Evidence map›Paper›PMID 36162331›Full record

ArticleNeoplasia (New York, N.Y.)2022

Targeting GRP78 suppresses oncogenic KRAS protein expression and reduces viability of cancer cells bearing various KRAS mutations.

Dat P Ha, Bo Huang, Han Wang, Daisy Flores Rangel, Richard Van Krieken, Ze Liu, Soma Samanta, Nouri Neamati, Amy S Lee

Open access · goldAbstract read
In one paragraph

Article in Neoplasia (New York, N.Y.), 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
3.2field-weighted citation impact, top 7% 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

21 citing papers in PubMed, 30 citations in OpenAlex.

  1. Targeting WFS1 overcomes KRASNPJ precision oncology · 2026
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  5. 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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  6. Review
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  14. 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
    Article
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  16. Review
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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

9 authors at 2 institutions 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.
Bo HuangDepartment of Biochemistry and Molecular Medicine, University of Southern California, Keck School of Medicine, Los Angeles, California, USA; USC Norris Comprehensive Cancer Center.
Han WangDepartment of Biochemistry and Molecular Medicine, University of Southern California, Keck School of Medicine, Los Angeles, California, USA; USC Norris Comprehensive Cancer Center.
Daisy Flores RangelDepartment of Biochemistry and Molecular Medicine, University of Southern California, Keck School of Medicine, Los Angeles, California, USA; USC Norris Comprehensive Cancer Center.
Richard Van KriekenDepartment of Biochemistry and Molecular Medicine, University of Southern California, Keck School of Medicine, Los Angeles, California, USA; USC Norris Comprehensive Cancer Center.
Ze LiuDepartment of Biochemistry and Molecular Medicine, University of Southern California, Keck School of Medicine, Los Angeles, California, USA; USC Norris Comprehensive Cancer Center.
Soma SamantaDepartment of Medicinal Chemistry, College of Pharmacy, Rogel Cancer Center, University of Michigan, Ann Arbor, Michigan, USA.
Nouri NeamatiDepartment of Medicinal Chemistry, College of Pharmacy, Rogel Cancer Center, University of Michigan, Ann Arbor, Michigan, USA.
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 · USUniversity of Michigan · 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
ROS-targeted therapy for pancreatic cancer - Diversity SupplementR01CA188252 · NCI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI NEAMATI, NOURI · 2015 to 2020
$2.6M
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 CA188252NCI NIH HHS R01 CA238029
6 · The paper itself

Abstract

KRAS is the most commonly mutated oncogene in human cancers with limited therapeutic options, thus there is a critical need to identify novel targets and inhibiting agents. The 78-kDa glucose-regulated protein GRP78, which is upregulated in KRAS cancers, is an essential chaperone and the master regulator of the unfolded protein response (UPR). Following up on our recent discoveries that GRP78 haploinsufficiency suppresses both KRAS

Indexed as

Endoplasmic Reticulum Chaperone BiPProto-Oncogene Proteins p21(ras)CarcinogenesisCell Line, TumorCell Transformation, NeoplasticGlucoseHumansMutationRNA, Small InterferingEndoplasmic Reticulum Chaperone BiPGlucoseKRAS protein, humanProto-Oncogene Proteins p21(ras)RNA, Small InterferingColon cancerGRP78KRASLung cancerPancreatic cancerSmall molecule inhibitors

Identifiers

PMID36162331
PMCPMC9516447
OpenAlexW4297025417

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.