Evidence map›Paper›PMID 29643475›Full record

ArticleOncogene2018

Tumor-derived exosomal lnc-Sox2ot promotes EMT and stemness by acting as a ceRNA in pancreatic ductal adenocarcinoma.

Zhonghu Li, Peng Jiang, Jie Li, Minjie Peng, Xin Zhao, Xi Zhang, Kai Chen, Yujun Zhang, Hui Liu, Lang Gan and 4 more

Abstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 161 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
161citing papers in PubMed, 2 pooled it
12.3field-weighted citation impact, top 1% 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

161 citing papers in PubMed, 2 syntheses or guidelines pooled it, 264 citations in OpenAlex.

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  14. Small extracellular vesicles (sEVs) in pancreatic cancer progression and diagnosis.Journal of controlled release : official journal of the Controlled Release Society · 2025
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101 more citing papers are in PubMed but not listed here.

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

14 authors at 2 institutions in 1 country.

Zhonghu LiHepatobiliary Surgery Institute, Southwest Hospital, Third Military Medical University, Chongqing, China.
Peng JiangHepatobiliary Surgery Institute, Southwest Hospital, Third Military Medical University, Chongqing, China.
Jie LiHepatobiliary Surgery Institute, Southwest Hospital, Third Military Medical University, Chongqing, China.
Minjie PengHepatobiliary Surgery Institute, Southwest Hospital, Third Military Medical University, Chongqing, China.
Xin ZhaoHepatobiliary Surgery Institute, Southwest Hospital, Third Military Medical University, Chongqing, China.
Xi ZhangHepatobiliary Surgery Institute, Southwest Hospital, Third Military Medical University, Chongqing, China.
Kai ChenHepatobiliary Surgery Institute, Southwest Hospital, Third Military Medical University, Chongqing, China.
Yujun ZhangHepatobiliary Surgery Institute, Southwest Hospital, Third Military Medical University, Chongqing, China.
Hui LiuHepatobiliary Surgery Institute, Southwest Hospital, Third Military Medical University, Chongqing, China.
Lang GanHepatobiliary Surgery Institute, Southwest Hospital, Third Military Medical University, Chongqing, China.
Huaqiang BiHepatobiliary Surgery Institute, Southwest Hospital, Third Military Medical University, Chongqing, China.
Ping ZhenHepatobiliary Surgery Institute, Southwest Hospital, Third Military Medical University, Chongqing, China.
Jin ZhuHepatobiliary Surgery Institute, Southwest Hospital, Third Military Medical University, Chongqing, China.
Xiaowu LiHepatobiliary Surgery Institute, Southwest Hospital, Third Military Medical University, Chongqing, China. lixw1966@163.com.
Southwest Hospital · CNArmy Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Long noncoding RNAs (lncRNAs) or exosomes have recently been shown to play vital regulatory or communication roles in cancer biology. However, the roles and mechanisms of exosomal lncRNAs in tumor invasion or metastasis of pancreatic ductal adenocarcinoma (PDAC) remain unknown. In this study, we aimed to investigate the detailed roles and mechanisms of tumor-generated exosomes in progression and metastasis of PDAC in vitro and in vivo. We identified a lncRNA-Sox2ot from exosomes of highly invasive PDAC cells, and analyzed the expression of Sox2ot in the plasma samples and found that the plasma exosomal Sox2ot expression was high and correlated with TNM stage and overall survival rate of PDAC patients. Further research showed that Sox2ot promotes epithelial-mesenchymal transition (EMT) and stem cell like properties by regulating Sox2 expression. Sox2ot competitively binds to the miR-200 family to regulate the expression of Sox2, thus promoting invasion and metastasis of PDAC. We also confirmed the transmission of the exosomes from producer cells to recipient PDAC cells, exosomal Sox2ot can promote tumor invasion and metastasis in vitro and in vivo. We further confirmed tumor generated exosomes could excrete to tumor cell or blood circulation in vivo condition. Finally, we observed a decreased exosomal Sox2ot expression in postoperative blood samples of PDAC patients. The exosomal lncRNA Sox2ot plays important roles in tumor progression and may be a useful maker for pancreatic cancer prognosis.

Indexed as

AnimalsCarcinoma, Pancreatic DuctalCell Line, TumorCell MovementDisease ProgressionEpithelial-Mesenchymal TransitionExosomesGene Expression Regulation, NeoplasticHumansMaleMiceMice, NudeNeoplasm InvasivenessPancreatic NeoplasmsPrognosisRNA, Long NoncodingRNA, Long NoncodingSOX2 protein, humanSOXB1 Transcription Factors

Identifiers

PMID29643475
OpenAlexW2796759472

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.