Evidence map›Paper›PMID 41869444›Full record

ArticleJournal of Cancer2026

C4orf3 Regulates HIF-1α Degradation Under Hypoxic Conditions and Contributes to the Malignant Phenotype in Small Cell Lung Cancer.

Keita Sakanashi, Hideya Onishi, Naoya Iwamoto, Yoshiyuki Nakanishi, Shinsaku Itoyama, Shogo Masuda, Keigo Ozono, Kosuke Yanai, Katsuya Nakamura, Masayo Nagami and 4 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Journal of Cancer, 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

14 authors.

Keita SakanashiDepartment of Surgery and Oncology, Graduate School of Medical Sciences, Kyushu University, 3-1-1 Maidashi, Higashi-ku, Fukuoka 812-8582, Japan; Department of Surgery and Oncology, Graduate School of Medical Sciences, Kyushu University, Fukuoka, Japan.
Hideya OnishiPancreatobiliary Surgery/ Kidney and Pancreas Transplantation, Kyushu University Hospital, 3-1-1 Maidashi, Higashi-ku, Fukuoka 812-8582, Japan.
Naoya IwamotoDepartment of Surgery and Oncology, Graduate School of Medical Sciences, Kyushu University, 3-1-1 Maidashi, Higashi-ku, Fukuoka 812-8582, Japan; Department of Surgery and Oncology, Graduate School of Medical Sciences, Kyushu University, Fukuoka, Japan.
Yoshiyuki NakanishiDepartment of Surgery and Oncology, Graduate School of Medical Sciences, Kyushu University, 3-1-1 Maidashi, Higashi-ku, Fukuoka 812-8582, Japan; Department of Surgery and Oncology, Graduate School of Medical Sciences, Kyushu University, Fukuoka, Japan.
Shinsaku ItoyamaDepartment of Otorhinolaryngology Graduate School of Medical Sciences Kyushu University Fukuoka, Japan.
Shogo MasudaDepartment of Otorhinolaryngology Graduate School of Medical Sciences Kyushu University Fukuoka, Japan.
Keigo OzonoDepartment of Respiratory Surgery, Hamanomachi Hospital, Fukuoka, Japan.
Kosuke YanaiYakuin Internal Medicine and Cardiology Clinic, Fukuoka, Japan.
Katsuya NakamuraDepartment of Respiratory Surgery, Japan Community Health Care Organisation, Kyushu Hospital, Kitakyushu, Japan.
Masayo NagamiFukuoka General Cancer Clinic, Fukuoka, Japan.
Kenichi NishiyamaDepartment of Pathology, Japanese Red Cross Fukuoka Hospital, Fukuoka, Japan.
Masayuki KojimaDepartment of Surgery and Oncology, Graduate School of Medical Sciences, Kyushu University, Fukuoka, Japan; Japanese Red Cross, Fukuoka Hospital, Fukuoka, Japan.
Yoshinao OdaDepartment of Anatomical Pathology, Graduate School of Medical Sciences, Kyushu University, Fukuoka, Japan.
Masafumi NakamuraDepartment of Surgery and Oncology, Graduate School of Medical Sciences, Kyushu University, 3-1-1 Maidashi, Higashi-ku, Fukuoka 812-8582, Japan; Department of Surgery and Oncology, Graduate School of Medical Sciences, Kyushu University, Fukuoka, Japan.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Hypoxia is a critical feature of the tumour microenvironment in small cell lung cancer (SCLC) and contributes to malignant progression through hypoxia-inducible factor 1 alpha (HIF-1α)-mediated transcriptional programs. However, the upstream regulators that maintain HIF-1α stability under hypoxic conditions remain incompletely understood. In this study, we identified the chromosome 4 open reading frame 3 (C4orf3) as a hypoxia-inducible gene and investigated its functional significance in SCLC. C4orf3 expression is upregulated under hypoxic conditions, and its knockdown suppresses cell proliferation, migration, and invasion

Identifiers

PMID41869444
PMCPMC13003554

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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.