Role of the runt‐related transcription factor (RUNX) family in prostate cancer

Ashe, Hannah; Krakowiak, Patryk; Hasterok, Sylwia; Sleppy, Rosalie; Roller, Devin G.; Gioeli, Daniel

doi:10.1111/febs.15804

Cited by 12 publications

(7 citation statements)

References 82 publications

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“…To expand on this observation, we performed CRISPR-Cas9 mediated RUNX1-KO in another T-ALL cell line (Jurkat), AML (HL60) and prostate adenocarcinoma (DU145) cell lines, contexts where increased RUNX1 expression is associated with disease progression. 30 , 31 , 32 Consistent with the KOPTK1 observations, RUNX1-KO led to ∼50% reduction of H3K27ac levels in all three cell lines ( Figures 1 H and S3 A–S3D) suggesting that RUNX1 associated loss of genome-wide H3K27ac density may be generalizable across cancer types.…”

Section: Resultssupporting

confidence: 81%

RUNX1 colludes with NOTCH1 to reprogram chromatin in T cell acute lymphoblastic leukemia

et al. 2023

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Section: Resultssupporting

confidence: 81%

RUNX1 colludes with NOTCH1 to reprogram chromatin in T cell acute lymphoblastic leukemia

et al. 2023

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“…RUNX2 has been shown to play an important role in mediating prostate cancer bone metastasis, especially in tumors with PTEN loss (Zhang et al, 2011). RUNX3 has a tumor suppressor role and its loss is associated with tumor progression (Ashe et al, 2021). Interestingly, the ABC transporter disorders pathway was also found up-regulated in the high-risk group predicted by signature 2, a biological process linked to chemoresistance and potentially worse survival in this group (Robey et al, 2018).…”

Section: Discussionmentioning

confidence: 99%

Multi-omics biomarkers aid prostate cancer prognostication

Omar

Benedetti

et al. 2022

Preprint

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Effective biomarkers and diagnostic tools are urgently needed in clinical settings for improved management of prostate cancer patients, especially to reduce over-treatment of indolent tumors and for early identification of aggressive disease. Gene expression signatures are currently the "gold standard" to provide guide clinical decision, however their clinical utility and interpretability is questionable. Multi-modal molecular profiling provides an holistic approach to systematically unravel the biological complexity underlying cancer pathogenesis, hence biomarkers developed using such an integrated approach hold the potential to more accurately capture cancer-driving alterations than signatures based on a single omics modality. Currently, however, robust and reproducible multi-omics biomarkers are still lacking for prostate cancer. In this study, we analyzed transcriptomics and metabolomics profiles jointly in a prostate cancer cohort and identified two prognostic signatures with high statistical powers (signature1: EGLN3, succinate, trans-4-hydroxyprolin; and signature2: IL6, SLC22A2, histamine). Our approach leveraged a priori biological knowledge of the cellular metabolism and gene circuitry, enabling the identification of dysregulated network modules. Functional bioinformatics analyses suggest that these signatures can capture relevant molecular alterations in prostate cancer tissues, including dysregulations of cellular signaling, cell cycle progression, and immune system modulation, stratifying patients in distinct risk groups. Next, we trained two gene expression signatures as a proxy for the multi-omics ones, extending our investigation to publicly available data, further confirming their prognostic values in independent patient cohorts. In summary, the analysis of multi-modal molecular grounded in cellular network biology represents a promising approach for the development of robust prognostic biomarkers of detecting and discriminating high grade disease.

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“…The CBFβ functions as a co-activator to RUNX, resulting in RUNX being relieved from its autoinhibited state, facilitating the CBF complex binding to DNA and regulation of target gene expression ( 97 ). In recent years, there has been growing recognition of RUNX transcription factors in promoting cell growth and metastatic potential of prostate cancer via matrix metalloproteinase signaling ( 24 ). Therefore, targeting such essential PPIs may disrupt the transcription process of oncogenic genes, resulting the anticarcinogenic effects.…”

Section: Exploiting Other Proteins In a Transcriptional Complexmentioning

confidence: 99%

Transcription Factors as Novel Therapeutic Targets and Drivers of Prostate Cancer Progression

2022

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Prostate cancer is the second most diagnosed cancer among men worldwide. Androgen deprivation therapy, the most common targeted therapeutic option, is circumvented as prostate cancer progresses from androgen dependent to castrate-resistant disease. Whilst the nuclear receptor transcription factor, androgen receptor, drives the growth of prostate tumor during initial stage of the disease, androgen resistance is associated with poorly differentiated prostate cancer. In the recent years, increased research has highlighted the aberrant transcriptional activities of a small number of transcription factors. Along with androgen receptors, dysregulation of these transcription factors contributes to both the poorly differentiated phenotypes of prostate cancer cells and the initiation and progression of prostate carcinoma. As master regulators of cell fate decisions, these transcription factors may provide opportunity for the development of novel therapeutic targets for the management of prostate cancer. Whilst some transcriptional regulators have previously been notoriously difficult to directly target, technological advances offer potential for the indirect therapeutic targeting of these transcription factors and the capacity to reprogram cancer cell phenotype. This mini review will discuss how recent advances in our understanding of transcriptional regulators and material science pave the way to utilize these regulatory molecules as therapeutic targets in prostate cancer.

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Role of the runt‐related transcription factor (RUNX) family in prostate cancer

Cited by 12 publications

References 82 publications

RUNX1 colludes with NOTCH1 to reprogram chromatin in T cell acute lymphoblastic leukemia

RUNX1 colludes with NOTCH1 to reprogram chromatin in T cell acute lymphoblastic leukemia

Multi-omics biomarkers aid prostate cancer prognostication

Transcription Factors as Novel Therapeutic Targets and Drivers of Prostate Cancer Progression

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