MEIS1 functions as a potential AR negative regulator

Cui, Liang; Li, Mingyang; Feng, Fan; Yang, Yutao; Hang, Xingyi; Cui, Jiahuan; Gao, Jiangping

doi:10.1016/j.yexcr.2014.08.023

Cited by 27 publications

(29 citation statements)

References 33 publications

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“…Decreased expression of MEIS1 is predicted as worse overall survival (OS) while elevated level of MEIS1 was associated with improved OS in prostate cancer [3, 13]. Our previous work also indicated that MEIS1 functions as a negative AR regulator and inhibits the ligand-dependent growth of certain kinds of prostate cancer [16]. Based on the previous discovery of MEIS1, to further reveal its function and develop potential therapy in human cancer treatment are accessible.…”

Section: Discussionmentioning

confidence: 99%

“…The MEIS1 expression vector or its small interfering RNA (siRNA) was as previously described [16]. Adenovirus vectors of MEIS1 were generated following the methods as described by Niu et al [21].…”

Section: Methodsmentioning

confidence: 99%

“…Xu et al showed that MEIS1 would interact with Hox (homeobox protein family) and Pbx1 (pre-B-cell leukemia homeobox 1) [15]. Our previous work also indicated that MEIS1 is a negative regulator of androgen receptor (AR) pathway [16]. To unmask thorough roles by which MEIS1 affect cancer physiology, more studies should be done.…”

Section: Introductionmentioning

confidence: 99%

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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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Section: Discussionmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

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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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“…In PCa, MEIS1 functions to direct transcriptional specificity and activity of HOXB13 and act as a negative regulator of AR [20,45]. Therefore, we next determined whether HOXB13 expression or AR activity were altered in the context of MYC activity.…”

Section: Myc Negatively Regulates Meis1 Expressionmentioning

confidence: 99%

MEIS1 down-regulation by MYC mediates prostate cancer development through elevated HOXB13 expression and AR activity

Whitlock¹,

Trostel²,

Wilkinson³

et al. 2019

Preprint

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Localized prostate cancer develops very slowly in most men, with the androgen receptor (AR) and MYC transcription factors amongst the most well-characterized drivers of prostate tumorigenesis. Canonically, MYC up-regulation in luminal prostate cancer cells functions to oppose the terminally differentiating effects of AR. However, the effects of MYC up-regulation are pleiotropic and inconsistent with a poorly proliferative phenotype. Here we show that increased MYC expression and activity are associated with the down-regulation of MEIS1, a HOX-family transcription factor. Using RNA-seq to profile a series of human prostate cancer specimens laser capture microdissected on the basis of MYC immunohistochemistry, MYC activity and MEIS1 expression were inversely correlated. Knockdown of MYC expression in prostate cancer cells increased expression of MEIS1 and increased occupancy of MYC at the MEIS1 locus. Finally, we show in laser capture microdissected human prostate cancer samples and the prostate TCGA cohort that MEIS1 expression is inversely proportional to AR activity as well as HOXB13, a known interacting protein of both AR and MEIS1. Collectively, our data demonstrate that elevated MYC in a subset of primary prostate cancers functions in a negative role in regulating MEIS1 expression, and that this down-regulation may contribute to MYC-driven development and progression.

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“…The homeodomain protein Meis1 is a three amino acid loop extension transcription factor, which participates in various physiological processes, including growth, proliferation and prevention of the accumulation of reactive oxygen species (16). Specifically, the Meis1/pre-B-cell leukemia homeobox 1/homeobox A9 complex is able to activate oncogenic genes, resulting in cell hyperproliferation (17).…”

Section: Introductionmentioning

confidence: 99%

Cardioprotective potential of Dendrobium officinale Kimura et Migo against myocardial ischemia in mice

Dou

Zhang

et al. 2016

Molecular Medicine Reports

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Dendrobium officinale Kimura et Migo has been used for thousands of years to promote body fluid production; however, little is currently known regarding its effects on the heart. The present study aimed to explore the cardioprotective potential of the water extract of Dendrobium officinale Kimura et Migo (DOE) on myocardial ischemia in mice. A mouse model of myocardial ischemia was induced following ligation of the left anterior descending coronary artery. Prior to the operation, mice were administered a vehicle or DOE for 2 weeks. Following the operation, ST elevation was measured. To estimate the extent of myocardial damage, infarct size analysis and histopathological examination were performed. The activities of cardiac marker enzymes [creatine kinase (CK)-MB and lactate dehydrogenase (LDH)] and antioxidative indicators [malondialdehyde (MDA) and superoxide dismutase (SOD)] were also analyzed to explore the underlying mechanisms. Treatment with DOE decreased infarct size and the number of apoptotic cardiomyocytes; reduced serum CK-MB, LDH and MDA activities; and increased SOD levels. According to western blotting, DOE conferred protection against myocardial ischemic injury via the regulation of Meis1 expression. These results indicated that DOE may exert potential cardioprotective effects against myocardial ischemia; these effects may be associated with its antioxidant activity, and its ability to inhibit cardiac cell apoptosis and to regulate Meis1 expression.

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MEIS1 functions as a potential AR negative regulator

Cited by 27 publications

References 33 publications

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

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

MEIS1 down-regulation by MYC mediates prostate cancer development through elevated HOXB13 expression and AR activity

Cardioprotective potential of Dendrobium officinale Kimura et Migo against myocardial ischemia in mice

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