Evidence map›Paper›PMID 36805500›Full record

ArticleCancer letters2023

Lymphocyte antigen 6K signaling to aurora kinase promotes advancement of the cell cycle and the growth of cancer cells, which is inhibited by LY6K-NSC243928 interaction.

Benson Chellakkan Selvanesan, Sheelu Varghese, Justyna Andrys-Olek, Ricardo Hernandez Arriaza, Rahul Prakash, Purushottam Babu Tiwari, Daniel Hupalo, Yuriy Gusev, Megha Nitin Patel, Sara Contente and 8 more

Open access · hybridAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cancer letters, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
0.6field-weighted citation impact, top 31% 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

4 citing papers in PubMed, 4 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
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

18 authors at 6 institutions in 3 countries.

Benson Chellakkan SelvanesanDepartment of Pathology, Uniformed Services University of the Health Sciences, Bethesda, MD, USA; Henry M. Jackson Foundation, Bethesda, MD, USA.
Sheelu VargheseDepartment of Pathology, Uniformed Services University of the Health Sciences, Bethesda, MD, USA; Henry M. Jackson Foundation, Bethesda, MD, USA.
Justyna Andrys-OlekJerzy Haber Institute of Catalysis and Surface Chemistry Polish Academy of Sciences, Cracow, Poland.
Ricardo Hernandez ArriazaDepartment of Chemistry and Biochemistry, University of South Carolina, Columbia, SC, USA.
Rahul PrakashDepartment of Chemistry and Biochemistry, University of South Carolina, Columbia, SC, USA.
Purushottam Babu TiwariDepartment of Oncology, Georgetown University Medical Center, Washington, DC, USA.
Daniel HupaloHenry M. Jackson Foundation, Bethesda, MD, USA; Department of Anatomy, Physiology, and Genetics, Uniformed Services University of the Health Sciences, Bethesda, MD, USA.
Yuriy GusevDepartment of Oncology, Georgetown University Medical Center, Washington, DC, USA.
Megha Nitin PatelDepartment of Chemistry and Biochemistry, University of South Carolina, Columbia, SC, USA.
Sara ContenteDepartment of Pathology, Uniformed Services University of the Health Sciences, Bethesda, MD, USA.
Miloslav SandaMax Planck Institute for Heart and Lung Research, Ludwigstrasse, 43, 61231, Bad Nauheim, Germany.
Aykut UrenDepartment of Oncology, Georgetown University Medical Center, Washington, DC, USA.
Matthew D WilkersonDepartment of Anatomy, Physiology, and Genetics, Uniformed Services University of the Health Sciences, Bethesda, MD, USA; John P. Murtha Cancer Center, Bethesda, MD, USA.
Clifton Lee DalgardDepartment of Anatomy, Physiology, and Genetics, Uniformed Services University of the Health Sciences, Bethesda, MD, USA; John P. Murtha Cancer Center, Bethesda, MD, USA.
Linda S ShimizuDepartment of Chemistry and Biochemistry, University of South Carolina, Columbia, SC, USA.
Maksymilian ChruszczDepartment of Chemistry and Biochemistry, University of South Carolina, Columbia, SC, USA.
Tomasz BorowskiJerzy Haber Institute of Catalysis and Surface Chemistry Polish Academy of Sciences, Cracow, Poland.
Geeta UpadhyayDepartment of Pathology, Uniformed Services University of the Health Sciences, Bethesda, MD, USA; John P. Murtha Cancer Center, Bethesda, MD, USA. Electronic address: geeta.upadhyay@usuhs.edu.
University of South Carolina · USUniformed Services University of the Health Sciences · USGeorgetown University · USHenry M. Jackson Foundation · USJerzy Haber Institute of Catalysis and Surface Chemistry, Polish Academy of Sciences · PLMax Planck Institute for Heart and Lung Research · DE

Funding

Tissue Culture Shared ResourceP30CA051008 · NCI · GEORGETOWN UNIVERSITY · PI Louis M Weiner · 1990 to 2026
$71.5M
Role of Ly6K in TGF-beta and immune escape pathways of triple negative breast cancerR01CA227694 · NCI · HENRY M. JACKSON FDN FOR THE ADV MIL/MED · PI Geeta Upadhyay · 2018 to 2026
$2.4M
Biacore 4000 High Throughput SystemS10OD019982 · OD · GEORGETOWN UNIVERSITY · PI UREN, AYKUT · 2015 to 2015
$484k
Use of Ly6K specific CAR T-cells to treat primary and metastatic triple negative breast cancerR21CA256424 · NCI · HENRY M. JACKSON FDN FOR THE ADV MIL/MED · PI UPADHYAY, GEETA · 2021 to 2022
$389k
NCI NIH HHS P30 CA051008NCI NIH HHS R01 CA227694NCI NIH HHS R21 CA256424NIH HHS S10 OD019982
6 · The paper itself

Abstract

Lymphocyte antigen 6K (LY6K) is a small GPI-linked protein that is normally expressed in testes. Increased expression of LY6K is significantly associated with poor survival outcomes in many solid cancers, including cancers of the breast, ovary, gastrointestinal tract, head and neck, brain, bladder, and lung. LY6K is required for ERK-AKT and TGF-β pathways in cancer cells and is required for in vivo tumor growth. In this report, we describe a novel role for LY6K in mitosis and cytokinesis through aurora B kinase and its substrate histone H3 signaling axis. Further, we describe the structural basis of the molecular interaction of small molecule NSC243928 with LY6K protein and the disruption of LY6K-aurora B signaling in cell cycle progression due to LY6K-NSC243928 interaction. Overall, disruption of LY6K function via NSC243928 led to failed cytokinesis, multinucleated cells, DNA damage, senescence, and apoptosis of cancer cells. LY6K is not required for vital organ function, thus inhibition of LY6K signaling is an ideal therapeutic approach for hard-to-treat cancers that lack targeted therapy such as triple-negative breast cancer.

Indexed as

NeoplasmsAcridinesAntigens, LyAurora Kinase BAurora KinasesCell CycleCell DivisionCell Line, TumorFemaleGPI-Linked ProteinsHumansLymphocytesSulfonamidesAcridinesAntigens, LyAurora Kinase BAurora KinasesGPI-Linked ProteinsLY6K protein, humanNSC243928SulfonamidesAurora BLY6KNSC243928Triple negative breast cancer

Identifiers

PMID36805500
PMCPMC10044439
OpenAlexW4321073981

What OpenQuestion holds

Textmetadata
LicenceTDM
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.