Evidence map›Paper›PMID 33298873›Full record

ArticleCell death discovery2020

A novel lncRNA PTTG3P/miR-132/212-3p/FoxM1 feedback loop facilitates tumorigenesis and metastasis of pancreatic cancer.

Wenyu Liu, Jian Tang, Huiqing Zhang, Fanyang Kong, Huiyun Zhu, Ping Li, Zhaoshen Li, Xiangyu Kong, Kaixuan Wang

Open access · goldAbstract read
In one paragraph

Article in Cell death discovery, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
1.4field-weighted citation impact, top 20% 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

20 citing papers in PubMed, 24 citations in OpenAlex.

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  14. LncRNA PTTG3P induced aberrant glycosylated IgA1 production and B cell growth in IgA nephropathy.Environmental science and pollution research international · 2021
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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

9 authors at 3 institutions in 1 country.

Wenyu LiuDepartment of General Surgery, Changhai Hospital, Second Military Medical University, Shanghai, 200433, China.
Jian TangDepartment of Gastroenterology, Changhai Hospital, Second Military Medical University, Shanghai, 200433, China.
Huiqing ZhangDepartment of Gastrointestinal Medical Oncology, Jiangxi Cancer Hospital, Nanchang, Jiangxi, 330029, China.
Fanyang KongDepartment of Gastroenterology, Changhai Hospital, Second Military Medical University, Shanghai, 200433, China.
Huiyun ZhuDepartment of Gastroenterology, Changhai Hospital, Second Military Medical University, Shanghai, 200433, China.
Ping LiDepartment of Gastroenterology, Changhai Hospital, Second Military Medical University, Shanghai, 200433, China.
Zhaoshen LiDepartment of Gastroenterology, Changhai Hospital, Second Military Medical University, Shanghai, 200433, China. zhaoshenli5610@hotmail.com.
Xiangyu KongDepartment of Gastroenterology, Changhai Hospital, Second Military Medical University, Shanghai, 200433, China. xiangyukong185@hotmail.com.
Kaixuan WangDepartment of Gastroenterology, Changhai Hospital, Second Military Medical University, Shanghai, 200433, China. wangkaixuan224007@163.com.
Changhai Hospital · CNSecond Military Medical University · CNJiangxi Provincial Cancer Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Pseudogene pituitary tumor-transforming 3 (PTTG3P) is emerging as a key player in the development and progression of cancer. However, the biological role and clinical significance of PTTG3P in pancreatic ductal adenocarcinoma (PDAC) remain unclear. Here, we found that PTTG3P was significantly upregulated in PDAC tissues. Elevated PTTG3P expression correlated with larger tumor size and worse differentiation, and reduced overall survival. Bioinformatics and experimental evidence revealed that PTTG3P promoted malignant phenotypes and FoxM1 signaling pathway in PDAC cells. Mechanistically, PTTG3P functions as a microRNA sponge to positively regulate the expression of FoxM1 through sponging miR-132/212-3p. Moreover, it showed that FoxM1 transcriptionally activated PTTG3P expression, thus forming a feedback loop to promote the aggressiveness of PDAC cells. Taken together, our findings suggest that PTTG3P promotes PDAC progression through PTTG3P/miR-132/212-3p/FoxM1 feedforward circuitry and it may serve as a promising diagnostic marker or target for treatment in PDAC patients.

Identifiers

PMID33298873
PMCPMC7705684
OpenAlexW3109157530

What Socratic holds

Textmetadata
LicenceCC BY
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.