Evidence map›Paper›PMID 21321117›Full record

ArticleThe Journal of biological chemistry2011

Overexpression of IL-32alpha increases natural killer cell-mediated killing through up-regulation of Fas and UL16-binding protein 2 (ULBP2) expression in human chronic myeloid leukemia cells.

Soyoung Cheon, Ji Hyung Lee, Sunyoung Park, Sa Ik Bang, Wang Jae Lee, Do-Young Yoon, Sung-Soo Yoon, Taesung Kim, Hyeyoung Min, Byung Joo Cho and 5 more

Abstract read
In one paragraph

Article in The Journal of biological chemistry, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
–field-weighted citation impact
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

23 citing papers in PubMed.

  1. Review
  2. Article
  3. Frontiers in molecular biosciences · 2022
    Article
  4. Review
  5. Interleukin 32 Promotes Foxp3Frontiers in cell and developmental biology · 2021
    Article
  6. Article
  7. Interleukin 32 expression in human melanoma.Journal of translational medicine · 2019
    Article
  8. Review
  9. Review
  10. Review
  11. Article
  12. Article
  13. Review
  14. Article
  15. Article
  16. Article
  17. Article
  18. Review
  19. The role of IL-32 in cutaneous T-cell lymphoma.The Journal of investigative dermatology · 2014
    Article
  20. Novel insights into the biology of interleukin-32.Cellular and molecular life sciences : CMLS · 2013
    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

15 authors.

Soyoung CheonDepartment of Life Science, Sookmyung Women's University, and Konkuk University Hospital, Seoul 140-742, Republic of Korea.
Ji Hyung Lee
Sunyoung Park
Sa Ik Bang
Wang Jae Lee
Do-Young Yoon
Sung-Soo Yoon
Taesung Kim
Hyeyoung Min
Byung Joo Cho
Hyong Joo Lee
Ki Woong Lee
Seung Hwan Jeong
Hyunjeong Park
Daeho Cho

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

IL-32 was recently identified as a proinflammatory cytokine that is induced by IL-18 in natural killer (NK) cells and is highly correlated with inflammatory disorders. However, the relationship between IL-32 and tumor progression is still unknown. In this study, we investigated whether overexpression of IL-32 affects susceptibility of chronic myeloid leukemia (CML) cells to NK cells. Interestingly, IL-32α-overexpressing CML cell lines, K562, Kcl22, and BV173, showed higher NK cell-mediated killing. Flow cytometry analysis revealed that overexpression of IL-32α induced increased expression of Fas and UL16-binding protein 2 (ULBP2) in CML cells. The direct relationship between overexpression of surface molecules by IL-32α and increased NK cell-mediated killing was confirmed by Fas or ULBP2 siRNA transfection. IL-32α-induced Fas and ULBP2 expression are regulated p38 MAPK. In addition, the transcription factor Ets1 plays a key role in ULBP2 specific expression by IL-32α overexpression in ULBP family members. Taken together, these data show that IL-32α stimulates Fas and ULBP2 expression via activation of p38 MAPK, which increases NK susceptibility of CML cells. Enhanced NK cell susceptibility of CML cells by IL-32α overexpression may improve the efficiency of NK cell-based immunotherapy.

Indexed as

Blotting, WesternCell LineCell Line, Tumorfas ReceptorFlow CytometryGPI-Linked ProteinsHumansIntercellular Signaling Peptides and ProteinsInterleukinsKiller Cells, NaturalLeukemia, Myelogenous, Chronic, BCR-ABL Positivep38 Mitogen-Activated Protein KinasesProto-Oncogene Protein c-ets-1Reverse Transcriptase Polymerase Chain ReactionRNA, Small InterferingETS1 protein, humanFAS protein, humanfas ReceptorGPI-Linked ProteinsIL32 protein, humanIntercellular Signaling Peptides and ProteinsInterleukinsp38 Mitogen-Activated Protein KinasesProto-Oncogene Protein c-ets-1RNA, Small InterferingULBP2 protein, human

Identifiers

PMID21321117
PMCPMC3069408

What OpenQuestion holds

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Registered trials

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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.