Evidence map›Paper›PMID 38342100›Full record

ArticleCancer science2024

Gap junction beta-4 accelerates cell cycle progression and metastasis through MET-AKT activation in pancreatic cancer.

Joji Muramatsu, Yohei Arihara, Makoto Yoshida, Tomohiro Kubo, Hajime Nakamura, Kazuma Ishikawa, Hiromi Fujita, Shintaro Sugita, Takumi Konno, Takashi Kojima and 3 more

Open access · goldAbstract read
In one paragraph

Article in Cancer science, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
1.4field-weighted citation impact, top 20% 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

6 citing papers in PubMed, 6 citations in OpenAlex.

  1. Beyond the gap: moonlighting functions of connexins in cancer.Cell communication and signaling : CCS · 2026
    Review
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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

13 authors at 2 institutions in 1 country.

Joji MuramatsuDepartment of Medical Oncology, Sapporo Medical University School of Medicine, Sapporo, Japan.ORCID https://orcid.org/0000-0002-7711-5450
Yohei AriharaDepartment of Medical Oncology, Sapporo Medical University School of Medicine, Sapporo, Japan.
Makoto YoshidaDepartment of Medical Oncology, Sapporo Medical University School of Medicine, Sapporo, Japan.
Tomohiro KuboDepartment of Medical Oncology, Sapporo Medical University School of Medicine, Sapporo, Japan.
Hajime NakamuraDepartment of Medical Oncology, Sapporo Medical University School of Medicine, Sapporo, Japan.
Kazuma IshikawaDepartment of Medical Oncology, Sapporo Medical University School of Medicine, Sapporo, Japan.
Hiromi FujitaDepartment of Surgical Pathology, Sapporo Medical University School of Medicine, Sapporo, Japan.
Shintaro SugitaDepartment of Surgical Pathology, Sapporo Medical University School of Medicine, Sapporo, Japan.
Takumi KonnoDepartment of Cell Science, Research Institute for Frontiers Medicine, Sapporo Medical University School of Medicine, Sapporo, Japan.
Takashi KojimaDepartment of Cell Science, Research Institute for Frontiers Medicine, Sapporo Medical University School of Medicine, Sapporo, Japan.
Yutaka KawanoDepartment of Community Medicine and Medical Science, Tokushima University Graduate School of Biomedical Sciences, Tokushima, Japan.
Masayoshi KobuneDepartment of Hematology, Sapporo Medical University School of Medicine, Sapporo, Japan.
Kohichi TakadaDepartment of Medical Oncology, Sapporo Medical University School of Medicine, Sapporo, Japan.
Sapporo Medical University · JPTokushima University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Despite continuing advances in the development of effective new therapies, including immunotherapies, the prognosis of pancreatic cancer remains extremely poor. Gap junction proteins have become attractive targets for potential cancer therapy. However, the role of gap junction beta-4 (GJB4) protein remains unexplored in pancreatic cancer. Through bioinformatic analyses we discovered pancreatic cancer tissues showed higher levels of GJB4 transcripts compared to normal pancreatic tissues and this had a negative effect on overall survival in patients that had pancreatic cancer. The high expression of nuclear GJB4 was identified as a negative prognostic factor in such patients. Knockdown of GJB4 in cultured pancreatic cancer cells resulted in G

Indexed as

Cell ProliferationConnexinsPancreatic NeoplasmsProto-Oncogene Proteins c-aktProto-Oncogene Proteins c-metAnimalsCell CycleCell Line, TumorCell MovementFemaleGene Expression Regulation, NeoplasticHumansMaleMiceMice, NudeNeoplasm Metastasisconnexin 30.3ConnexinsProto-Oncogene Proteins c-aktProto-Oncogene Proteins c-metcell cycle arrestGJB4MET–AKTmetastasispancreatic cancer

Identifiers

PMID38342100
PMCPMC11093205
OpenAlexW4391733194

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.