Ask about this productRelated genes to: PFDN4 antibody
- Gene:
- PFDN4 NIH gene
- Name:
- prefoldin subunit 4
- Previous symbol:
- -
- Synonyms:
- PFD4, C-1, C1
- Chromosome:
- 20q13.2
- Locus Type:
- gene with protein product
- Date approved:
- 1998-08-06
- Date modifiied:
- 2014-11-19
Related products to: PFDN4 antibody
Related articles to: PFDN4 antibody
- Stomach adenocarcinoma (STAD) is the most common gastrointestinal cancer. A clear diagnosis and molecular targeted therapy have important implications for prolonging survival of patients. RAD51 is the central catalyst of homologous recombination that plays important role in maintaining genomic integrity. However, the clinical significance of RAD51 expression in STAD patients remains unclear. This study aimed to assess the association of RAD51 expression with clinicopathological characteristics and patient outcomes. - Source: PubMed
Publication date: 2025/04/11
Jian BaiyuZhang HaoFan LiLi YangWu NanWang NingningLi LingminLi XueyanGe PenglingNiu YingcaiLiu Jicheng - PFDN4, a subunit of the prefoldin complex, has been previously shown to be upregulated in breast and colorectal cancers, where its expression correlates with poor clinical outcomes. This study investigates PFDN4 expression across various cancer types, with a specific focus on its role in hepatocellular carcinoma (HCC) development and progression. Analysis of TCGA data revealed that PFDN4 is highly expressed in several cancers and is associated with poor prognosis. Further validation through multiple databases, tissue microarrays, and clinical samples confirmed that PFDN4 protein levels are significantly elevated in HCC tissues. Meanwhile, multiple database multivariate and univariate Cox regression analyses suggest that PFDN4 is an independent prognostic marker for HCC. To evaluate the functional effects of PFDN4, we established stable HCC cell lines with PFDN4 knockdown and overexpression. Using CCK-8, EdU, wound healing, and Transwell assays, we found that PFDN4 knockdown significantly suppressed cell proliferation, migration, and invasion, while its overexpression enhanced these behaviors. These findings were further validated in vivo. Mechanistically, transcriptome sequencing suggested that PFDN4 modulates HCC cell behavior through the MAPK/ERK signaling pathway, a result confirmed by Western blot and the use of the MAPK/ERK inhibitor SCH772984. Additionally, single-cell RNA sequencing data revealed that PFDN4 is primarily expressed in several immune cell types, including B cells, CD8 + Tex, DC, ILC, mast cells, macrophages, Tprolif, and Treg. In conclusion, our study demonstrates that PFDN4 is upregulated in HCC and drives tumor progression via the MAPK/ERK pathway, highlighting its potential as both a prognostic marker and therapeutic target for HCC. - Source: PubMed
Publication date: 2024/12/06
Ye JingWang JianguoLiu RongqiangChen ChenWang Weixing - Cerebral cavernous malformations (CCMs) are vascular abnormalities associated with deregulated angiogenesis. Their pathogenesis and optimal treatment remain unclear. This study aims to investigate the molecular signatures of cuproptosis, a newly identified type of cell death, associated with CCMs development. - Source: PubMed
Publication date: 2024/06/05
Chen ChengweiBao YutingJu SihanJiang ConglinZou XiangZhang XinChen Liang - Breast cancer is the most common malignancy and its incidence is increasing. It is currently mainly treated by clinical chemotherapy, but chemoresistance remains poorly understood. Prefolded proteins 4 (PFDN4) are molecular chaperone complexes that bind to newly synthesized polypeptides and allow them to fold correctly to stabilize protein formation. This study aimed to investigate the role of PFDN4 in chemotherapy resistance in breast cancer. Our study found that PFDN4 was highly expressed in breast cancer compared to normal tissues and was statistically significantly associated with stage, nodal status, subclasses (luminal, HER2 positive and triple negative), triple-negative subtype and disease-specific survival by TCGA database analysis. CRISPR knockout of PFDN4 inhibited the growth of 89% of breast cancer cell lines, and the triple-negative cell line exhibited a stronger inhibitory effect than the non-triple-negative cell line. High PFDN4 expression was associated with poor overall survival in chemotherapy and resistance to doxorubicin and paclitaxel through the CREBP1/AURKA pathway in the triple-negative MDAMB231 cell line. This study provides insightful evidence for the value of PFDN4 in poor prognosis and chemotherapy resistance in breast cancer patients. - Source: PubMed
Publication date: 2024/03/31
Wang Shih-HoYeh Cheng-HsiWu Chia-WeiHsu Chia-YiTsai Eing-MeiHung Chao-MingWang Yi-WenHsieh Tsung-Hua - The condition of hepatic fibrosis is hazardous. Therefore, it is vital that we investigate the mechanism of hepatic fibrosis to provide new targets for treatment. - Source: PubMed
Publication date: 2023/11/28
Shi LiuFeng GongYang XueliangZhang YangZhang YuCheng JunLin Shumei