Evidence map›Paper›PMID 27626681›Full record

ArticleOncotarget2016

Overexpression of LLT1 (OCIL, CLEC2D) on prostate cancer cells inhibits NK cell-mediated killing through LLT1-NKRP1A (CD161) interaction.

Stephen O Mathew, Pankaj Chaudhary, Sheila B Powers, Jamboor K Vishwanatha, Porunelloor A Mathew

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.

0numbers the graph read from it
0cells of the map it votes in
44citing papers in PubMed
1.9field-weighted citation impact, top 15% 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

44 citing papers in PubMed, 65 citations in OpenAlex.

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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

5 authors at 2 institutions in 1 country.

Stephen O MathewDepartment of Cell Biology and Immunology and Institute for Cancer Research, University of North Texas Health Science Center, Fort Worth, TX 76107, USA.
Pankaj ChaudharyDepartment of Molecular and Medical Genetics and Institute for Cancer Research, University of North Texas Health Science Center, Fort Worth, TX 76107, USA.
Sheila B PowersDepartment of Cell Biology and Immunology and Institute for Cancer Research, University of North Texas Health Science Center, Fort Worth, TX 76107, USA.
Jamboor K VishwanathaDepartment of Molecular and Medical Genetics and Institute for Cancer Research, University of North Texas Health Science Center, Fort Worth, TX 76107, USA.
Porunelloor A MathewDepartment of Cell Biology and Immunology and Institute for Cancer Research, University of North Texas Health Science Center, Fort Worth, TX 76107, USA.
University of North Texas · USUniversity of North Texas Health Science Center · US

Funding

Texas Minority Health, Research and Outreach (MiHERO)S21MD012472 · NIMHD · UNIVERSITY OF NORTH TEXAS HLTH SCI CTR · PI JAMBOOR K. VISHWANATHA · 2017 to 2026
$18.0M
NIMHD NIH HHS S21 MD012472
6 · The paper itself

Abstract

Prostate cancer is the most common type of cancer diagnosed and the second leading cause of cancer-related death in American men. Natural Killer (NK) cells are the first line of defense against cancer and infections. NK cell function is regulated by a delicate balance between signals received through activating and inhibitory receptors. Previously, we identified Lectin-like transcript-1 (LLT1/OCIL/CLEC2D) as a counter-receptor for the NK cell inhibitory receptor NKRP1A (CD161). Interaction of LLT1 expressed on target cells with NKRP1A inhibits NK cell activation. In this study, we have found that LLT1 was overexpressed on prostate cancer cell lines (DU145, LNCaP, 22Rv1 and PC3) and in primary prostate cancer tissues both at the mRNA and protein level. We further showed that LLT1 is retained intracellularly in normal prostate cells with minimal cell surface expression. Blocking LLT1 interaction with NKRP1A by anti-LLT1 mAb on prostate cancer cells increased the NK-mediated cytotoxicity of prostate cancer cells. The results indicate that prostate cancer cells may evade immune attack by NK cells by expressing LLT1 to inhibit NK cell-mediated cytolytic activity through LLT1-NKRP1A interaction. Blocking LLT1-NKRP1A interaction will make prostate cancer cells susceptible to killing by NK cells and therefore may be a new therapeutic option for treatment of prostate cancer.

Indexed as

Antibodies, BlockingCell Line, TumorCytotoxicity, ImmunologicGene Expression Regulation, NeoplasticHumansJurkat CellsKiller Cells, NaturalLectins, C-TypeMaleNK Cell Lectin-Like Receptor Subfamily BProstatic NeoplasmsProtein BindingReceptors, Cell SurfaceAntibodies, BlockingCLEC2D protein, humanKLRB1 protein, humanLectins, C-TypeNK Cell Lectin-Like Receptor Subfamily BReceptors, Cell SurfaceLLT1LLT1-NKRP1A interactionNK cellsNKRP1A (CD161)prostate cancer

Identifiers

PMID27626681
PMCPMC5356580
OpenAlexW2516362774

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.