Evidence map›Paper›PMID 32774721›Full record

ArticleAmerican journal of translational research2020

MAGEA3 promotes proliferation and suppresses apoptosis in cervical cancer cells by inhibiting the KAP1/p53 signaling pathway.

Xinping Gao, Qing Li, Guobin Chen, Haipeng He, Ying Ma

Open access · greenAbstract read
In one paragraph

Article in American journal of translational research, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
1.0field-weighted citation impact, top 25% of its field
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

19 citing papers in PubMed, 21 citations in OpenAlex.

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  7. KAP1 in antiviral immunity: dual roles in viral silencing and immune regulation.Frontiers in cellular and infection microbiology · 2025
    Review
  8. Multifaceted role ofMedComm · 2024
    Review
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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

5 authors at 3 institutions in 1 country.

Xinping GaoDepartment of Obstetrics and Gynecology, Shenzhen SAMII Medical Center Shenzhen, Guangdong, China.
Qing LiDepartment of Obstetrics and Gynecology, Affiliated Hospital of Hebei University, Hebei University Medical College Baoding, Hebei, China.
Guobin ChenDepartment of Obstetrics and Gynecology, Shenzhen Maternity and Child Healthcare Hospital Shenzhen, Guangdong, China.
Haipeng HeDepartment of Obstetrics and Gynecology, Affiliated Hospital of Hebei University, Hebei University Medical College Baoding, Hebei, China.
Ying MaDepartment of Obstetrics and Gynecology, Affiliated Hospital of Hebei University, Hebei University Medical College Baoding, Hebei, China.
Affiliated Hospital of Hebei University · CNShenzhen Genoimmune Medical Institute · CNShenzhen Maternity and Child Healthcare Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Melanoma-associated antigen A3 (MAGEA3), a member of the cancer-testis antigen (CTA) family, is aberrantly expressed in various cancer types. Accumulating evidence indicates that MAGEA3 plays a vital role in the pathogenesis and development of various cancers. However, the underlying mechanisms behind the tumor-promoting effect of MAGEA3 remain unclear, particularly in cervical cancer (CC). The present study investigated the effects of MAGEA3 on CC cell proliferation and apoptosis as well as the underlying molecular mechanism. Cell Counting Kit-8 (CCK-8), 5-ethynyl-2'-deoxyuridine (EdU), and flow cytometry assays were used to evaluate the effects of MAGE-A3 on proliferation, cell cycle, and apoptosis. Co-immunoprecipitation (Co-IP), dual-luciferase reporter, western blotting, and quantitative RT-PCR assays were performed to investigate the regulatory mechanisms of MAGEA3 in CC cells. Compared to the control, MAGE-A3 overexpression markedly promoted the proliferation of SiHa cells in vitro and in vivo, increased the proportion of cells in S phase, and suppressed apoptosis. However, MAGEA3 knockdown inhibited proliferation, blocked the cell cycle in G1 phase, and induced apoptosis in HeLa cells. Further mechanistic study revealed that MAGEA3 interacts with KAP1, thereby suppressing p53 transcriptional activity, thus suppressing p53-mediated regulation of the expression of genes involved in the cell cycle (p21, cyclin D1) and apoptosis (Bax, Bcl-2, and PUMA). Collectively, our results, both in vivo and in vitro, indicate that the expression of MAGEA3 contributes to CC cell proliferation and tumor growth and exerts tumor-promoting effects by regulating the KAP1/p53 signaling pathway.

Indexed as

apoptosiscell cyclecervical cancerKRAB domain-associated protein 1 (KAP1)Melanoma-associated antigen A3 (MAGEA3)p53

Identifiers

PMID32774721
PMCPMC7407682
OpenAlexW3049208014

What OpenQuestion holds

Textmetadata
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 OpenQuestion graph.