Evidence map›Paper›PMID 39367898›Full record

ArticleClinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico2025

Inhibiting SNX10 induces autophagy to suppress invasion and EMT and inhibits the PI3K/AKT pathway in cervical cancer.

Dan Liao, Yanxian He, Bin He, Saitian Zeng, Yejia Cui, Cuifen Li, Haohai Huang

Abstract read
PubMed Publisher
In one paragraph

Article in Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing 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

7 citing papers in PubMed.

  1. Article
  2. Article
  3. Article
  4. Targeting proteostasis pathways for cancer therapy.Journal of pharmaceutical analysis · 2025
    Review
  5. Article
  6. Review
  7. 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

7 authors.

Dan LiaoDepartment of Gynaecology, Affiliated Dongguan Songshan Lake Central Hospital, Guangdong Medical University, No.1, Huangzhou Xianglong Road of Shilong Town, Dongguan, 523326, Guangdong, China. 26312526@qq.com.
Yanxian HeDepartment of Gynaecology, Affiliated Dongguan Songshan Lake Central Hospital, Guangdong Medical University, No.1, Huangzhou Xianglong Road of Shilong Town, Dongguan, 523326, Guangdong, China.
Bin HeClinical Translational Medical Center, Affiliated Dongguan Songshan Lake Central Hospital, Guangdong Medical University, Dongguan, Guangdong, China.
Saitian ZengDepartment of Gynaecology, Affiliated Dongguan Songshan Lake Central Hospital, Guangdong Medical University, No.1, Huangzhou Xianglong Road of Shilong Town, Dongguan, 523326, Guangdong, China.
Yejia CuiDepartment of Clinical Laboratory, Affiliated Dongguan Songshan Lake Central Hospital, Guangdong Medical University, Dongguan, Guangdong, China.
Cuifen LiDepartment of Gynaecology, Affiliated Dongguan Songshan Lake Central Hospital, Guangdong Medical University, No.1, Huangzhou Xianglong Road of Shilong Town, Dongguan, 523326, Guangdong, China.
Haohai HuangClinical Translational Medical Center, Affiliated Dongguan Songshan Lake Central Hospital, Guangdong Medical University, Dongguan, Guangdong, China. haohaihuang@hotmail.com.ORCID http://orcid.org/0009-0002-9017-708X

Funding

Medical Scientific Research Foundation of Guangdong Province A2023476National Natural Science Foundation of China 82303389
6 · The paper itself

Abstract

purposeCervical cancer (CC) is a prevalent malignancy among women with high morbidity and poor prognosis. Sorting nexin 10 (SNX10) is a newly recognized cancer regulatory factor, while its action on CC progression remains elusive. Hence, this study studied the effect of SNX10 on CC development and investigated the mechanism.

methodsThe SNX10 level in CC and the overall survival of CC cases with different SNX10 expressions were determined by bioinformatics analysis in GEPIA. The SNX10 expression in tumor tissues and clinical significance were studied in 64 CC cases. The overall survival was assessed using Kaplan-Meier analysis. The formation of LC3 was evaluated using immunofluorescence. Cell invasion was measured using the Transwell assay. Epithelial-to-mesenchymal transition (EMT) was determined by observing cell morphology and assessing EMT marker levels. A xenograft tumor was constructed to evaluate tumor growth.

resultsSNX10 was elevated in CC tissues and cells, and the CC cases with high SNX10 levels exhibited poor overall survival. Besides, SNX10 correlated with the FIGO stage, lymph node invasion, and stromal invasion of CC. SNX10 silencing induced CC cell autophagy and suppressed CC cell invasion and EMT. Meanwhile, silenced SNX10 could suppress invasion and EMT via inducing autophagy. Furthermore, SNX10 inhibition suppressed the PI3K/AKT pathway. Moreover, silenced SNX10 restrained the tumor growth, autophagy, and EMT of CC in vivo.

conclusionSNX10 was enhanced in CC and correlated with poor prognosis. Silenced SNX10 induced autophagy to suppress invasion and EMT and inhibited the PI3K/AKT pathway in CC, making SNX10 a valuable molecule for CC therapy.

Indexed as

AutophagyEpithelial-Mesenchymal TransitionPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktSorting NexinsUterine Cervical NeoplasmsAnimalsCell MovementFemaleHumansMiceMice, Inbred BALB CMice, NudeMiddle AgedNeoplasm InvasivenessPrognosisPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktSNX10 protein, humanSorting NexinsAutophagyCervical cancerInvasionMigrationPI3K/AKTSNX10

Identifiers

PMID39367898

What OpenQuestion holds

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Registered trials

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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.