Evidence map›Paper›PMID 31177911›Full record

ArticleAutophagy2020

TGFB1-induced autophagy affects the pattern of pancreatic cancer progression in distinct ways depending on SMAD4 status.

Chen Liang, Jin Xu, Qingcai Meng, Bo Zhang, Jiang Liu, Jie Hua, Yiyin Zhang, Si Shi, Xianjun Yu

Open access · bronzeAbstract read
In one paragraph

Article in Autophagy, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 59 papers.

0numbers the graph read from it
0cells of the map it votes in
59citing papers in PubMed
6.8field-weighted citation impact, top 2% 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

59 citing papers in PubMed, 107 citations in OpenAlex.

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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 1 institution in 1 country.

Chen LiangDepartment of Pancreatic Surgery, Fudan University Shanghai Cancer Center, Shanghai, China.ORCID 0000-0003-0578-7589
Jin XuDepartment of Pancreatic Surgery, Fudan University Shanghai Cancer Center, Shanghai, China.
Qingcai MengDepartment of Pancreatic Surgery, Fudan University Shanghai Cancer Center, Shanghai, China.
Bo ZhangDepartment of Pancreatic Surgery, Fudan University Shanghai Cancer Center, Shanghai, China.
Jiang LiuDepartment of Pancreatic Surgery, Fudan University Shanghai Cancer Center, Shanghai, China.
Jie HuaDepartment of Pancreatic Surgery, Fudan University Shanghai Cancer Center, Shanghai, China.
Yiyin ZhangDepartment of Pancreatic Surgery, Fudan University Shanghai Cancer Center, Shanghai, China.
Si ShiDepartment of Pancreatic Surgery, Fudan University Shanghai Cancer Center, Shanghai, China.ORCID 0000-0002-6652-0629
Xianjun YuDepartment of Pancreatic Surgery, Fudan University Shanghai Cancer Center, Shanghai, China.
Shanghai Medical College of Fudan University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Pancreatic ductal adenocarcinoma (PDAC) is one of the most aggressive and lethal malignancies. Given that macroautophagy/autophagy activation is prevalent in PDAC, the dual roles of autophagy could be involved in PDAC heterogeneity. In this work, we demonstrated that TGFB1 induced autophagic flux through SMAD4-dependent or SMAD4-independent pathways based on a distinct genetic context. In SMAD4-positive PDAC cells, TGFB1-induced autophagy promoted proliferation and inhibited migration by decreasing the nuclear translocation of SMAD4. Conversely, TGFB1-induced autophagy inhibited proliferation and promoted migration in SMAD4-negative cells through the regulation of MAPK/ERK activation. TGFB1 expression also positively correlated with LC3B expression in PDAC specimens. A high level of LC3B was associated with unfavorable overall survival (OS) and disease-free survival (DFS) in SMAD4-negative PDAC patients, although LC3B could not predict OS and DFS for the 110 PDAC patients. Thus, TGFB1-induced autophagy contributed to the different patterns of PDAC progression. This knowledge can aid in improving our understanding of the molecular classification of PDAC and might guide the development of therapeutic strategies for PDAC, especially for SMAD4-negative PDAC.

Indexed as

AutophagyDisease ProgressionAdenocarcinomaCarcinoma, Pancreatic DuctalCell Line, TumorCell NucleusFemaleHumansMaleMAP Kinase Signaling SystemMicrotubule-Associated ProteinsMiddle AgedPancreatic NeoplasmsPrognosisSequestosome-1 ProteinSmad4 ProteinMAP1LC3B protein, humanMicrotubule-Associated ProteinsSequestosome-1 ProteinSmad4 ProteinSQSTM1 protein, humanTGFB1 protein, humanTransforming Growth Factor beta1Autophagic fluxLC3Bmetastasispancreatic ductal adenocarcinomaproliferation

Identifiers

PMID31177911
PMCPMC6999639
OpenAlexW2949637147

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.