Evidence map›Paper›PMID 40176181›Full record

ArticleJournal of ovarian research2025

Modified screening of MYC promotor region elements using the CRISPR library in ovarian cancer.

Akiko Yamamoto, Yosuke Tanaka, Sachiko Ishibashi, Masumi Ikeda, Keisuke Sugita, Masanori Ono, Hirotaka Nishi, Morito Kurata

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Journal of ovarian research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. Article
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.

Akiko Yamamoto *Department of Obstetrics and Gynecology, Tokyo Medical University, 6-7-1Shinjuku-Ku, Tokyo , Nishishinjuku, 1600023, Japan. akko-y@tokyo-med.ac.jp.
Yosuke Tanaka *Bioresource Research Center, Institute of Science Tokyo, Tokyo, Japan.
Sachiko IshibashiDepartment of Comprehensive Pathology, Graduate School of Institute of Science Tokyo, Tokyo, Japan.
Masumi IkedaDepartment of Comprehensive Pathology, Graduate School of Institute of Science Tokyo, Tokyo, Japan.
Keisuke SugitaDepartment of Comprehensive Pathology, Graduate School of Institute of Science Tokyo, Tokyo, Japan.
Masanori OnoDepartment of Obstetrics and Gynecology, Tokyo Medical University, 6-7-1Shinjuku-Ku, Tokyo , Nishishinjuku, 1600023, Japan.
Hirotaka NishiDepartment of Obstetrics and Gynecology, Tokyo Medical University, 6-7-1Shinjuku-Ku, Tokyo , Nishishinjuku, 1600023, Japan.
Morito KurataDepartment of Comprehensive Pathology, Graduate School of Institute of Science Tokyo, Tokyo, Japan.

Funding

KAKENHI 21K16800
6 · The paper itself

Abstract

Ovarian cancer remains one of the most lethal gynecological malignancies owing to its high recurrence rate and chemotherapeutic resistance. MYC is a well-known proto-oncogene that is frequently amplified in ovarian cancer and has been implicated in drug resistance. Previously, we established a new promoter-reporter system combined with a CRISPR activation library to identify unknown MYC regulators, and M1AP was identified as a novel MYC regulator. However, considering the insufficient explanation for the absence of guide RNA (gRNA) of MYC, this present study explored methods to prevent the gRNA of MYC itself from binding. This study first modified the promoter-reporter vector to improve its quality, then conducted CRISPR screening and analyzed candidate genes as MYC promoter regulators using next-generation sequencing in OVSAHO ovarian cancer cells. Eighty-six genes had ≥ 1000 reads, and Pearson's correlation coefficient analysis was performed on the cBioPortal of the Cancer Genomics database. Fourteen genes were identified as candidate MYC regulators with positive and significant correlations with MYC. Seven genes, including CYP4v2, ASPH, ANP32D, PCED1A, ABI1, FUZ, and HOOK2, demonstrated significantly higher luciferase activity than the control genes. Four genes, including ABI1, PCED1A, HOOK2, and CYP4v2, activated the MYC promoter, which showed over twofold higher activity than the control when overexpressed using a vector. In conclusion, four genes that activate MYC promoters were identified in an ovarian cancer cell line using the CRISPR library system with a modified promoter-reporter tool. These results will prove helpful in the development of novel treatment strategies for ovarian cancer.

Indexed as

Clustered Regularly Interspaced Short Palindromic RepeatsOvarian NeoplasmsPromoter Regions, GeneticProto-Oncogene Proteins c-mycCell Line, TumorCRISPR-Cas SystemsFemaleGene Expression Regulation, NeoplasticGene LibraryHumansProto-Oncogene MasMAS1 protein, humanMYC protein, humanProto-Oncogene MasProto-Oncogene Proteins c-mycCRISPRLuciferase assayMYCOncogeneOvarian cancer

Identifiers

PMID40176181
PMCPMC11963443

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LicenceCC BY-NC-ND
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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.