Evidence map›Paper›PMID 31432134›Full record

ArticleMolecular medicine reports2019

Upregulation of Myc promotes the evasion of NK cell‑mediated immunity through suppression of NKG2D ligands in K562 cells.

Young-Shin Lee, Woong Heo, Cheol-Hun Son, Chi-Dug Kang, You-Soo Park, Jaeho Bae

Open access · hybridAbstract read
In one paragraph

Article in Molecular medicine reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.2field-weighted citation impact, top 21% 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

13 citing papers in PubMed, 19 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Review
  5. Targeting Myc-driven stress addiction in colorectal cancer.Drug resistance updates : reviews and commentaries in antimicrobial and anticancer chemotherapy · 2023
    Review
  6. Article
  7. Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. Review
  13. Targeting ADAM10 in Cancer and Autoimmunity.Frontiers in immunology · 2020
    Review
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

6 authors at 2 institutions in 1 country.

Young-Shin LeeDepartment of Biochemistry, Pusan National University School of Medicine, Yangsan, Gyeongsangnam 50612, Republic of Korea.
Woong HeoDepartment of Biochemistry, Pusan National University School of Medicine, Yangsan, Gyeongsangnam 50612, Republic of Korea.
Cheol-Hun SonDepartment of Research Center, Dongnam Institute of Radiological and Medical Sciences, Gijang, Busan 46033, Republic of Korea.
Chi-Dug KangDepartment of Biochemistry, Pusan National University School of Medicine, Yangsan, Gyeongsangnam 50612, Republic of Korea.
You-Soo ParkDepartment of Research Center, Dongnam Institute of Radiological and Medical Sciences, Gijang, Busan 46033, Republic of Korea.
Jaeho BaeDepartment of Biochemistry, Pusan National University School of Medicine, Yangsan, Gyeongsangnam 50612, Republic of Korea.
Pusan National University · KRDongnam Institute of Radiological & Medical Sciences · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

c‑Myc is a characteristic oncogene with dual functions in cell proliferation and apoptosis. Since the overexpression of the c‑Myc proto‑oncogene is a common event in the development and growth of various human types of cancer, the present study investigated whether oncogenic c‑Myc can alter natural killer (NK) cell‑mediated immunity through the expression of associated genes, using PCR, western blotting and flow cytometry assays. Furthermore, whether c‑Myc could influence the expression levels of natural killer group 2 member D (NKG2D) ligands, which are well known NK activation molecules, as well as NK cell‑mediated immunity, was investigated. c‑Myc was inhibited by 10058‑F4 treatment and small interfering RNA transfection. Upregulation of c‑Myc was achieved by transfection with a pCMV6‑myc vector. The inhibition of c‑Myc increased MHC class I polyeptide‑related sequence B and UL16 binding protein 1 expressions among NKG2D ligands, and the overexpression of c‑Myc suppressed the expression of all NKG2D ligands, except MHC class I polyeptide‑related sequence A. Furthermore, the alteration of c‑Myc activity altered the susceptibility of K562 cells to NK cells. These results suggested that the overexpression of c‑Myc may contribute to the immune escape of cancer cells and cell proliferation. Combined treatment with NK‑based cancer immunotherapy and inhibition of c‑Myc may achieve improved therapeutic results.

Indexed as

Immunity, CellularTumor EscapeGene Expression Regulation, LeukemicHumansK562 CellsKiller Cells, NaturalNK Cell Lectin-Like Receptor Subfamily KProto-Oncogene Proteins c-mycUp-RegulationKLRK1 protein, humanMYC protein, humanNK Cell Lectin-Like Receptor Subfamily KProto-Oncogene Proteins c-myc

Identifiers

PMID31432134
PMCPMC6755160
OpenAlexW2967261874

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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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.