Evidence map›Paper›PMID 41635546›Full record

ArticleOncology letters2026

DHX15 overexpression suppresses colorectal cancer cell line proliferation.

Yuki Ii, Kosuke Saita, Toshiro Iwagawa, Shingo Ito, Kiichi Sugimoto, Kazuhiro Sakamoto, Sumiko Watanabe

Abstract read
In one paragraph

Article in Oncology letters, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

7 authors.

Yuki IiDepartment of Coloproctological Surgery, Juntendo University Graduate School of Medicine, Tokyo 113-8421, Japan.
Kosuke SaitaDepartment of Retinal Biology and Pathology, Graduate School of Medicine, University of Tokyo, Tokyo 113-8655, Japan.
Toshiro IwagawaDepartment of Retinal Biology and Pathology, Graduate School of Medicine, University of Tokyo, Tokyo 113-8655, Japan.
Shingo ItoDepartment of Gastrointestinal Surgery, Shonan Kamakura General Hospital, Kanagawa 247-0072, Japan.
Kiichi SugimotoDepartment of Coloproctological Surgery, Juntendo University Graduate School of Medicine, Tokyo 113-8421, Japan.
Kazuhiro SakamotoDepartment of Coloproctological Surgery, Juntendo University Graduate School of Medicine, Tokyo 113-8421, Japan.
Sumiko WatanabeDepartment of Retinal Biology and Pathology, Graduate School of Medicine, University of Tokyo, Tokyo 113-8655, Japan.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

DEAH (Asp-Glu-Ala-His) box helicase 15 (DHX15) is a member of the DEAD box RNA helicase family that carries out a key role in innate immunity against viral infections. It is involved in tumorigenesis as a tumor-promoting factor in various types of cancer, but it has also been suggested to act as a tumor suppressor. However, the role of DHX15 in colorectal cancer (CRC) remains largely unknown. In the present study, we examined the role of DHX15 in CRC. Immunostaining of clinical samples from patients with CRC identified DHX15 proteins in the cell nuclei of both tumor and adjacent normal tissues. DHX15 overexpression was revealed to reduce the cell number of various CRC cell lines, as well as the number of Ki67-positive proliferating cells. However, the number of AC3-positive apoptotic cells was comparable between the control and DHX15-overexpressing cells. The possible downstream mechanisms of DHX15 were further examined which revealed that activation of the Wnt/β-catenin and NF-κB signaling pathways were not affected by DHX15 expression. However, DHX15 overexpression resulted in fewer LC3 puncta in HCT116 and DLD1 cells. Taken together, DHX15 may negatively affect CRC cell proliferation, and autophagy may potentially be involved in the downstream mechanism of DHX15.

Indexed as

autophagycell proliferationcolorectal cancerDHX15tumorigenesis

Identifiers

PMID41635546
PMCPMC12863016

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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.