Androgen receptor and osteoglycin gene expression predicting prognosis of metastatic prostate cancer.

This study aimed to identify the predictive factors associated with the oncological outcomes of metastatic hormone-sensitive prostate cancer-related genes. A nomogram for predicting prostate cancer-specific survival (CSS) was constructed based on biopsy samples obtained from 103 patients with metastatic hormone-sensitive prostate cancer. We analyzed the association between clinical data and mRNA expression levels.

Inhibition of PSF activity overcomes resistance to treatment in cancers harboring mutant p53.

Mutations in the TP53 tumor suppressor genes are prevalent in aggressive cancers. Pharmacological reactivation of dysfunctional p53 due to mutations is a promising strategy for treating such cancers. Recently, a multifunctional proline- and glutamine-rich protein, PTB-associated splicing factor (PSF), was identified as a key driver of aggressive cancers.

Anillin actin-binding protein expression correlates with poor prognosis for prostate cancer patients.

Objective: Octamer transcription factor 1 (OCT1), a transcription factor that interacts with androgen receptor, is involved in prostate cancer (PCa) progression. The OCT1 target gene, Anillin actin-binding protein (), is highly expressed in castration-resistant PCa tissue; however, it remains unclear whether ANLN expression in hormone-sensitive PCa tissue could be used as a predictive biomarker for poor prognosis of patients. We aimed to investigate ANLN expression in PCa tissue obtained via radical prostatectomy and its correlation with clinical parameters.

ERRα and ERRγ coordinate expression of genes associated with Alzheimer's disease, inhibiting to suppress tau phosphorylation.

Alzheimer's disease (AD) is a prevalent neurodegenerative disease characterized by cognitive decline and learning/memory impairment associated with neuronal cell loss. Estrogen-related receptor α (ERRα) and ERRγ, which are highly expressed in the brain, have emerged as potential AD regulators, with unelucidated underlying mechanisms. Here, we identified genome-wide binding sites for ERRα and ERRγ in human neuronal cells.

Identification of DNA damage response-related genes as biomarkers for castration-resistant prostate cancer.

Although hormone therapy is effective for the treatment of prostate cancer (Pca), many patients develop a lethal type of Pca called castration-resistant prostate cancer (CRPC). Dysregulation of DNA damage response (DDR)-related genes leads to Pca progression. Here, we explored DDR-related signals upregulated in CRPC tissues.

Expression and function of estrogen receptors and estrogen-related receptors in the brain and their association with Alzheimer's disease.

While estrogens are well known for their pivotal role in the female reproductive system, they also play a crucial function in regulating physiological processes associated with learning and memory in the brain. Moreover, they have neuroprotective effects in the pathogenesis of Alzheimer's disease (AD). Importantly, AD has a higher incidence in older and postmenopausal women than in men, and estrogen treatment might reduce the risk of AD in these women.

Identification of small-molecule inhibitors against the interaction of RNA-binding protein PSF and its target RNA for cancer treatment.

Diverse cellular activities are modulated through a variety of RNAs, including long noncoding RNAs (lncRNAs), by binding to certain proteins. The inhibition of oncogenic proteins or RNAs is expected to suppress cancer cell proliferation. We have previously demonstrated that PSF interaction with its target RNAs, such as androgen-induced lncRNA , is critical for hormone therapy resistance in prostate and breast cancers.

Stress granules sequester Alzheimer's disease-associated gene transcripts and regulate disease-related neuronal proteostasis.

Environmental and physiological stresses can accelerate Alzheimer's disease (AD) pathogenesis. Under stress, a cytoplasmic membraneless structure termed a stress granule (SG) is formed and is associated with various neurodegenerative disorders, including AD. SGs contain translationally arrested mRNAs, suggesting that impaired RNA metabolism in neurons causes AD progression; however, the underlying mechanism remains unclear.

Ribonuclease H2 Subunit A Preserves Genomic Integrity and Promotes Prostate Cancer Progression.

Unlabelled: Homeostasis of genomic integrity should be regulated to promote proliferation and inhibit DNA damage-induced cell death in cancer. Ribonuclease H2 (RNase H2) maintains genome stability by controlling DNA:RNA hybrid and R-loop levels. Here, we identified that RNase H2 subunit A (RNASEH2A), a component of RNase H2, is highly expressed in castration-resistant prostate cancer (CRPC) tissues compared with localized prostate cancer.

Targeting phase separation on enhancers induced by transcription factor complex formations as a new strategy for treating drug-resistant cancers.

The limited options for treating patients with drug-resistant cancers have emphasized the need to identify alternative treatment targets. Tumor cells have large super-enhancers (SEs) in the vicinity of important oncogenes for activation. The physical process of liquid-liquid phase separation (LLPS) contributes to the assembly of several membrane-less organelles in mammalian cells.

Antitumor effects of pyrrole-imidazole polyamide modified with alkylating agent on prostate cancer cells.

Androgens and androgen receptor (AR) have a central role in prostate cancer progression by regulating its downstream signaling. Although androgen depletion therapy (ADT) is the primary treatment for most prostate cancers, they acquires resistance to ADT and become castration resistant prostate cancers (CRPC). AR complex formation with multiple transcription factors is important for enhancer activity and transcriptional regulation, which can contribute to cancer progression and resistance to ADT.

Transcriptional and Post-Transcriptional Regulations of Amyloid-β Precursor Protein APP mRNA.

Alzheimer's disease (AD) is an age-associated neurodegenerative disorder characterized by progressive impairment of memory, thinking, behavior, and dementia. Based on ample evidence showing neurotoxicity of amyloid-β (Aβ) aggregates in AD, proteolytically derived from amyloid precursor protein (APP), it has been assumed that misfolding of Aβ plays a crucial role in the AD pathogenesis. Additionally, extra copies of the gene caused by chromosomal duplication in patients with Down syndrome can promote AD pathogenesis, indicating the pathological involvement of the gene dose in AD.

Subtype-specific collaborative transcription factor networks are promoted by OCT4 in the progression of prostate cancer.

Interactive networks of transcription factors (TFs) have critical roles in epigenetic and gene regulation for cancer progression. It is required to clarify underlying mechanisms for transcriptional activation through concerted efforts of TFs. Here, we show the essential role of disease phase-specific TF collaboration changes in advanced prostate cancer (PC).

Targeting Epigenetic and Posttranscriptional Gene Regulation by PSF Impairs Hormone Therapy-Refractory Cancer Growth.

RNA-binding protein PSF functions as an epigenetic modifier by interacting with long noncoding RNAs and the corepressor complex. PSF also promotes RNA splicing events to enhance oncogenic signals. In this study, we conducted an chemical array screen and identified multiple small molecules that interact with PSF.

Identification of long non-coding RNAs in advanced prostate cancer associated with androgen receptor splicing factors.

The molecular and cellular mechanisms of development of castration-resistant prostate cancer (CRPC) remain elusive. Here, we analyzed the comprehensive and unbiased expression profiles of both protein-coding and long non-coding RNAs (lncRNAs) using RNA-sequencing to reveal the clinically relevant molecular signatures in CRPC tissues. For protein-coding genes upregulated in CRPC, we found that mitochondria-associated pathway, androgen receptor (AR), and spliceosome associated genes were enriched.