Evidence map›Paper›PMID 34966448›Full record

ArticleOncology letters2022

Inositol 1,4,5-trisphosphate receptor type 3 is involved in resistance to apoptosis and maintenance of human hepatocellular carcinoma.

Marcone Loiola Dos Santos, Andressa França, Antônio Carlos Melo Lima Filho, Rodrigo M Florentino, Paulo Henrique Diniz, Fernanda Oliveira Lemos, Carlos Alberto Xavier Gonçalves, Vitor Lima Coelho, Cristiano Xavier Lima, Giselle Foureaux and 3 more

Open access · diamondAbstract read
In one paragraph

Article in Oncology letters, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
0.3field-weighted citation impact, top 39% of its field
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

5 citing papers in PubMed, 4 citations in OpenAlex.

  1. Article
  2. Cannabidiol-Ion Channel Interactions Represent a Promising Preventive and Therapeutic Strategy in Hepatocellular Carcinoma.Pathophysiology : the official journal of the International Society for Pathophysiology · 2026
    Review
  3. Article
  4. Article
  5. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

13 authors at 4 institutions in 2 countries.

Marcone Loiola Dos SantosDepartment of Morphology, Federal University of Minas Gerais, Belo Horizonte, Minas Gerais 31270-901, Brazil.
Andressa FrançaDepartment of Physiology and Biophysics, Federal University of Minas Gerais, Belo Horizonte, Minas Gerais 31270-901, Brazil.
Antônio Carlos Melo Lima FilhoDepartment of Physiology and Biophysics, Federal University of Minas Gerais, Belo Horizonte, Minas Gerais 31270-901, Brazil.
Rodrigo M FlorentinoDepartment of Physiology and Biophysics, Federal University of Minas Gerais, Belo Horizonte, Minas Gerais 31270-901, Brazil.
Paulo Henrique DinizDepartment of Internal Medicine, Federal University of Minas Gerais, Belo Horizonte, Minas Gerais 31270-901, Brazil.
Fernanda Oliveira LemosDepartment of Physiology and Biophysics, Federal University of Minas Gerais, Belo Horizonte, Minas Gerais 31270-901, Brazil.
Carlos Alberto Xavier GonçalvesCoordination of Biotechnology, SENAI's Innovation Institute for Biosynthetics and Fibers, SENAI CETIQT, Rio de Janeiro 20961-020, Brazil.
Vitor Lima CoelhoCoordination of Biotechnology, SENAI's Innovation Institute for Biosynthetics and Fibers, SENAI CETIQT, Rio de Janeiro 20961-020, Brazil.
Cristiano Xavier LimaDepartment of Surgery, Federal University of Minas Gerais, Belo Horizonte, Minas Gerais 30 130-100, Brazil.
Giselle FoureauxDepartment of Morphology, Federal University of Minas Gerais, Belo Horizonte, Minas Gerais 31270-901, Brazil.
Michael H NathansonSection of Digestive Diseases, Department of Internal Medicine, Yale University School of Medicine, New Haven, CT 06520-8056, USA.
Paula Vieira Teixeira VidigalDepartment of Pathological Anatomy and Forensic Medicine of Hospital das Clínicas, Federal University of Minas Gerais, Belo Horizonte, Minas Gerais 30 130-100, Brazil.
M Fátima LeiteDepartment of Physiology and Biophysics, Federal University of Minas Gerais, Belo Horizonte, Minas Gerais 31270-901, Brazil.
Universidade Federal de Minas Gerais · BRServiço Nacional de Aprendizagem Industrial · BRHospital das Clínicas da Universidade Federal de Minas Gerais · BRYale University · US

Funding

Yale Clinical and Translational Science Award (U Component)UL1TR001863 · NCATS · YALE UNIVERSITY · PI John H. Krystal, LUCILA OHNO-MACHADO · 2016 to 2026
$102.9M
Yale Liver CenterP30DK034989 · NIDDK · YALE UNIVERSITY · PI WAJAHAT Zafar MEHAL · 1986 to 2026
$31.1M
Translational CoreP01DK057751 · NIDDK · YALE UNIVERSITY · PI YANG, XIAOYONG · 2001 to 2020
$25.6M
Interactions between neutrophils and cholangiocytes in alcoholic hepatitisR01AA028765 · NIAAA · YALE UNIVERSITY · PI NATHANSON, MICHAEL H · 2021 to 2025
$3.5M
Ca2+ waves in hepatocytes: Mechanisms and effectsR01DK114041 · NIDDK · YALE UNIVERSITY · PI NATHANSON, MICHAEL H · 2018 to 2022
$2.6M
Molecular regulation of cholestasis in cholangiocytesR01DK112797 · NIDDK · YALE UNIVERSITY · PI NATHANSON, MICHAEL H · 2018 to 2021
$1.9M
Pacific Bioscience Sequel II sequencing system for the Yale Center for Genome Analysis (YCGA)S10OD028669 · OD · YALE UNIVERSITY · PI MANE, SHRIKANT M · 2020 to 2020
$407k
NCATS NIH HHS UL1 TR001863NIAAA NIH HHS R01 AA028765NIDDK NIH HHS P01 DK057751NIDDK NIH HHS P30 DK034989NIDDK NIH HHS R01 DK112797NIDDK NIH HHS R01 DK114041NIH HHS S10 OD028669
6 · The paper itself

Abstract

The expression of the inositol 1,4,5-trisphosphate receptor type 3 (ITRP3) in hepatocytes is a common event in the pathogenesis of hepatocellular carcinoma (HCC), regardless of the type of underlying liver disease. However, it is not known whether ITPR3 expression in hepatocytes is involved in tumor maintenance. The aim of the present study was to determine whether there is an association between ITPR3 expression and clinical and morphological parameters using HCC samples obtained from liver explants from patients (n=53) with different etiologies of underlying chronic liver disease (CLD). ITPR3 expression, mitosis and apoptosis were analyzed in human liver samples by immunohistochemistry. Clinical and event-free survival data were combined to assess the relationship between ITPR3 and liver cancer growth in patients. RNA sequencing analysis was performed to identify apoptotic genes altered by ITPR3 expression in a liver tumor cell line. ITPR3 was highly expressed in HCC tumor cells relative to adjacent CLD tissue and healthy livers. There was an inverse correlation between ITPR3 expression and mitotic and apoptotic indices in HCC, suggesting that ITPR3 contributed to the maintenance of HCC by promoting resistance to apoptosis. This was confirmed by the upregulation of CTSB, CHOP and GADD45, genes involved in the apoptotic pathway in HCC. The expression of ITPR3 in the liver may be a promising prognostic marker of HCC.

Indexed as

apoptosiscalcium signalingchronic diseasesliver cancermitosis

Identifiers

PMID34966448
PMCPMC8669656
OpenAlexW3217513719

What OpenQuestion holds

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LicenceCC BY-NC-ND
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Registered trials

None linked

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.