ArticleNature communications2017
TRIB2 confers resistance to anti-cancer therapy by activating the serine/threonine protein kinase AKT.
Article in Nature communications, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 45 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
45 citing papers in PubMed, 71 citations in OpenAlex.
- Pseudokinase STK40 promotes TScience advances · 2024Article
- Association of WHSC1/NSD2 and T-cell infiltration with prostate cancer metastasis and prognosis.Scientific reports · 2023Article
- FUS-dependent microRNA deregulations identify TRIB2 as a druggable target for ALS motor neurons.iScience · 2023Article
- TRIB1 confers therapeutic resistance in GBM cells by activating the ERK and Akt pathways.Scientific reports · 2023Article
- The 'omics of obesity in B-cell acute lymphoblastic leukemia.Journal of the National Cancer Institute. Monographs · 2023Article
- TRIB2 safeguards naive T cell homeostasis during aging.Cell reports · 2023Article
- Effect of COP1 in Promoting the Tumorigenesis of Gastric Cancer by Down-Regulation of CDH18 via PI3K/AKT Signal Pathway.Analytical cellular pathology (Amsterdam) · 2023Article
- Multiplexed cellular profiling identifies an organoselenium compound as an inhibitor of CRM1-mediated nuclear export.Traffic (Copenhagen, Denmark) · 2022Article
- A novel 7 RNA-based signature for prediction of prognosis and therapeutic responses of wild-type BRAF cutaneous melanoma.Biological procedures online · 2022Article
- TRIB2 regulates the expression of miR‑33a‑5p through the ERK/c‑Fos pathway to affect the imatinib resistance of chronic myeloid leukemia cells.International journal of oncology · 2022Article
- Tribbles 2 pseudokinase confers enzalutamide resistance in prostate cancer by promoting lineage plasticity.The Journal of biological chemistry · 2022Article
- Article
- Comprehensive Profiling of Mammalian Tribbles Interactomes Implicates TRIB3 in Gene Repression.Cancers · 2021Article
- Functional annotation of noncoding mutations in cancer.Life science alliance · 2021Article
- A methyltransferase-like 14/miR-99a-5p/tribble 2 positive feedback circuit promotes cancer stem cell persistence and radioresistance via histone deacetylase 2-mediated epigenetic modulation in esophageal squamous cell carcinoma.Clinical and translational medicine · 2021Article
- TRIB2 Stimulates Cancer Stem-Like Properties through Activating the AKT-GSK3β-β-Catenin Signaling Axis.Molecules and cells · 2021Article
- Upregulation of TRIB2 by Wnt/β-catenin activation in BRAFCancer chemotherapy and pharmacology · 2021Article
- Review
- Tribbles Pseudokinases in Colorectal Cancer.Cancers · 2021Review
- Review
Corrections and comments
- Retracted
Authors and funding
15 authors at 8 institutions in 6 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Intrinsic and acquired resistance to chemotherapy is the fundamental reason for treatment failure for many cancer patients. The identification of molecular mechanisms involved in drug resistance or sensitization is imperative. Here we report that tribbles homologue 2 (TRIB2) ablates forkhead box O activation and disrupts the p53/MDM2 regulatory axis, conferring resistance to various chemotherapeutics. TRIB2 suppression is exerted via direct interaction with AKT a key signalling protein in cell proliferation, survival and metabolism pathways. Ectopic or intrinsic high expression of TRIB2 induces drug resistance by promoting phospho-AKT (at Ser473) via its COP1 domain. TRIB2 expression is significantly increased in tumour tissues from patients correlating with an increased phosphorylation of AKT, FOXO3a, MDM2 and an impaired therapeutic response. This culminates in an extremely poor clinical outcome. Our study reveals a novel regulatory mechanism underlying drug resistance and suggests that TRIB2 functions as a regulatory component of the PI3K network, activating AKT in cancer cells.
Indexed as
Identifiers
What OpenQuestion holds
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 OpenQuestion graph.