Evidence map›Paper›PMID 30342037›Full record

ArticleGastroenterology2019

Inhibition of AURKA Reduces Proliferation and Survival of Gastrointestinal Cancer Cells With Activated KRAS by Preventing Activation of RPS6KB1.

Lihong Wang-Bishop, Zheng Chen, Ahmed Gomaa, Albert Craig Lockhart, Safia Salaria, Jialiang Wang, Keeli B Lewis, Jeffrey Ecsedy, Kay Washington, Robert Daniel Beauchamp and 1 more

Open access · greenAbstract read
In one paragraph

Article in Gastroenterology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 papers.

0numbers the graph read from it
0cells of the map it votes in
55citing papers in PubMed
5.9field-weighted citation impact, top 3% 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

55 citing papers in PubMed, 87 citations in OpenAlex.

  1. Article
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  5. Aurora-A drives sorafenib resistance by scaffolding stress granule assembly via phase separation.Proceedings of the National Academy of Sciences of the United States of America · 2026
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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

11 authors at 4 institutions in 1 country.

Lihong Wang-BishopDepartment of Chemical and Biomolecular Engineering, Vanderbilt University, Nashville, Tennessee.
Zheng ChenDepartment of Surgery, Miller School of Medicine, University of Miami, Miami, Florida.
Ahmed GomaaDepartment of Surgery, Miller School of Medicine, University of Miami, Miami, Florida.
Albert Craig LockhartDivision of Medical Oncology, Miller School of Medicine, University of Miami, Miami, Florida; Sylvester Comprehensive Cancer Center, Miller School of Medicine, University of Miami, Miami, Florida.
Safia SalariaSection of Surgical Sciences, Vanderbilt University Medical Center, Nashville, Tennessee.
Jialiang WangSection of Surgical Sciences, Vanderbilt University Medical Center, Nashville, Tennessee.
Keeli B LewisSection of Surgical Sciences, Vanderbilt University Medical Center, Nashville, Tennessee.
Jeffrey EcsedyTranslational Medicine, Millennium Pharmaceuticals, Inc., Cambridge, Massachusetts.
Kay WashingtonSection of Surgical Sciences, Vanderbilt University Medical Center, Nashville, Tennessee.
Robert Daniel BeauchampSection of Surgical Sciences, Vanderbilt University Medical Center, Nashville, Tennessee; Department of Pathology, Vanderbilt University Medical Center, Nashville, Tennessee.
Wael El-RifaiDepartment of Surgery, Miller School of Medicine, University of Miami, Miami, Florida; Sylvester Comprehensive Cancer Center, Miller School of Medicine, University of Miami, Miami, Florida; Department of Veterans Affairs, Miami VA Healthcare system, Miami, Florida. Electronic address: welrifai@med.miami.edu.
Vanderbilt University Medical Center · USUniversity of Miami · USMillennium Engineering and Integration (United States) · USVanderbilt University · US

Funding

Translational Analysis CoreP30DK058404 · NIDDK · VANDERBILT UNIVERSITY MEDICAL CENTER · PI RICHARD M. PEEK · 2002 to 2026
$29.9M
Vanderbilt-Ingram Cancer Center SPORE in Gastrointestinal CancerP50CA236733 · NCI · VANDERBILT UNIVERSITY MEDICAL CENTER · PI STEPHEN W. FESIK · 2019 to 2026
$19.6M
The Role of Aurora Kinase in Upper Gastrointestinal AdenocarcinomasR01CA131225 · NCI · VANDERBILT UNIVERSITY MEDICAL CENTER · PI EL-RIFAI, WAEL · 2009 to 2018
$3.3M
Molecular Pathobiology of Gastric CarcinogenesisI01BX001179 · VA · VETERANS HEALTH ADMINISTRATION · PI EL-RIFAI, WAEL · 2012 to 2024
–
BLRD Research Career Scientist Award ApplicationIK6BX003787 · VA · VETERANS HEALTH ADMINISTRATION · PI WAEL EL-RIFAI · 2017 to 2026
–
BLRD VA I01 BX001179BLRD VA IK6 BX003787NCI NIH HHS P50 CA236733NCI NIH HHS R01 CA131225NIDDK NIH HHS P30 DK058404
6 · The paper itself

Abstract

BACKGROUND &

aimsActivation of KRAS signaling and overexpression of the aurora kinase A (AURKA) are often detected in luminal gastrointestinal cancers. We investigated regulation of ribosomal protein S6 kinase B1 (RPS6KB1) by AURKA and the effects of alisertib, an AURKA inhibitor, in mice xenograft tumors grown from human gastrointestinal cancer cells with mutant, activated forms of KRAS.

methodsWe tested the effects of alisertib or AURKA overexpression or knockdown in 10 upper gastrointestinal or colon cancer cell lines with KRAS mutations or amplifications using the CellTiter-Glo luminescence and clonogenic cell survival assays. We used the proximity ligation in situ assay to evaluate protein co-localization and immunoprecipitation to study protein interactions. Nude mice with xenograft tumors grown from HCT116, SNU-601, SW480, or SNU-1 cells were given oral alisertib (40 mg/kg, 5 times/wk) for 4 weeks. Tumor samples were collected and analyzed by immunoblots and immunohistochemistry. Tissue microarrays from 151 paraffin-embedded human colon tumors, with adjacent normal and adenoma tissues, were analyzed by immunohistochemistry for levels of AURKA.

resultsAlisertib reduced proliferation and survival of the cell lines tested. AURKA knockdown or inhibition with alisertib reduced levels of phosphorylated RPS6KB1 (at T389) and increased levels of proteins that induce apoptosis, including BIM, cleaved PARP, and cleaved caspase 3. AURKA co-localized and interacted with RPS6KB1, mediating RPS6KB1 phosphorylation at T389. We detected AURKA-dependent phosphorylation of RPS6KB1 in cell lines with mutations in KRAS but not in cells with wild-type KRAS. Administration of alisertib to mice with xenograft tumors significantly reduced tumor volumes (P < .001). Alisertib reduced phosphorylation of RPS6KB1 and Ki-67 and increased levels of cleaved caspase 3 in tumor tissues. In analyses of tissue microarrays, we found significant overexpression of AURKA in gastrointestinal tumor tissues compared with non-tumor tissues (P = .0003).

conclusionIn studies of gastrointestinal cancer cell lines with activated KRAS, we found AURKA to phosphorylate RPS6KB1, promoting cell proliferation and survival and growth of xenograft tumors in mice. Agents that inhibit AURKA might slow the growth of gastrointestinal tumors with activation of KRAS.

Indexed as

AnimalsAurora Kinase AAzepinesCell DeathCell Line, TumorCell ProliferationGastrointestinal NeoplasmsGene Expression Regulation, NeoplasticHumansMiceMice, NudeMolecular Targeted TherapyProtein Kinase InhibitorsProto-Oncogene Proteins p21(ras)PyrimidinesRandom AllocationAurka protein, mouseAurora Kinase AAzepinesHras protein, mouseMLN 8237Protein Kinase InhibitorsProto-Oncogene Proteins p21(ras)PyrimidinesColon CancerMutationOncogenicSignal Transduction

Identifiers

PMID30342037
PMCPMC6368861
OpenAlexW2897103727

What OpenQuestion holds

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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.