Evidence map›Paper›PMID 27471397›Full record

ArticleOncoTargets and therapy2016

Interleukin-32α inactivates JAK2/STAT3 signaling and reverses interleukin-6-induced epithelial-mesenchymal transition, invasion, and metastasis in pancreatic cancer cells.

Jingfeng Chen, Silu Wang, Jiadong Su, Guanyu Chu, Heyi You, Zongjing Chen, Hongwei Sun, Bicheng Chen, Mengtao Zhou

Open access · goldAbstract read
In one paragraph

Article in OncoTargets and therapy, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed, 1 pooled it
2.5field-weighted citation impact, top 9% 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

26 citing papers in PubMed, 1 synthesis or guideline pooled it, 51 citations in OpenAlex.

  1. Pooled it
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  5. Review
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  14. Lung cancer and epithelial-mesenchymal transition.General thoracic and cardiovascular surgery · 2021
    Review
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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 2 institutions in 1 country.

Jingfeng ChenDepartment of Surgery, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou; Department of Surgery, The Sixth Affiliated Hospital of Wenzhou Medical University, Lishui.
Silu WangDepartment of Surgery, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou.
Jiadong SuDepartment of Surgery, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou.
Guanyu ChuDepartment of Surgery, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou.
Heyi YouDepartment of Surgery, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou.
Zongjing ChenDepartment of Surgery, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou.
Hongwei SunDepartment of Surgery, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou.
Bicheng ChenDepartment of Surgery, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou; Zhejiang Provincial Top Key Discipline in Surgery, Wenzhou Key Laboratory of Surgery, Department of Surgery, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, Zhejiang Province, People's Republic of China.
Mengtao ZhouDepartment of Surgery, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou.
Wenzhou Medical University · CNFirst Affiliated Hospital of Wenzhou Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Interleukin (IL)-32 is a newly discovered cytokine that has multifaceted roles in inflammatory bowel disease, cancer, and autoimmune diseases and participates in cell apoptosis, cancer cell growth inhibition, accentuation of inflammation, and angiogenesis. Here, we investigated the potential effects of IL-32α on epithelial-mesenchymal transition, metastasis, and invasion, and the JAK2/STAT3 signaling pathway in pancreatic cancer cells. The human pancreatic cancer cell lines PANC-1 and SW1990 were used. Epithelial-mesenchymal transition-related markers, including E-cadherin, N-cadherin, Vimentin, Snail, and Zeb1, as well as extracellular matrix metalloproteinases (MMPs), including MMP2, MMP7, and MMP9, were detected by immunofluorescence, Western blotting, and real-time polymerase chain reaction. The activation of JAK2/STAT3 signaling proteins was detected by Western blotting. Wound healing assays, real-time polymerase chain reaction, and Western blotting were performed to assess cell migration and invasion. The effects of IL-32α on the IL-6-induced activation of JAK2/STAT3 were also evaluated. In vitro, we found that IL-32α inhibits the expressions of the related markers N-cadherin, Vimentin, Snail, and Zeb1, as well as JAK2/STAT3 proteins, in a dose-dependent manner in pancreatic cancer cell lines. Furthermore, E-cadherin expression was increased significantly after IL-32α treatment. IL-32α downregulated the expression of MMPs, including MMP2, MMP7, and MMP9, and decreased wound healing in pancreatic cancer cells. These consistent changes were also found in IL-6-induced pancreatic cancer cells following IL-32α treatment. This study showed that reversion of epithelial-mesenchymal transition, inhibition of invasiveness and metastasis, and activation of the JAK2/STAT3 signaling pathway could be achieved through the application of exogenous IL-32α.

Indexed as

EMTIL-32αJAK2MMPsSTAT3

Identifiers

PMID27471397
PMCPMC4948719
OpenAlexW2467938813

What OpenQuestion holds

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LicenceCC BY-NC
Read underepoch 390

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.