ArticleDevelopmental cell2022
Functional genetic screen identifies ITPR3/calcium/RELB axis as a driver of colorectal cancer metastatic liver colonization.
Article in Developmental cell, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers, 1 of them a synthesis that pooled it.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
17 citing papers in PubMed, 1 synthesis or guideline pooled it, 21 citations in OpenAlex.
- Gene expression regulation by CaCellular & molecular biology letters · 2026Pooled it
- Metabolites and cancer metastasis.Oncogene · 2026Review
- Colorectal cancers with distinct metastatic potential trigger divergent early T cell responses.bioRxiv : the preprint server for biology · 2026Article
- S100A14 promotes colorectal cancer progression and anti-PD-1 resistance via UPF1-mediated activation of the non-canonical NF-κB signaling.Cell death & disease · 2026Article
- GABPB1 activates transcription of ITPR3 and EMT in OSCC progression.Functional & integrative genomics · 2026Article
- Identification and experimental validation of biomarkers associated with paraptosis in meningioma.Medicine · 2025Article
- The role of calcium signaling in organotropic metastasis of cancer.Acta pharmacologica Sinica · 2025Review
- Loss of STIM2, but not of STIM1, drives colorectal cancer metastasis through metabolic reprogramming and the ATF4 ER stress pathway.Science signaling · 2025Article
- In vivo CRISPR activation screen identifies acyl-CoA-binding protein as a driver of bone metastasis.Science translational medicine · 2025Article
- Transcriptomic validation and clinical translation of CCDC78 as a prognostic biomarker in colorectal cancer.American journal of cancer research · 2025Article
- Breast cancer cells utilize T3 to trigger proliferation through cellular CaCell communication and signaling : CCS · 2024Article
- LTBR acts as a novel immune checkpoint of tumor-associated macrophages for cancer immunotherapy.iMeta · 2024Article
- Knockdown of SCN5A alters metabolic-associated genes and aggravates hypertrophy in the cardiomyoblast.Molecular biology reports · 2024Article
- Article
- Type 3 IP3 receptor: Its structure, functions, and related disease implications.Channels (Austin, Tex.) · 2023Review
- Structural titration reveals CaNature communications · 2023Article
- Microbiome and Metabolomics in Liver Cancer: Scientific Technology.International journal of molecular sciences · 2022Review
Corrections and comments
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
Abstract
Metastatic colonization is the primary cause of death from colorectal cancer (CRC). We employed genome-scale in vivo short hairpin RNA (shRNA) screening and validation to identify 26 promoters of CRC liver colonization. Among these genes, we identified a cluster that contains multiple targetable genes, including ITPR3, which promoted liver-metastatic colonization and elicited similar downstream gene expression programs. ITPR3 is a caffeine-sensitive inositol 1,4,5-triphosphate (IP3) receptor that releases calcium from the endoplasmic reticulum and enhanced metastatic colonization by inducing expression of RELB, a transcription factor that is associated with non-canonical NF-κB signaling. Genetic, cell biological, pharmacologic, and clinical association studies revealed that ITPR3 and RELB drive CRC colony formation by promoting cell survival upon substratum detachment or hypoxic exposure. RELB was sufficient to drive colonization downstream of ITPR3. Our findings implicate the ITPR3/calcium/RELB axis in CRC metastatic colony formation and uncover multiple clinico-pathologically associated targetable proteins as drivers of CRC metastatic colonization.
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Registered trials
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 Socratic graph.