Ask about this productRelated genes to: PABPC5 antibody
- Gene:
- PABPC5 NIH gene
- Name:
- poly(A) binding protein cytoplasmic 5
- Previous symbol:
- -
- Synonyms:
- PABP5
- Chromosome:
- Xq21.31
- Locus Type:
- gene with protein product
- Date approved:
- 2002-02-14
- Date modifiied:
- 2016-10-05
Related products to: PABPC5 antibody
Related articles to: PABPC5 antibody
- Alternative splicing contributes to the carcinogenic process of non-small cell lung cancer. Although extensive efforts have characterized cancer-associated alternative splicing events, the upstream regulators governing these aberrant splicing events remain poorly understood. - Source: PubMed
Publication date: 2026/03/02
Yan YuMeng HuaGuo HuanWei ShengCheng Shanshan - Glioma, especially high-grade gliomas like glioblastoma, are aggressive and highly treatment-resistant brain tumors with poor prognosis. Despite advances in therapeutic strategies, the mechanisms driving glioma progression remain inadequately understood, with dysregulated apoptosis playing a central role in malignancy. RNA-binding proteins(RBPs) such as the poly(A)-binding protein family, including , have gained attention due to their roles in regulating mRNA stability and translation. ’s role in glioma pathogenesis remains poorly characterized despite its identification as a key regulator of the mitochondria-associated programmed cell death index (mtPCDI) in low-grade glioma (LGG). This study thoroughly investigated the oncogenic functions of . TCGA-GBM analysis revealed significant decreasing trend in expression with increasing glioma grade(G2 vs. G3: < 0.05; G2vsG4: < 0.0001;). However, immunohistochemistry and Western blotting demonstrated that PABPC5 protein levels were elevated in Grade 4 tumors compare to Grades 1–3. Notably, expression levels showed no correlation with overall survival ( = 0.92). Lentiviral infection of knockdown in glioblastoma cells (U87/U251) significantly suppressed malignant phenotypes while inducing pro-apoptotic molecular alterations: upregulated BAX and cleaved caspase−3 protein expression, enhanced ROS production, and reduced Bcl−2 and caspase−3 levels. In vivo validation showed that knocdown substantially inhibited subcutaneous tumor growth and increased apoptosis (TUNEL:3.164-fold increase, < 0.001). Consistent with in vitro findings, immunofluorescence(IF)analysis of tumor tissues confirmed altered Bcl−2/cleaved-caspase−3 expression patterns and mitochondrial ultrastructural changes. This work establishes PABPC5 as a novel biomarker for glioma pathological grading and reveals its functional role in apoptosis regulation. These findings provide a mechanistic foundation for developing therapeutic strategies targeting apoptosis-resistant glioma. - Source: PubMed
Publication date: 2026/01/30
Mujite AZheng YitongLiu WenLi YabinMa XiaohuHu BatuluLiu TengfeiSu WudeQin HuWang Yongxin - A 70-year-old man undergoing treatment for immunoglobulin G4-related disease developed a liver mass on computed tomography during routine imaging examination. The tumor was located in the hepatic S1/4 region, was 38 mm in size, and showed arterial enhancement on dynamic contrast-enhanced computed tomography. We performed a liver biopsy and diagnosed moderately differentiated hepatocellular carcinoma. The patient underwent proton beam therapy. The tumor remained unchanged but enlarged after 4 years. The patient was diagnosed with hepatocellular carcinoma recurrence and received hepatic arterial chemoembolization. However, 1 year later, the patient developed jaundice, and the liver tumor grew in size. Unfortunately, the patient passed away. Autopsy revealed that the tumor consisted of spindle-shaped cells exhibiting nuclear atypia and a fission pattern and tested positive for α-smooth muscle actin and vimentin. No hepatocellular carcinoma components were observed, and the patient was pathologically diagnosed with hepatic leiomyosarcoma. Next-generation sequencing revealed somatic mutations in CACNA2D4, CTNNB1, DOCK5, IPO8, MTMR1, PABPC5, SEMA6D, and ZFP36L1. Based on the genetic mutation, sarcomatoid hepatocarcinoma was the most likely pathogenesis in this case. This mutation is indicative of the transition from sarcomatoid hepatocarcinoma to hepatic leiomyosarcoma. - Source: PubMed
Publication date: 2024/03/09
Numata YutoAkutsu NoriyukiIdogawa MasashiWagatsuma KoheiNumata YasunaoIshigami KeisuikeNakamura TomoyaHirano TakehiroKawakami YujiroMasaki YoshiharuMurota AyakoSasaki ShigeruNakase Hiroshi - Although mutations of genes are crucial events in tumorigenesis and development, the association between gene mutations and lung cancer metastasis is still largely unknown. The goal of this study is to identify driver and novel genes associated with non-small cell lung cancer (NSCLC) metastasis. Candidate genes were identified using a novel comprehensive analysis, which was based on bioinformatics technology and meta-analysis. Firstly, EGFR, KRAS, ALK, TP53, BRAF and PIK3CA were identified as candidate driver genes. Further meta-analysis identified that EGFR (Pooled OR 1.33, 95% CI 1.19, 1.50; P < .001) and ALK (Pooled OR 1.52, 95% CI 1.22, 1.89; P < .001) mutations were associated with distant metastasis of NSCLC. Besides, ALK (Pooled OR 2.40, 95% CI 1.71, 3.38; P < .001) mutation was associated with lymph node metastasis of NSCLC. In addition, thirteen novel gene mutations were identified to be correlated with NSCLC metastasis, including SMARCA1, GGCX, KIF24, LRRK1, LILRA4, OR2T10, EDNRB, NR1H4, ARID4A, PRKCI, PABPC5, ACAN and TLN1. Furthermore, elevated mRNA expression level of SMARCA1 and EDNRB was associated with poor overall survival in lung adenocarcinoma (LUAD) and lung squamous cell carcinoma (LUSC), respectively. Additionally, pathway and protein-protein interactions network analyses found the two genes were correlated with epithelial-mesenchymal transition process. In conclusion, mutations of EGFR and ALK were significantly correlated with NSCLC metastasis. In addition, thirteen novel genes were identified to be associated with NSCLC metastasis, especially SMARCA1 in LUAD and EDNRB in LUSC. - Source: PubMed
Publication date: 2021/07/10
Wu YongfengNi HengYang DexinNiu YuequnChen KelieXu JinmingWang FangTang SongShi YuZhang HongheHu JianXia DajingWu Yihua - Glioma is the most common primary malignancy in the brain, and vasculogenic mimicry (VM) is one of the blood supply methods. Here we investigated the possibility that lncRNAs regulate the stability of transcription factors through the SMD pathway, which affects proliferation, migration, invasion, and the ability to form VMs in glioma. Expression of , , and was detected by real-time qPCR or western blot in glioma. Cell Counting Kit-8, Transwell assays, and VM tube formation were used to investigate , , and function in cell proliferation, migration, invasion, and VM, respectively. ChIP assays were used to ascertain the interaction between and or . and were highly expressed in glioma cells. was lowly expressed. bound to increase its stability. Knockdown reduced the degradation of ZNF331 mRNA by the SMD pathway. inhibited transcription through binding to the promoter region of and and inhibited the ability to form VMs in glioma cells. The feedback loop plays an important role in regulating VM formation in glioma and provides new targets for glioma treatment. - Source: PubMed
Publication date: 2020/03/30
Jing FangkunRuan XueleiLiu XiaobaiYang ChunqingWang DiZheng JianXue YixueShen ShuyuanShao LianqiYang YangWang PingMa JunLiu Yunhui