Ask about this productRelated genes to: RASSF6 antibody
- Gene:
- RASSF6 NIH gene
- Name:
- Ras association domain family member 6
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 4q13.3
- Locus Type:
- gene with protein product
- Date approved:
- 2003-04-24
- Date modifiied:
- 2016-10-05
Related products to: RASSF6 antibody
Related articles to: RASSF6 antibody
- Colorectal cancer (CRC) exhibits substantial molecular heterogeneity, yet detailed single-cell transcriptomic data from Japanese patients remain limited. Here, we performed single-cell RNA sequencing (scRNA-seq) on tumor tissues and adjacent normal tissues from four Japanese CRC patients to characterize malignant cell populations. We identified a common cancer-associated cell cluster observed across all four cases, characterized by high expression of the long noncoding RNA KCNQ1 opposite strand/antisense transcript 1 (KCNQ1OT1). Further analysis revealed a marked decrease in Ras Association Domain Family Member 6 (RASSF6) expression within this cluster, despite clinical datasets reporting that elevated RASSF6 expression correlates with poor overall survival in Western cohorts. Reanalysis of publicly available bulk RNA-seq data from independent East Asian cohorts confirmed that RASSF6 expression was consistently reduced in tumor tissues compared with adjacent normal colon tissues, while KCNQ1OT1 expression showed no apparent differences across cohorts. Collectively, our single-cell analysis delineates a recurrent cancer-associated transcriptional state observed within this cohort and highlights distinct gene expression features that may be underappreciated by bulk or population-averaged analyses, underscoring the value of single-cell profiling for refining molecular interpretations of CRC. - Source: PubMed
Publication date: 2026/03/02
Iwabuchi SadahiroSawada KentaroKojima MotohiroOzawa MihoTaniguchi HiroyaBando HideakiAbe KazumiKuze YutaImamura KiyomiKashima YukieHirohashi YoshihikoTajima AtsushiTorigoe ToshihikoSuzuki YutakaYoshino TakayukiHashimoto Shinichi - Pseudorabies virus (PRV), a zoonotic swine alphaherpesvirus, poses a severe threat to global pig production and public health. - Source: PubMed
Publication date: 2025/11/30
Shu XianghuaSun YalongWang ShanqiangYang DayongLi XingZhang YingSong Chunlian - : Breast cancer represents a diverse group of malignancies and continues to rank among the leading causes of cancer-related deaths in women. Altered Hippo pathway signaling has been increasingly recognized as a contributor to tumor growth, therapeutic resistance, and metastatic spread. This study aimed to identify miRNAs targeting Hippo pathway-related genes that are consistently dysregulated across all five breast cancer subtypes. : The study cohort included patients representing five breast cancer subtypes: 130 luminal A, 96 HER2-positive luminal B, 100 HER2-negative luminal B, 36 non-luminal HER2-positive, and 43 triple-negative breast cancer (TNBC). Tumor samples were collected during surgery, along with adjacent healthy tissue that served as controls. Expression of Hippo-related genes was analyzed using mRNA microarrays and validated with reverse transcription quantitative polymerase chain reaction (RT-qPCR). Protein levels were assessed via enzyme-linked immunosorbent assay (ELISA), while miRNA expression profiling was performed with miRNA microarrays. Potential mRNA targets were predicted using the miRDB database. : We identified consistent downregulation of , , and , alongside overexpression of and . miRNA analysis revealed that is potentially regulated by miR-522-3p, by miR-199b-5p and miR-30a-3p, whereas , , and appeared to be predominantly regulated at the transcriptional level. These alterations reflect both the suppression of upstream Hippo activation and activation of downstream oncogenic effectors across all subtypes. : Our findings reveal a conserved Hippo dysregulation program in breast cancer, highlighting subtype-independent Hippo-related genes and their miRNA regulators as potential universal biomarkers and therapeutic targets, complementing subtype-specific treatment strategies. - Source: PubMed
Publication date: 2025/09/25
Król-Jatręga KatarzynaMitka-Krysiak ElżbietaBoroń KacperZmarzły NikolaOssowski PiotrPlata-Babula AleksandraOrdon PawełKulej WojciechSirek TomaszGajdeczka JuliaPrudnikov YuriyBereza KrzysztofNowotny-Czupryna OlgaBoroń DariuszGrabarek Beniamin Oskar - Periodontitis, a chronic inflammatory disease of periodontal tissues, is linked to immune response and epigenetic modifications, with DNA methylation playing a crucial role. This study integrates transcriptomic and DNA methylation profiles from periodontitis patients to explore the immune microenvironment and identify potential biomarkers and therapeutic targets. - Source: PubMed
Publication date: 2025/10/10
Jin LingYuan Zhong-ZhengLiu Yin - The neurodevelopmental toxicity of bisphenol A (BPA) and its substitutes has garnered significant attention. However, the association between two widely detected environmental contaminants-BPAF and BPB-and adolescent depression, along with their underlying mechanisms, remain largely unclear. Here, we established a prenatal BPB/BPAF exposure animal model and demonstrated that such exposure induces depression- and anxiety-like behaviors in weanling male offspring. Through RNA sequencing of cortical tissues, combined with screening of depression-associated transcription factors (TFs), functional enrichment analysis of target genes, and identification of hub genes, we revealed that BPB and BPAF drive disease progression via distinct transcriptional regulatory networks and biological processes. Specifically, BPB significantly downregulate the TFs Lhx8 and Foxp1, targeting hub genes (e.g., Alb, Apoa1, Apoa2, Fga, Serpina1b, Fos, Rassf6, Rassf10, Rassf7, Moap1) to disrupt neuropeptide-, synapse-, transcription- related biological processes. In contrast, BPAF significantly upregulate the TF Neurod1, which modulate hub genes (e.g., Rpl26, Mrpl3,Rpl35, Mrpl1, Kcnd3) involved in neuronal cell body and cerebral cortex development. Molecular docking further confirmed potential binding interactions between BPB and Lhx8/ Foxp1, as well as BPAF and Neurod1, mediated by hydrogen bonding or hydrophobic interactions. These findings demonstrate that BPB and BPAF induce depression-like behavior in male offspring through compound-specific disruption of transcriptional networks, which alter neurodevelopmental pathways, potentially due to their divergent binding affinities to distinct TFs. This research offers new perspectives on the neurodevelopmental toxicity associated with BPA alternatives, offering critical implications for risk assessment and therapeutic targeting of BPAF/BPB-related neuropsychiatric disorders. - Source: PubMed
Publication date: 2025/09/11
Chen NannanLiu YuetongZhouguo YiranCai XueyiPan XinyiGuo RuiYan Wei