Evidence map›Paper›PMID 27123137›Full record

ArticleOncology letters2016

Smad4 inhibits cell migration via suppression of JNK activity in human pancreatic carcinoma PANC-1 cells.

Xueying Zhang, Junxia Cao, Yujun Pei, Jiyan Zhang, Qingyang Wang

Open access · diamondAbstract read
In one paragraph

Article in Oncology letters, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
1.6field-weighted citation impact, top 17% 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

15 citing papers in PubMed, 18 citations in OpenAlex.

  1. Article
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  7. JNK signaling as a target for anticancer therapy.Pharmacological reports : PR · 2021
    Review
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  15. SMAD4 Loss Is Associated with Cetuximab Resistance and Induction of MAPK/JNK Activation in Head and Neck Cancer Cells.Clinical cancer research : an official journal of the American Association for Cancer Research · 2017
    Article
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

5 authors at 1 institution.

Xueying ZhangDepartment of Molecular Immunology, Institute of Basic Medical Sciences, Beijing 100850, P.R. China.
Junxia CaoDepartment of Molecular Immunology, Institute of Basic Medical Sciences, Beijing 100850, P.R. China.
Yujun PeiDepartment of Molecular Immunology, Institute of Basic Medical Sciences, Beijing 100850, P.R. China.
Jiyan ZhangDepartment of Molecular Immunology, Institute of Basic Medical Sciences, Beijing 100850, P.R. China.
Qingyang WangDepartment of Molecular Immunology, Institute of Basic Medical Sciences, Beijing 100850, P.R. China.
Institute of Basic Medical Sciences of the Chinese Academy of Medical Sciences

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Smad4 is a common Smad and is a key downstream regulator of the transforming growth factor-β signaling pathway, in which Smad4 often acts as a potent tumor suppressor and functions in a highly context-dependent manner, particularly in pancreatic cancer. However, little is known regarding whether Smad4 regulates other signaling pathways involved in pancreatic cancer. The present study demonstrated that Smad4 downregulates c-Jun N-terminal kinase (JNK) activity using a Smad4 loss-of-function or gain-of-function analysis. Additionally, stable overexpression of Smad4 clearly affected the migration of human pancreatic epithelioid carcinoma PANC-1 cells, but did not affect cell growth. In addition, the present study revealed that upregulation of mitogen-activated protein kinase phosphatase-1 is required for the reduction of JNK activity by Smad4, leading to a decrease in vascular endothelial growth factor expression and inhibiting cell migration. Overall, the present findings indicate that Smad4 may suppress JNK activation and inhibit the tumor characteristics of pancreatic cancer cells.

Indexed as

cell migrationJNKpancreatic cancerSmad4

Identifiers

PMID27123137
PMCPMC4840846
OpenAlexW2324929837

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.