Evidence map›Paper›PMID 38907071›Full record

ArticleMolecular biotechnology2025

EPB41L3 Inhibits the Progression of Cervical Cancer Via the ERK/p38 MAPK Signaling Pathway.

Gulixian Tuerxun, Wenyun Li, Guligeina Abudurexiti, Qian Zhuo, Awahan Tuerdi, Guzalinuer Abulizi

Abstract read
PubMed Publisher
In one paragraph

Article in Molecular biotechnology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing 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

4 citing papers in PubMed.

  1. Article
  2. Organoid technology in cervical cancer research.American journal of cancer research · 2025
    Review
  3. Article
  4. 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

6 authors.

Gulixian TuerxunFifth Department of Gynecologic Surgery, Affiliated Tumor Hospital, Xinjiang Medical University, No. 789 East Suzhou Street, Xinshi District, Urumqi, 830000, China.
Wenyun LiFifth Department of Gynecologic Surgery, Affiliated Tumor Hospital, Xinjiang Medical University, No. 789 East Suzhou Street, Xinshi District, Urumqi, 830000, China.
Guligeina AbudurexitiFifth Department of Gynecologic Surgery, Affiliated Tumor Hospital, Xinjiang Medical University, No. 789 East Suzhou Street, Xinshi District, Urumqi, 830000, China.
Qian ZhuoFifth Department of Gynecologic Surgery, Affiliated Tumor Hospital, Xinjiang Medical University, No. 789 East Suzhou Street, Xinshi District, Urumqi, 830000, China.
Awahan TuerdiMaternal and Child Health Service Center Shayibake District, Urumqi, China.
Guzalinuer AbuliziFifth Department of Gynecologic Surgery, Affiliated Tumor Hospital, Xinjiang Medical University, No. 789 East Suzhou Street, Xinshi District, Urumqi, 830000, China. 00157@xjmu.edu.cn.ORCID http://orcid.org/0009-0008-0857-8479

Funding

Natural Science Foundation of Xinjiang Uygur Autonomous Region 2022D01C506
6 · The paper itself

Abstract

This study was aimed to uncover the character and potential regulatory mechanism of EPB41L3 in cervical cancer (CC). CC cells were injected into BALB/c nude mice (female) to construct a xenograft tumor model. Real-time quantitative polymerase chain reaction (qRT-PCR) and western blot were performed to evaluate the expression of EPB41L3, ERK/p38 MAPK signal markers in CC tissues and cells. Cell counting kit-8 (CCK-8) and Transwell was applied to analyze the viability, invasion, and migration of CC cell lines. EPB41L3 was substantially decreased both in CC tissues and cells. Cell viability, invasion, and migration of CC cells were reduced by overexpressing EPB41L3. Bioinformatics analysis prerdicted that EPB41L3 was strongly related to the ERK/p38 MAPK pathway. Compared with Ad-nc mice, the volume and weight of tumors and ERK/p38 MAPK signal markers were down-regulated in Ad-EPB41L3 mice. After knocking down EPB41L3 with EPB41L3 siRNA (siEPB41L3), the ERK/p38 MAPK pathway was activated. Moreover, SB203580 treatment reversed the effect of EPB41L3 silencing on the improvement in viability, migration, and invasion of CC cells. EPB41L3 suppresses the progression of CC via activating the ERK/p38 MAPK pathway. EPB41L3 may serve as an effective therapeutic target for CC.

Indexed as

MAP Kinase Signaling Systemp38 Mitogen-Activated Protein KinasesUterine Cervical NeoplasmsAnimalsCell Line, TumorCell MovementCell ProliferationCell SurvivalDisease ProgressionFemaleGene Expression Regulation, NeoplasticHumansMiceMice, Inbred BALB CMice, NudeXenograft Model Antitumor Assaysp38 Mitogen-Activated Protein KinasesCervical cancerEPB41L3ERKInvasionMigrationp38 MAPK pathway

Identifiers

PMID38907071

What OpenQuestion holds

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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 OpenQuestion graph.