Evidence map›Paper›PMID 16965397›Full record

ArticleCancer science2006

Expression profile of LIT1/KCNQ1OT1 and epigenetic status at the KvDMR1 in colorectal cancers.

Seiji Nakano, Kazuhiro Murakami, Makiko Meguro, Hidenobu Soejima, Ken Higashimoto, Takeshi Urano, Hiroyuki Kugoh, Tsunehiro Mukai, Masahide Ikeguchi, Mitsuo Oshimura

Open access · greenAbstract read
In one paragraph

Article in Cancer science, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 58 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
58citing papers in PubMed, 1 pooled it
1.9field-weighted citation impact, top 14% 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

58 citing papers in PubMed, 1 synthesis or guideline pooled it, 104 citations in OpenAlex.

  1. Perspectives of long non-coding RNAs in cancer.Molecular biology reports · 2017
    Pooled it
  2. Review
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  11. Epigenetic reprogramming in cancer: From diagnosis to treatment.Frontiers in cell and developmental biology · 2023
    Review
  12. Long Non-coding RNAs and CRISPR-Cas Edition in Tumorigenesis.Advances in experimental medicine and biology · 2023
    Article
  13. Review
  14. Review
  15. Review
  16. Article
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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

10 authors at 3 institutions in 1 country.

Seiji NakanoDepartment of Biomedical Science, Institute of Regenerative Medicine and Biofunction, Graduate School of Medical Science, Tottori University, 86 Nishimachi, Yonago, Tottori 683-8503, Japan.
Kazuhiro Murakami
Makiko Meguro
Hidenobu Soejima
Ken Higashimoto
Takeshi Urano
Hiroyuki Kugoh
Tsunehiro Mukai
Masahide Ikeguchi
Mitsuo Oshimura
Tottori University · JPSaga University · JPNagoya University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The human chromosome region 11p15.5 contains a number of maternally and paternally imprinted genes, and the LIT1/KCNQ1OT1 locus acts as an imprinting center in the proximal domain of 11p15.5. Loss of imprinting (LOI) of LIT1 and its correlation with methylation status at a differentially methylated region, the KvDMR1, were investigated in 69 colorectal cancer tissue specimens. LIT1 expression profiles were also examined by RNA-fluorescence in situ hybridization in 13 colorectal cancer cell lines. In 69 colorectal cancer tissue specimens, LOI of LIT1 was observed in nine of the 17 (53%) informative cases. Moreover, LOI of LIT1 was only observed in tumor samples. In the cell lines, methylation status at the KvDMR1 correlated well with LIT1 expression profiles. Loss of expression of LIT1 also correlated with enrichment of H3 lysine 9 (H3-K9) dimethylation and reduction of H3 lysine 4 (H3-K4) dimethylation. Thus, LIT1 expression appears to be controlled by epigenetic modifications at the KvDMR1, although CDKN1C expression, which is considered to be controlled by LIT1, was not associated with epigenetic status at the KvDMR1 in some colorectal cancer cell lines. Therefore, these findings suggest that LOI of LIT1 via epigenetic disruption plays an important role in colorectal carcinogenesis, but it is not necessarily associated with CDKN1C expression.

Indexed as

Epigenesis, GeneticGene Expression Regulation, NeoplasticChromatin ImmunoprecipitationChromosomes, Human, Pair 11Colorectal NeoplasmsCyclin-Dependent Kinase Inhibitor p57DNA MethylationGenomic ImprintingHumansIn Situ Hybridization, FluorescenceInsulin-Like Growth Factor IIMembrane ProteinsPotassium Channels, Voltage-GatedProteinsRNA, Long NoncodingRNA, UntranslatedCDKN1C protein, humanCyclin-Dependent Kinase Inhibitor p57H19 long non-coding RNAIGF2 protein, humanInsulin-Like Growth Factor IIKCNQ1OT1 long non-coding RNA, humanMembrane ProteinsPotassium Channels, Voltage-GatedProteinsRNA, Long NoncodingRNA, Untranslated

Identifiers

PMID16965397
PMCPMC11158715
OpenAlexW2063977955

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.