Evidence map›Paper›PMID 34768108›Full record

ArticleNeoplasia (New York, N.Y.)2021

Suppression of ER-stress induction of GRP78 as an anti-neoplastic mechanism of the cardiac glycoside Lanatoside C in pancreatic cancer: Lanatoside C suppresses GRP78 stress induction.

Dat P Ha, Yuan-Li Tsai, Amy S Lee

Open access · goldAbstract read
In one paragraph

Article in Neoplasia (New York, N.Y.), 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed, 2 pooled it
2.1field-weighted citation impact, top 14% 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

17 citing papers in PubMed, 2 syntheses or guidelines pooled it, 26 citations in OpenAlex.

  1. Pooled it
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  3. Review
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  6. Stress-induced translocation of the endoplasmic reticulum chaperone GRP78/BiP and its impact on human disease and therapy.Proceedings of the National Academy of Sciences of the United States of America · 2025
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  13. ER chaperone GRP78/BiP translocates to the nucleus under stress and acts as a transcriptional regulator.Proceedings of the National Academy of Sciences of the United States of America · 2023
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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

3 authors at 1 institution in 1 country.

Dat P HaDepartment of Biochemistry and Molecular Medicine, University of Southern California, Keck School of Medicine, Los Angeles, California, USA; USC Norris Comprehensive Cancer Center.
Yuan-Li TsaiDepartment of Biochemistry and Molecular Medicine, University of Southern California, Keck School of Medicine, Los Angeles, California, USA; USC Norris Comprehensive Cancer Center.
Amy S LeeDepartment of Biochemistry and Molecular Medicine, University of Southern California, Keck School of Medicine, Los Angeles, California, USA; USC Norris Comprehensive Cancer Center. Electronic address: amylee@usc.edu.
University of Southern California · US

Funding

USC/NORRIS COMPREHENSIVE CANCER CENTER (CORE) SUPPORTP30CA014089 · NCI · UNIVERSITY OF SOUTHERN CALIFORNIA · PI MYLES G COCKBURN · 1985 to 2026
$181.4M
STRESS INDUCTION OF THE GLUCOSE REGULATED PROTEINSR01CA027607 · NCI · UNIVERSITY OF SOUTHERN CALIFORNIA · PI LEE, AMY S · 1985 to 2021
$11.1M
Targeting Cancer through Suppressing Stress Induction of GRP78/BiPR01CA238029 · NCI · UNIVERSITY OF SOUTHERN CALIFORNIA · PI LEE, AMY S · 2020 to 2022
$1.1M
NCI NIH HHS P30 CA014089NCI NIH HHS R01 CA027607NCI NIH HHS R01 CA238029
6 · The paper itself

Abstract

The 78 kilodalton glucose-regulated protein (GRP78) is a major endoplasmic reticulum (ER) molecular chaperone with antiapoptotic properties and a key regulator of the unfolded protein response (UPR). ER-stress induction of GRP78 in cancer cells represents a major pro-survival branch of the UPR. Pancreatic ductal adenocarcinoma (PDAC) remains a highly lethal disease and high level of GRP78 is associated with aggressive disease and poor survival. Recently, we reported that PDAC exhibited high level of ER stress and that GRP78 haploinsufficiency is sufficient to suppress pancreatic tumorigenesis in mice, suggesting the utility of inhibitors of GRP78 expression in combating pancreatic cancer. Screening of clinically relevant compound libraries revealed that cardiac glycosides (CGs) can inhibit ER-stress induction of GRP78 in pancreatic and other types of human cancers. Using the FDA-approved CG compound Lanatoside C (LanC) and human pancreatic cancer cell lines as model systems, we discovered that LanC preferably suppressed ER stress induction of GRP78 and to a lesser extent GRP94. The suppression is at the post-transcriptional level and dependent on the Na

Indexed as

Carcinoma, Pancreatic DuctalCardiac GlycosidesCell Line, TumorEndoplasmic Reticulum Chaperone BiPEndoplasmic Reticulum StressHumansLanatosidesPancreatic NeoplasmsUnfolded Protein ResponseCardiac GlycosidesEndoplasmic Reticulum Chaperone BiPHSPA5 protein, humanlanatoside CLanatosidesBiPCardiac GlycosidesER-stressGRP78Lanatoside CPancreatic Cancer

Identifiers

PMID34768108
PMCPMC8591401
OpenAlexW3212432902

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
Read underepoch 390

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.