Evidence map›Paper›PMID 22131883›Full record

ArticleNeoplasia (New York, N.Y.)2011

Activation of the long terminal repeat of human endogenous retrovirus K by melanoma-specific transcription factor MITF-M.

Iyoko Katoh, Anna Mírová, Shun-ichi Kurata, Yasushi Murakami, Kenji Horikawa, Natsuko Nakakuki, Takunobu Sakai, Kunihiko Hashimoto, Ayako Maruyama, Takaaki Yonaga and 3 more

Open access · goldAbstract read
In one paragraph

Article in Neoplasia (New York, N.Y.), 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed
6.6field-weighted citation impact, top 4% 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

35 citing papers in PubMed, 48 citations in OpenAlex.

  1. Review
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  6. Human Endogenous Retroviruses in Diseases.Sub-cellular biochemistry · 2023
    Article
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  9. Review
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  17. Downregulation of Human Endogenous Retrovirus Type K (HERV-K) ViralClinical cancer research : an official journal of the American Association for Cancer Research · 2017
    Article
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  20. 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

13 authors at 4 institutions in 2 countries.

Iyoko KatohDepartment of Microbiology, Interdisciplinary Graduate School of Medicine and Engineering, University of Yamanashi, Chuo, Yamanashi, Japan. iyoko@yamanashi.ac.jp
Anna Mírová
Shun-ichi Kurata
Yasushi Murakami
Kenji Horikawa
Natsuko Nakakuki
Takunobu Sakai
Kunihiko Hashimoto
Ayako Maruyama
Takaaki Yonaga
Nahoko Fukunishi
Kohji Moriishi
Hirohisa Hirai
University of Yamanashi · JPTokyo Medical and Dental University · JPCharles University · CZKyoto University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The human and Old World primate genomes possess conserved endogenous retrovirus sequences that have been implicated in evolution, reproduction, and carcinogenesis. Human endogenous retrovirus (HERV)-K with 5'LTR-gag-pro-pol-env-rec/np9-3'LTR sequences represents the newest retrovirus family that integrated into the human genome 1 to 5 million years ago. Although a high-level expression of HERV-K in melanomas, breast cancers, and teratocarcinomas has been demonstrated, the mechanism of the lineage-specific activation of the long terminal repeat (LTR) remains obscure. We studied chromosomal HERV-K expression in MeWo melanoma cells in comparison with the basal expression in human embryonic kidney 293 (HEK293) cells. Cloned LTR of HERV-K (HML-2.HOM) was also characterized by mutation and transactivation experiments. We detected multiple transcriptional initiator (Inr) sites in the LTR by rapid amplification of complementary DNA ends (5' RACE). HEK293 and MeWo showed different Inr usage. The most potent Inr was associated with a TATA box and three binding motifs of microphthalmia-associated transcription factor (MITF). Both chromosomal HERV-K expression and the cloned LTR function were strongly activated in HEK293 by transfection with MITF-M, a melanocyte/melanoma-specific isoform of MITF. Coexpression of MITF and the HERV-K core antigen was detected in retinal pigmented epithelium by an immunofluorescence analysis. Although malignant melanoma lines MeWo, G361, and SK-MEL-28 showed enhanced HERV-K transcription compared with normal melanocytes, the level of MITF-M messenger RNA persisted from normal to transformed melanocytes. Thus, MITF-M may be a prerequisite for the pigmented cell lineage-specific function of HERV-K LTR, leading to the high-level expression in malignant melanomas.

Indexed as

Transcriptional ActivationAdultAnimalsBase SequenceCells, CulturedEndogenous RetrovirusesFemaleFetusGene Expression Regulation, NeoplasticGene Expression Regulation, ViralGenes, NeoplasmHEK293 CellsHumansMacaca mulattaMaleMelanomaMicrophthalmia-Associated Transcription Factor

Identifiers

PMID22131883
PMCPMC3223611
OpenAlexW24850402

What OpenQuestion holds

Textmetadata
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.