Evidence map›Paper›PMID 41566108›Full record

ArticleDiscover oncology2026

SOX30 is a diagnostic biomarker that suppresses ovarian cancer progression through an autophagy mediated mechanism.

Qian Li, Peng Guo, Keying Chen, Jing Gu, Na Sun, Yating Deng, Fei Wang, Jun Ding, Jinyi Liu, Fei Han

Abstract read
In one paragraph

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

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0citing papers in PubMed
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1 · What the graph read from it

What it found

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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

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3 · Its place in the literature

Who cites it

0 citing papers in PubMed.

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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

10 authors.

Qian Li *Department of Toxicology, School of Public Health, Chongqing Medical University, No.1, Medical College Road, Yuzhong District, Chongqing, 400016, China.
Peng Guo *Department of Hepatobiliary Surgery, Third Affiliated Hospital of Chongqing Medical University, No.1, Shuanghu Branch Road, Huixing Street, Yubei District, Chongqing, 401120, China.
Keying Chen *Department of Toxicology, School of Public Health, Chongqing Medical University, No.1, Medical College Road, Yuzhong District, Chongqing, 400016, China.
Jing GuInstitute of Toxicology, College of Preventive Medicine, Army Medical University, 30 Gaotanyan Street, Shapingba District, Chongqing, 400038, China.
Na SunBreast and Thyroid Surgery, Southwest Hospital, Army Medical University, 30 Gaotanyan Street, Shapingba District, Chongqing, 400038, China.
Yating DengDepartment of Toxicology, School of Public Health, Chongqing Medical University, No.1, Medical College Road, Yuzhong District, Chongqing, 400016, China.
Fei WangDepartment of Toxicology, School of Public Health, Chongqing Medical University, No.1, Medical College Road, Yuzhong District, Chongqing, 400016, China.
Jun DingDepartment of Hepatobiliary Surgery, Third Affiliated Hospital of Chongqing Medical University, No.1, Shuanghu Branch Road, Huixing Street, Yubei District, Chongqing, 401120, China.
Jinyi LiuInstitute of Toxicology, College of Preventive Medicine, Army Medical University, 30 Gaotanyan Street, Shapingba District, Chongqing, 400038, China. jinyiliutmmu@163.com.
Fei HanDepartment of Toxicology, School of Public Health, Chongqing Medical University, No.1, Medical College Road, Yuzhong District, Chongqing, 400016, China. flyskyhf@cqmu.edu.cn.

Funding

Future Medical Youth Innovation Team of Chongqing Medical University W0151the National Natural Science Foundation of China 82073137the Natural Science Foundation of Chongqing cstc2021jcyj-msxmX0985
6 · The paper itself

Abstract

introductionThe discovery and identification of novel diagnostic markers and effective therapeutic targets for ovarian cancer are urgently required. Recent studies have demonstrated that SOX30 suppresses tumor metastasis and serves as a prognostic and chemotherapeutic marker in advanced-stage ovarian cancer. In this study, we aim to investigate the expression patterns, regulatory mechanisms, and diagnostic potential of SOX30, as well as its SOX30 in tumor growth and the underlying mechanisms in ovarian cancer.

methodsUsing data from The Cancer Genome Atlas (TCGA) database, we comprehensively analyzed the association between SOX30 expression levels and copy number variations (CNVs) as well as DNA methylation in ovarian cancer. The functional role of SOX30 in tumor growth was evaluated through MTS assays, colony formation assays, rescue experiments, and xenograft models. Flow cytometry, western blotting, and confocal microscopy were employed to explore the effects of SOX30 on apoptosis and autophagy. Additionally, co-expression analysis of SOX30-related genes and functional enrichment analysis were performed to uncover potential biological pathways.

resultsSOX30 was frequently overexpressed in ovarian cancer, closely associated with copy number amplification, and effectively distinguished tumor tissues from normal tissues. Functionally, SOX30 significantly inhibited cancer cell proliferation in vitro and suppressed tumor growth in vivo, inducting slight cell apoptosis but marked autophagy in ovarian cancer cells. Mechanistically, the inhibitory effect of SOX30 on cancer cell proliferation was dependent on the regulation of autophagy. At the molecular level, SOX30 modulated biological processes and signaling pathways related to autophagy rather than apoptosis in ovarian cancer. Furthermore, SOX30 showed a strong positive correlation with key autophagy-related genes in ovarian cancer.

conclusionsOur findings identify SOX30 as a promising diagnostic marker and therapeutic target in ovarian cancer, and highlight the previously underappreciated role of SOX30 in suppressing cancer cell proliferation and tumor growth primarily through an autophagy-mediated mechanism, offering new insights into the pathogenesis and treatment of ovarian cancer.

Indexed as

AutophagyOvarian cancerSOX30Tumor growth

Identifiers

PMID41566108
PMCPMC12905037

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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.