ArticleCell death & disease2019
POTEE drives colorectal cancer development via regulating SPHK1/p65 signaling.
Article in Cell death & disease, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 39 citations in OpenAlex.
- MEOX1 Coordinates Autocrine-Paracrine Programs via SPHK1/S1P to Promote Lymph Node Metastasis in Ovarian Cancer.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- POTEF upregulation drives hepatocellular carcinoma progression via oncogenic signaling and immune modulation.Scientific reports · 2026Article
- Identification of TTLL8, POTEE, and PKMYT1 as immunogenic cancer-associated antigens and potential immunotherapy targets in ovarian cancer.Oncoimmunology · 2025Article
- Element-specific estimation of background mutation rates in whole cancer genomes through transfer learning.NPJ precision oncology · 2025Article
- NFκB signalling in colorectal cancer: Examining the central dogma of IKKα and IKKβ signalling.Heliyon · 2024Review
- POTEE promotes breast cancer cell malignancy by inducing invadopodia formation through the activation of SUMOylated Rac1.Molecular oncology · 2024Article
- GRK2 mediated degradation of SAV1 initiates hyperplasia of fibroblast-like synoviocytes in rheumatoid arthritis.Acta pharmaceutica Sinica. B · 2024Article
- Deciphering the omicron variant: integrated omics analysis reveals critical biomarkers and pathophysiological pathways.Journal of translational medicine · 2024Article
- Article
- POTEE mutation as a potential predictive biomarker for immune checkpoint inhibitors in lung adenocarcinoma.Investigational new drugs · 2023Article
- Histaminergic System and Inflammation-Related Genes in Normal Large Intestine andInternational journal of molecular sciences · 2023Article
- Metabolomic Analysis Reveals that SPHK1 Promotes Oral Squamous Cell Carcinoma Progression through NF-κB Activation.Annals of surgical oncology · 2022Article
- Gastric Cancer Pre-Stage Detection and Early Diagnosis of Gastritis Using Serum Protein Signatures.Molecules (Basel, Switzerland) · 2022Article
- Whole genome sequencing of Malaysian colorectal cancer patients reveals specific druggable somatic mutations.Frontiers in molecular biosciences · 2022Article
- Article
- SPHK1 contributes to cisplatin resistance in bladder cancer cells via the NONO/STAT3 axis.International journal of molecular medicine · 2021Article
- S100P contributes to promoter demethylation and transcriptional activation of SLC2A5 to promote metastasis in colorectal cancer.British journal of cancer · 2021Article
- N-Myristoylation by NMT1 Is POTEE-Dependent to Stimulate Liver TumorigenesisFrontiers in oncology · 2021Article
- Article
- Evolution of Mutational Landscape and Tumor Immune-Microenvironment in Liver Oligo-Metastatic Colorectal Cancer.Cancers · 2020Article
Corrections and comments
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Authors and funding
10 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Aberrant gene expression plays critical roles in the development of colorectal cancer (CRC). Here we show that POTEE, which was identified as a member E of POTE ankyrin domain family, was significantly upregulated in colorectal tumors and predicted poor overall survival of CRC patients. In CRC cells, POTEE could act as an oncogene and could promote cell growth, cell-cycle progression, inhibit apoptosis, and elevates xenograft tumor growth. Mechanically, we used microarray analysis and identified a POTEE/SPHK1/p65 signaling axis, which affected the biological functions of CRC cells. Further evaluation showed that overexpression of POTEE could increase the protein expression of SPHK1, followed by promoting the phosphorylation and activation of p65 protein. Altogether, our findings suggested a POTEE/SPHK1/p65 signaling axis could promote colorectal tumorigenesis and POTEE might potentially serve as a novel biomarker for the diagnosis and an intervention of colorectal cancer.
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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.