ArticleOncotarget2019
Neurotensin as a source of cyclic AMP and co-mitogen in fibrolamellar hepatocellular carcinoma.
Article in Oncotarget, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
What it found
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Who cites it
9 citing papers in PubMed, 12 citations in OpenAlex.
- Clinical guideline for the diagnosis and treatment of fibrolamellar carcinoma.Hepatology (Baltimore, Md.) · 2026Article
- Procalcitonin as a potential tumor marker for fibrolamellar hepatocellular carcinoma: Insights from three patients and a literature review.Frontiers in medicine · 2026Article
- Multi-omics dissection of CPNE1 reveals its prognostic value and immune-regulatory function in liver cancer.Discover oncology · 2025Article
- A framework for fibrolamellar carcinoma research and clinical trials.Nature reviews. Gastroenterology & hepatology · 2022Review
- New Insights in the Control of Fat Homeostasis: The Role of Neurotensin.International journal of molecular sciences · 2022Review
- The cAMP-signaling cancers: Clinically-divergent disorders with a common central pathway.Frontiers in endocrinology · 2022Review
- Expression of neurotensin receptor-1 (NTSBreast cancer research and treatment · 2021Article
- DnaJ-PKAc fusion induces liver inflammation in a zebrafish model of fibrolamellar carcinoma.Disease models & mechanisms · 2020Article
- The role of Neurotensin and its receptors in non-gastrointestinal cancers: a review.Cell communication and signaling : CCS · 2020Review
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
Abstract
Fibrolamellar hepatocellular carcinomas (FL-HCCs) possess a unique mutation that encodes a chimeric form of protein kinase A (DNAJ-PKAc), which includes a chaperonin binding domain. DNAJ-PKAc retains most of the biochemical properties of the native enzyme, however, and activity remains dependent on cAMP. We thus speculated that a persistent source of cAMP is necessary to promote FL-HCC carcinogenesis, and that neurotensin (NTS) may drive cAMP production in this setting, given that NS serum and tumor levels are elevated in many patients with FL-HCC. We examined expression of NTS pathway components in human FL-HCCs and paired normal livers, and determined the role of NTS in driving proliferation in tumor slice cultures. Cultured hepatocytes were used to determine interactions between NTS and other proliferative pathways, and to determine the effects of NTS on cAMP production and PKA activity. We found that the NTS pathway is up-regulated in human FL-HCCs, and that NTS activates cAMP and PKA in hepatocytes. NTS increases proliferation in the presence of epidermal growth factor (EGF), and NTS-induced proliferation is dependent on NTSR1 and the EGFR/MEK pathway. We conclude that NTS serves as a co-mitogen in FL-HCC, and provides a source of cAMP to facilitate ongoing activation of DNAJ-PKAc.
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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 OpenQuestion graph.