0.25% agar in DMEM. Colonies number are the mean ± SE of three independent experiments scored after 3–4 weeks of growth [19].…”

Section: Methodsmentioning

confidence: 99%

FBI-1 Enhances ETS-1 Signaling Activity and Promotes Proliferation of Human Colorectal Carcinoma Cells

Zhu

Zhang

et al. 2014

PLoS ONE

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In this study, we investigated a potential regulatory role of FBI-1 in transcription factor activity of ETS-1. The protein interaction was identified between ETS-1 and FBI-1 in lovo cells. The accumulating data showed that FBI-1 promoted the recruitment of ETS-1 to endogenous promoter of its target genes and increase ETS-1 accumulation in the nuclear. Our work also indicated that the FBI-1 enhances ETS-1 transcription factor activity via down-regulating p53-mediated inhibition on ETS-1. Further, FBI-1 plays a role in regulation of colorectal carcinoma cells proliferation. These findings supported that FBI-1 might be a potential molecule target for treating colorectal carcinoma.

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Four-and-a-half-LIM protein 1 down-regulates estrogen receptor α activity through repression of AKT phosphorylation in human breast cancer cell

Cited by 34 publications

References 23 publications

Long interspersed nucleotide acid element-1 ORF-1 protein promotes proliferation and invasion of human colorectal cancer LoVo cells through enhancing ETS-1 activity

Long interspersed nucleotide acid element-1 ORF-1 protein promotes proliferation and invasion of human colorectal cancer LoVo cells through enhancing ETS-1 activity

MEIS1 inhibits clear cell renal cell carcinoma cells proliferation and in vitro invasion or migration

FBI-1 Enhances ETS-1 Signaling Activity and Promotes Proliferation of Human Colorectal Carcinoma Cells

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