Evidence map›Paper›PMID 33948367›Full record

ArticleAmerican journal of cancer research2021

MEX3A suppresses proliferation and EMT via inhibiting Akt signaling pathway in cervical cancer.

Yichi Xu, Shuya Pan, Hong Chen, Hongfei Qian, Zhiwei Wang, Xueqiong Zhu

Open access · greenAbstract read
In one paragraph

Article in American journal of cancer research, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
2.4field-weighted citation impact, top 11% 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

15 citing papers in PubMed, 21 citations in OpenAlex.

  1. EMT and cancer stem cells: Drivers of therapy resistance and promising therapeutic targets.Drug resistance updates : reviews and commentaries in antimicrobial and anticancer chemotherapy · 2025
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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

6 authors at 1 institution in 1 country.

Yichi XuCenter for Uterine Cancer Diagnosis & Therapy Research of Zhejiang Province, Department of Obstetrics and Gynecology, The Second Affiliated Hospital of Wenzhou Medical University Wenzhou, People's Republic of China.
Shuya PanCenter for Uterine Cancer Diagnosis & Therapy Research of Zhejiang Province, Department of Obstetrics and Gynecology, The Second Affiliated Hospital of Wenzhou Medical University Wenzhou, People's Republic of China.
Hong ChenCenter for Uterine Cancer Diagnosis & Therapy Research of Zhejiang Province, Department of Obstetrics and Gynecology, The Second Affiliated Hospital of Wenzhou Medical University Wenzhou, People's Republic of China.
Hongfei QianCenter for Uterine Cancer Diagnosis & Therapy Research of Zhejiang Province, Department of Obstetrics and Gynecology, The Second Affiliated Hospital of Wenzhou Medical University Wenzhou, People's Republic of China.
Zhiwei WangCenter for Uterine Cancer Diagnosis & Therapy Research of Zhejiang Province, Department of Obstetrics and Gynecology, The Second Affiliated Hospital of Wenzhou Medical University Wenzhou, People's Republic of China.
Xueqiong ZhuCenter for Uterine Cancer Diagnosis & Therapy Research of Zhejiang Province, Department of Obstetrics and Gynecology, The Second Affiliated Hospital of Wenzhou Medical University Wenzhou, People's Republic of China.
Wenzhou Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

MEX3A, one member of the human MEX3 gene family, exerts different effects on a variety of human cancer cells. However, the biological functions and regulatory mechanism have not been explored in cervical cancer. In our study, we used multiple approaches to determine the functions and underlying molecular mechanism of MEX3A in cervical tumorigenesis, including CCK-8 assay, BrdU assay, FACS for cell cycle and apoptosis, wound healing assay, Transwell migration and invasion assays, immunohistochemistry (IHC) assay, Transfection, real-time RT-PCR and Western blotting analysis. IHC results showed that the expression levels of MEX3A were decreased in cervical cancer patients with advanced clinical stages and lymph node involvement. Moreover, upregulation of MEX3A attenuated cell proliferation, migration and invasion and induced cell cycle arrest at G0/G1 phase in human cervical cancer cells, whereas knockdown of MEX3A exhibited the opposite effects. Mechanistically, MEX3A exerted its tumor suppressive functions via inactivation of Akt signaling pathway and inhibiting epithelial to mesenchymal transition (EMT). Importantly, Akt activation by its activator SC79 reversed the biological functions of MEX3A overexpression. Furthermore, MEX3A inhibited tumor growth in xenograft models. Overall, our investigation suggested that MEX3A participated in antitumor activity in cervical cancer by inhibition of the Akt signaling pathway and EMT. Hence, targeting MEX3A might have a therapeutic potential to treat cervical cancer.

Indexed as

Aktcervical cancerEMTinvasionMEX3Aproliferation

Identifiers

PMID33948367
PMCPMC8085868
OpenAlexW3159381592

What Socratic 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 Socratic graph.