Evidence map›Paper›PMID 39604563›Full record

ArticleBreast cancer (Tokyo, Japan)2025

The role of C1orf50 in breast cancer progression and prognosis.

Yusuke Otani, Atsushi Tanaka, Masaki Maekawa, Tirso Peña, Anna Rogachevskaya, Teruhiko Ando, Takuto Itano, Haruyoshi Katayama, Eiji Nakata, Toshifumi Ozaki and 4 more

Abstract read
In one paragraph

Article in Breast cancer (Tokyo, Japan), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing 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

4 citing papers in PubMed.

  1. Article
  2. 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

14 authors.

Yusuke Otani *Department of Pathology, Beth Israel Deaconess Medical Center, Boston, MA, USA.
Atsushi Tanaka *Department of Pathology, Beth Israel Deaconess Medical Center, Boston, MA, USA.
Masaki MaekawaDepartment of Pathology, Beth Israel Deaconess Medical Center, Boston, MA, USA.
Tirso PeñaDepartment of Pathology, Beth Israel Deaconess Medical Center, Boston, MA, USA.
Anna RogachevskayaDepartment of Pathology, Beth Israel Deaconess Medical Center, Boston, MA, USA.
Teruhiko AndoDepartment of Orthopedic Surgery, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, 2-5-1 Shikata-Cho, Kita-Ku, Okayama, 700-8558, Japan.
Takuto ItanoDepartment of Orthopedic Surgery, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, 2-5-1 Shikata-Cho, Kita-Ku, Okayama, 700-8558, Japan.
Haruyoshi KatayamaDepartment of Orthopedic Surgery, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, 2-5-1 Shikata-Cho, Kita-Ku, Okayama, 700-8558, Japan.
Eiji NakataDepartment of Orthopedic Surgery, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, 2-5-1 Shikata-Cho, Kita-Ku, Okayama, 700-8558, Japan.
Toshifumi OzakiDepartment of Orthopedic Surgery, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, 2-5-1 Shikata-Cho, Kita-Ku, Okayama, 700-8558, Japan.
Shinichi ToyookaDepartment of General Thoracic Surgery and Breast and Endocrinological Surgery, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, 2-5-1 Shikata-Cho, Kita-Ku, Okayama, 700-8558, Japan.
Hiroyoshi DoiharaDepartment of General Surgery, Kawasaki Medical School General Medical Center, 2-6-1 Nakasange, Kita-Ku, Okayama, 700-8505, Japan.
Michael H RoehrlDepartment of Pathology, Beth Israel Deaconess Medical Center, Boston, MA, USA.
Atsushi FujimuraDepartment of Cellular Physiology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, 2-5-1 Shikata-Cho, Kita-Ku, Okayama, 700-8558, Japan. atsushi.fujimura@okayama-u.ac.jp.ORCID http://orcid.org/0000-0002-8638-5460

Funding

Agency for Medical Research and Development JP19cm0106143Agency for Medical Research and Development JP22cm0106179Grant-in-Aid for Scientific Research from the Ministry of Education, Culture, Sports, Sciences, and Technology of Japan JP23K06676
6 · The paper itself

Abstract

Although the prognosis of breast cancer has significantly improved compared to other types of cancer, there are still some patients who expire due to recurrence or metastasis. Therefore, it is necessary to develop a method to identify patients with poor prognosis at the early stages of cancer. In the process of discovering new prognostic markers from genes of unknown function, we found that the expression of C1orf50 determines the prognosis of breast cancer patients, especially for those with Luminal A breast cancer. This study aims to elucidate the molecular role of C1orf50 in breast cancer progression. Bioinformatic analyses of the breast cancer dataset of TCGA, and in vitro analyses, reveal the molecular pathways influenced by C1orf50 expression. C1orf50 knockdown suppressed the cell cycle of breast cancer cells and weakened their ability to maintain the undifferentiated state and self-renewal capacity. Interestingly, upregulation of C1orf50 increased sensitivity to CDK4/6 inhibition. In addition, C1orf50 was found to be more abundant in breast cancer cells than in normal breast epithelium, suggesting C1orf50's involvement in breast cancer pathogenesis. Furthermore, the mRNA expression level of C1orf50 was positively correlated with the expression of PD-L1 and its related factors. These results suggest that C1orf50 promotes breast cancer progression through cell cycle upregulation, maintenance of cancer stemness, and immune evasion mechanisms. Our study uncovers the biological functions of C1orf50 in Luminal breast cancer progression, a finding not previously reported in any type of cancer.

Indexed as

Biomarkers, TumorBreast NeoplasmsB7-H1 AntigenCell Line, TumorCell ProliferationDisease ProgressionFemaleGene Expression Regulation, NeoplasticHumansPrognosisB7-H1 AntigenBiomarkers, TumorCD274 protein, humanC1orf50Cell cycleImmune evasionLuminal A breast cancerYAP/TAZ

Identifiers

PMID39604563
PMCPMC11842435

What Socratic 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 Socratic graph.