Evidence map›Paper›PMID 41339379›Full record

ArticleScientific reports2025

FAM172A promotes epithelial ovarian cancer progression and induces platinum resistance via the PI3K/AKT pathway.

Yuanyuan Wu, Jie Ma, Bo Wu, Zhixiang Li, Yan Li, Chenglei Zhang, Lijuan Wang, Jiarui Li, Yanru Ren, Yi Yang

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Scientific reports, 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. Review
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.

Yuanyuan Wu *School of Basic Medical Sciences, Ningxia Medical University, 1160 Shengli Street, Yinchuan750000 China, Yinchuan, 750000, China.
Jie Ma *School of Basic Medical Sciences, Ningxia Medical University, 1160 Shengli Street, Yinchuan750000 China, Yinchuan, 750000, China.
Bo WuDepartment of oncological surgery, Cancer Hospital, General Hospital of Ningxia Medical University, Yinchuan, 750000, China.
Zhixiang LiClinical Medical College of Ningxia Medical University, Yinchuan, 750000, China.
Yan LiSchool of Basic Medical Sciences, Ningxia Medical University, 1160 Shengli Street, Yinchuan750000 China, Yinchuan, 750000, China.
Chenglei ZhangMedical Laboratory, General Hospital of Ningxia Medical University, Yinchuan, 750000, China.
Lijuan WangDepartment of Endocrinology, General Hospital of Ningxia Medical University, Yinchuan, 750000, China.
Jiarui LiSchool of Basic Medical Sciences, Ningxia Medical University, 1160 Shengli Street, Yinchuan750000 China, Yinchuan, 750000, China.
Yanru RenSchool of Basic Medical Sciences, Ningxia Medical University, 1160 Shengli Street, Yinchuan750000 China, Yinchuan, 750000, China.
Yi YangSchool of Basic Medical Sciences, Ningxia Medical University, 1160 Shengli Street, Yinchuan750000 China, Yinchuan, 750000, China. yangyi@nxmu.edu.cn.

Funding

the Ningxia Natural Science Foundation No. 2021AAC03354
6 · The paper itself

Abstract

This study aimed to investigate the role of FAM172A in epithelial ovarian cancer (EOC), a highly lethal gynecological malignancy often diagnosed at late stages with limited treatment options. FAM172A expression was evaluated in EOC and normal ovarian tissues using western blotting and immunohistochemistry, and its association with patient prognosis, treatment response, and CA125 levels was assessed by multivariate regression analysis. Functional assays were performed to examine the effects of FAM172A on EOC cell proliferation, migration, and invasion. In vivo models were used to evaluate the influence of FAM172A on tumor growth, metastasis, and chemosensitivity. The underlying mechanism was explored by modulating the PI3K-Akt pathway with pharmacological inhibitors and activators. FAM172A was significantly upregulated in EOC tissues, and its elevated expression correlated with poor prognosis, chemotherapy resistance, and increased CA125 levels. Multivariate analysis identified FAM172A expression, platinum sensitivity, and CA125 as independent prognostic factors. In vitro, FAM172A promoted malignant behavior and conferred resistance to cisplatin. In vivo, knockdown of FAM172A suppressed tumor progression and enhanced the efficacy of cisplatin. Mechanistically, FAM172A exerted its effects through regulation of the PI3K-Akt pathway, and modulation of PI3K signaling rescued FAM172A-induced phenotypic changes. These findings highlight FAM172A as a critical promoter of EOC progression, associated with aggressive tumor characteristics and treatment failure. By activating the PI3K-Akt pathway, FAM172A represents a promising therapeutic target for EOC, potentially offering new strategies to improve patient outcomes, particularly in overcoming chemoresistance.

Indexed as

Carcinoma, Ovarian EpithelialDrug Resistance, NeoplasmOvarian NeoplasmsPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktAnimalsAntineoplastic AgentsCA-125 AntigenCell Line, TumorCell MovementCell ProliferationCisplatinDisease ProgressionFemaleGene Expression Regulation, NeoplasticHumansAntineoplastic AgentsCA-125 AntigenCisplatinPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktCisplatin sensitivityFAM172AOvarian cancerPI3K-Akt signaling pathwayPrognosis

Identifiers

PMID41339379
PMCPMC12678607

What Socratic holds

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LicenceCC BY
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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.