PRDM16 is associated with evasion of apoptosis by prostatic cancer cells according to RNA interference screening

Zhu, Shuchai; Xu, Yipeng; Song, Mei; Chen, Guiping; Wang, Hua; Zhao, Yang; Wang, Zongping; Li, Fangyin

doi:10.3892/mmr.2016.5605

Cited by 41 publications

(28 citation statements)

References 18 publications

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“…Commonly altered genes in the promoter region included PYCR1 and SHARPIN, which are known to be upregulated in PCa tissue and involved in processes such as proliferation and angiogenesis (55). Gene body methylation changes were observed in genes that regulate various tumorigenic processes, including NFATC1 (47) , PRDM16 (56), and OPCML (57). Pathway analysis also further highlighted key mechanisms that have been established in prostate tumor tissue studies, including the wnt pathway (16).…”

Section: Discussionmentioning

confidence: 99%

Dynamics of the cell-free DNA methylome of metastatic prostate cancer during androgen-targeting treatment

Peter

Bilenky

Isserlin

et al. 2020

Preprint

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27Aim: We examined methylation changes in cell-free DNA (cfDNA) in metastatic castration 28 resistant prostate cancer (mCRPC) during treatment. Materials and Methods: Genome-wide 29 methylation analysis of sequentially collected cfDNA samples derived from mCRPC patients 30 undergoing androgen-targeting therapy was performed. Results: Alterations in methylation 31 states previously implicated in prostate cancer progression were observed and patients that 32 maintained methylation changes throughout therapy tended to have a longer time to clinical 33 progression (TTP). Importantly, we also report that markers associated with a highly aggressive 34 form of the disease, Neuroendocrine-CRPC, were associated with a faster TTP. Conclusion: Our 35

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Section: Discussionmentioning

confidence: 99%

Dynamics of the cell-free DNA methylome of metastatic prostate cancer during androgen-targeting treatment

Peter

Bilenky

Isserlin

et al. 2020

Preprint

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“…PRDM3 (MDS1‐EVI1) is critical for the initiation and progression of MLL‐AF9‐induced AML. In prostatic cancers, PRDM16S (MEL1S) is overexpressed and has an antiapoptotic function …”

Section: Introductionmentioning

confidence: 99%

“…In prostatic cancers, PRDM16S (MEL1S) is overexpressed and has an antiapoptotic function. [5][6][7][8][9] PRDM5 (or PFM2) is a recently identified member of the PRDM protein family and is located at human chromosome region 4q26, which harbors many tumor suppressor genes active in several cancers. 10 PRDM5 participates in inducing committed murine blood cells to differentiate into hematopoietic stem cells and modulates the transcription of a subset of developmental regulators during mouse embryonic stem cell differentiation.…”

Section: Introductionmentioning

confidence: 99%

Overexpression of PRDM5 promotes acute myeloid leukemia cell proliferation and migration by activating the JNK pathway

Zhou¹,

Chen²,

et al. 2019

Cancer Medicine

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PRDM family proteins are dysregulated in many human diseases, especially hematological malignancies and solid cancers, and share a unique N‐terminal PR domain followed by zinc fingers toward the C terminus. With a high frequency of DNA promoter hypermethylation, PRDM5 is primarily considered as a tumor suppressor in solid tumors. However, little is known about the function of PRDM5 in blood malignancies, especially acute myeloid leukemia (AML). In this study, we showed that high PRDM5 expression levels were independently correlated with poor overall survival in AML patients. PRDM5 overexpression promoted cell proliferation, colony formation, and migration in vitro and enhanced tumorigenesis in an in vivo xenograft model. Furthermore, we found that PRDM5 overexpression promoted cell cycle progression with the decreased level of cell cycle inhibitors such as p16 and p21, and regulated the expression of epithelial‐mesenchymal transition markers ZO‐1 and Vimentin to promote migration. Moreover, we observed that PRDM5 upregulated the Jun N‐terminal kinase (JNK) signaling pathway and downregulated c‐Myc expression. Pharmacological inhibition of JNK by SP600125 partially abrogated PRDM5‐induced cell proliferation and migration. Taken together, our findings demonstrate that PRDM5 functions as an oncogenic driver in AML via JNK pathway, suggesting that PRDM5 is a potential therapeutic target for AML.

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“…However, another report failed to identify these sites as SETD4 substrates, and instead suggested H3K4 as the substrate of SETD4 in macrophages (36). Emerging evidence suggests that SETD4 may have an oncogenic activity (37)(38)(39). According to the TCGA database, oncogenic fusion of SETD4 was found to be with TMPRSS2 in prostate cancer, with FTCD in invasive ductal carcinoma, with KIAA1958 in serous ovarian cancer, and with B4Galt6 in lung squamous cancer.…”

Section: Introductionmentioning

confidence: 99%

Deletion of mouseSetd4promotes the recovery of hematopoietic failure

Feng

Yue

et al. 2019

Preprint

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Key points:• Deletion of Setd4 in adult mice improved the survival from hematopoietic failure.• Setd4 deficiency sensitized HSCs to radiation, but improved bone marrow environment niche.• The study suggests that SETD4 as a potential inhibitory target to improve bone marrow niche function for recovery of bone marrow failure.Abstract: Acquired hematopoietic failure is commonly caused by therapeutic and accidental exposure to toxic agents to the bone marrow (BM). Efficient recovery from the BM failure is not only dictated by the intrinsic sensitivity and proliferation capacity of the hematopoietic stem and progenitor cells, but also nourished by the BM environment niche. Identification of genetic factors that improve the recovery from hematopoietic failure is essential. Vertebrate SETD4 is a poorly characterized, putative non-histone methyl-transferase whose physiological substrates have not yet been fully identified. By inducing Setd4 deletion in adult mice, we found that loss of Setd4 improved the survival of whole body irradiation induced BM failure. This was associated with improved recoveries of long-term and short-term hematopoietic stem cells (HSC), and early progenitor cells. BM transplantation analyses surprisingly showed that the improved recovery was not due to a radiation resistance of the Setd4 deficient HSC, but that Setd4 deficient HSC were actually more sensitive to radiation. However, the Setd4 deficient mice were better recipients for allogeneic HSC transplantation. Furthermore, there was an enhanced splenic erythropoiesis in Setd4 deficient mice. These findings not only revealed a previously unrecognized role of the Setd4 as a unique modulator of hematopoiesis, but also underscored the critical role of the BM niche in the recovery of hematopoietic failure. These studies also implicated Setd4 as a potential target for therapeutic inhibition to improve the conditioning of the BM niche prior to allogeneic transplantation. Authorship Contributions: XF and ZS: designed the experiments, performed data analysis, and drafted the initial versions of manuscript. XF: performed most of the experiments; HL, JL, and MS: performed and assisted with some of the experiments. HL, and JY: performed some of the early studies led to the construction of the mouse models; LD, and SD: provided resources for some experiments, computational analysis, and edited the manuscript. ZS: directed and oversaw the project, secured funding for the study, completed the final version of the manuscript. Conflict of Interest statement:The authors declare that there were no competing interests.

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PRDM16 is associated with evasion of apoptosis by prostatic cancer cells according to RNA interference screening

Cited by 41 publications

References 18 publications

Dynamics of the cell-free DNA methylome of metastatic prostate cancer during androgen-targeting treatment

Dynamics of the cell-free DNA methylome of metastatic prostate cancer during androgen-targeting treatment

Overexpression of PRDM5 promotes acute myeloid leukemia cell proliferation and migration by activating the JNK pathway

Deletion of mouseSetd4promotes the recovery of hematopoietic failure

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