Evidence map›Paper›PMID 36612299›Full record

ArticleCancers2023

Long Non-Coding RNAs Associated with Mitogen-Activated Protein Kinase in Human Pancreatic Cancer.

Tomohiko Ishikawa, Shinichi Fukushige, Yuriko Saiki, Katsuya Hirose, Takako Hiyoshi, Takenori Ogawa, Yukio Katori, Toru Furukawa

Open access · goldAbstract read
In one paragraph

Article in Cancers, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
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

3 citing papers in PubMed, 8 citations in OpenAlex.

  1. Non-coding RNA profiling in BRAFScientific data · 2025
    Article
  2. Review
  3. 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

8 authors at 2 institutions in 1 country.

Tomohiko IshikawaDepartment of Investigative Pathology, Tohoku University Graduate School of Medicine, Sendai 980-8575, Japan.ORCID 0000-0003-3115-0047
Shinichi FukushigeDepartment of Investigative Pathology, Tohoku University Graduate School of Medicine, Sendai 980-8575, Japan.
Yuriko SaikiDepartment of Investigative Pathology, Tohoku University Graduate School of Medicine, Sendai 980-8575, Japan.
Katsuya HiroseDepartment of Investigative Pathology, Tohoku University Graduate School of Medicine, Sendai 980-8575, Japan.
Takako HiyoshiDepartment of Investigative Pathology, Tohoku University Graduate School of Medicine, Sendai 980-8575, Japan.
Takenori OgawaDepartment of Otolaryngology, Gifu University Graduate School of Medicine, Gifu 501-1194, Japan.
Yukio KatoriDepartment of Otolaryngology-Head and Neck Surgery, Tohoku University Graduate School of Medicine, Sendai 980-8574, Japan.
Toru FurukawaDepartment of Investigative Pathology, Tohoku University Graduate School of Medicine, Sendai 980-8575, Japan.ORCID 0000-0002-1083-2324
Tohoku University · JPGifu University · JP

Funding

Japan Society for the Promotion of Science JP22H02839
6 · The paper itself

Abstract

Long non-coding RNAs (lncRNAs) have emerged as a significant player in various cancers, including pancreatic cancer. However, how lncRNAs are aberrantly expressed in cancers is largely unknown. We hypothesized that lncRNAs would be regulated by signaling pathways and contribute to malignant phenotypes of cancer. In this study, to understand the significance of mitogen-activated protein kinase/extracellular signal-regulated kinase (MAPK/ERK), which is a major aberrant signaling pathway in pancreatic cancer, for the expression of lncRNAs, we performed comparative transcriptome analyses between pancreatic cancer cell lines with or without activation of MAPK. We identified 45 lncRNAs presumably associated with MAPK in pancreatic cancer cells; among these, LINC00941 was consistently upregulated by MAPK. The immediate genomic upstream region flanking LINC00941 was identified as a promoter region, the activity of which was found to be preferentially associated with MAPK activity via ETS-1 binding site. LINC00941 promoted cell proliferation in vitro. Moreover, TCGA data analysis indicated that high expression of LINC00941 was associated with poor prognosis of patients with pancreatic cancer. Transcriptomes comparing transcriptions between cells with and without LINC00941 knockdown revealed 3229 differentially expressed genes involved in 44 biological processes, including the glycoprotein biosynthetic process, beta-catenin-TCF complex assembly, and histone modification. These results indicate that MAPK mediates the aberrant expression of lncRNAs. LINC00941 is the lncRNA by MAPK most consistently promoted, and is implicated in the dismal prognosis of pancreatic cancer. MAPK-associated lncRNAs may play pivotal roles in malignant phenotypes of pancreatic cancer, and as such might represent both potentially valid therapeutic targets and diagnostic biomarkers.

Indexed as

lincRNAMAPKpancreatic cancerpromotersignal transductiontranscriptome

Identifiers

PMID36612299
PMCPMC9818929
OpenAlexW4313398348

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.