ArticleMicroarrays (Basel, Switzerland)2016
Small-Molecule Inhibition of Rho/MKL/SRF Transcription in Prostate Cancer Cells: Modulation of Cell Cycle, ER Stress, and Metastasis Gene Networks.
Article in Microarrays (Basel, Switzerland), 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
17 citing papers in PubMed, 27 citations in OpenAlex.
- A novel function of RHOA as a host-dependent factor in Glaesserella parasuis infection of LLC-PK1 cells.Veterinary research · 2025Article
- Pirin does not bind to p65 or regulate NFκB-dependent gene expression but does modulate cellular quercetin levels.Molecular pharmacology · 2025Article
- Pirin does not bind to p65 or regulate NFκB-dependent gene expression but does modulate cellular quercetin levels.bioRxiv : the preprint server for biology · 2024Article
- Transcriptional profiling of rare acantholytic disorders suggests common mechanisms of pathogenesis.JCI insight · 2023Article
- The endoplasmic reticulum stress response in prostate cancer.Nature reviews. Urology · 2022Review
- 'Cloudbuster': a Python-based open source application for three-dimensional reconstruction and quantification of stacked biological imaging samples.Interface focus · 2022Article
- Underappreciated roles for Rho GDP dissociation inhibitors (RhoGDIs) in cell function: Lessons learned from the pancreatic islet β-cell.Biochemical pharmacology · 2022Review
- Article
- Gene expression profile identifies distinct molecular subtypes and potential therapeutic genes in Merkel cell carcinoma.Translational oncology · 2020Article
- Splice switching an oncogenic ratio of SmgGDS isoforms as a strategy to diminish malignancy.Proceedings of the National Academy of Sciences of the United States of America · 2020Article
- MKL1 Mediates TGF-β Induced RhoJ Transcription to Promote Breast Cancer Cell Migration and Invasion.Frontiers in cell and developmental biology · 2020Article
- Identification of Pirin as a Molecular Target of the CCG-1423/CCG-203971 Series of Antifibrotic and Antimetastatic Compounds.ACS pharmacology & translational science · 2019Article
- SRF'ing and SAP'ing - the role of MRTF proteins in cell migration.Journal of cell science · 2018Review
- Pharmacological intervention of MKL/SRF signaling by CCG-1423 impedes endothelial cell migration and angiogenesis.Angiogenesis · 2017Article
- The prognostic utility of the transcription factor SRF in docetaxel-resistant prostate cancer: in-vitro discovery and in-vivo validation.BMC cancer · 2017Article
- Pharmacological Inhibition of Myocardin-related Transcription Factor Pathway Blocks Lung Metastases of RhoC-Overexpressing Melanoma.Molecular cancer therapeutics · 2017Article
- SRF inhibitors reduce prostate cancer cell proliferation through cell cycle arrest in an isogenic model of castrate-resistant prostate cancer.Cell cycle (Georgetown, Tex.)Article
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
Abstract
Metastasis is the major cause of cancer deaths and control of gene transcription has emerged as a critical contributing factor. RhoA- and RhoC-induced gene transcription via the actin-regulated transcriptional co-activator megakaryocytic leukemia (MKL) and serum response factor (SRF) drive metastasis in breast cancer and melanoma. We recently identified a compound, CCG-1423, which blocks Rho/MKL/SRF-mediated transcription and inhibits PC-3 prostate cancer cell invasion. Here, we undertook a genome-wide expression study in PC-3 cells to explore the mechanism and function of this compound. There was significant overlap in the genes modulated by CCG-1423 and Latrunculin B (Lat B), which blocks the Rho/MKL/SRF pathway by preventing actin polymerization. In contrast, the general transcription inhibitor 5,6-dichloro-1-β-d-ribofuranosyl-1H-benzimidazole (DRB) showed a markedly different pattern. Effects of CCG-1423 and Lat B on gene expression correlated with literature studies of MKL knock-down. Gene sets involved in DNA synthesis and repair, G1/S transition, and apoptosis were modulated by CCG-1423. It also upregulated genes involved in endoplasmic reticulum stress. Targets of the known Rho target transcription factor family E2F and genes related to melanoma progression and metastasis were strongly suppressed by CCG-1423. These results confirm the ability of our compound to inhibit expression of numerous Rho/MKL-dependent genes and show effects on stress pathways as well. This suggests a novel approach to targeting aggressive cancers and metastasis.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.