Evidence map›Paper›PMID 33061431›Full record

ArticleOncoTargets and therapy2020

Inactivation of Pancreatic Stellate Cells by Exendin-4 Inhibits the Migration and Invasion of Pancreatic Cancer Cells.

Meizhu Yan, Manru Shen, Linfang Xu, Jiying Huang, Guijun He, Min An, Xiaocui Li, Zhenjun Gao, Xin Meng

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in OncoTargets and therapy, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
0.3field-weighted citation impact, top 38% 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

8 citing papers in PubMed, 11 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 4 institutions in 1 country.

Meizhu Yan *Department of Gastroenterology, Zhongshan Hospital Qingpu Branch, Fudan University, Shanghai 201700, People's Republic of China.
Manru Shen *Department of Gastroenterology, Zhongshan Hospital Qingpu Branch, Fudan University, Shanghai 201700, People's Republic of China.
Linfang Xu *Department of Gastroenterology, Zhongshan Hospital Qingpu Branch, Fudan University, Shanghai 201700, People's Republic of China.
Jiying HuangDepartment of Gastroenterology, Zhongshan Hospital Qingpu Branch, Fudan University, Shanghai 201700, People's Republic of China.
Guijun HeDepartment of Gastroenterology, Zhongshan Hospital Qingpu Branch, Fudan University, Shanghai 201700, People's Republic of China.
Min AnDepartment of Gastroenterology, Zhongshan Hospital Qingpu Branch, Fudan University, Shanghai 201700, People's Republic of China.
Xiaocui LiDepartment of Gastroenterology, Zhongshan Hospital Qingpu Branch, Fudan University, Shanghai 201700, People's Republic of China.
Zhenjun GaoDepartment of Gastroenterology, Zhongshan Hospital Qingpu Branch, Fudan University, Shanghai 201700, People's Republic of China.
Xin MengDepartment of Hospital Infection Management, Zhongshan Hospital Qingpu Branch, Fudan University, Shanghai 201700, People's Republic of China.
Fudan University · CNThe First Affiliated Hospital, Sun Yat-sen University · CNZhongshan Hospital · CNSun Yat-sen University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundPancreatic stellate cells (PSCs) are precursor cells of cancer-associated fibroblasts that promote tumor proliferation, invasion, and metastasis. The glucagon-like peptide-1 receptor agonist exendin-4 has been reported to exhibit anticancer effects against several tumor cells; however, the function and mechanism underlying the effects of exendin-4 on pancreatic cancer cells remain unclear.

methodsGene expression levels were determined using quantitative real-time polymerase chain reaction (qRT-PCR) and Western blot assay. Cell viability, migration and invasion were assessed using the cell counting kit-8 (CCK-8), wound healing, and transwell assays, respectively. A xenografted tumor model was established in mouse to evaluate the effects of exendin-4 in vivo.

resultsExendin-4 treatment led to the inactivation of PSCs and suppressed their proliferation and migration. Moreover, we also found that exendin-4 attenuated NF-κB-dependent SDF-1 secretion. Furthermore, pancreatic cancer cells incubated with conditioned medium obtained from exendin-4-treated PSCs showed a decreased ability to proliferate, migrate, and invade as compared to the control cells, which is similar to the effects induced by the CXCR4 inhibitor, AMD3100. Consistent with in vitro results, we also confirmed that exendin-4 indirectly targeted pancreatic cancer cells in vivo by attenuating the function of PSCs and suppressing the deposition of extracellular matrix.

conclusionThese results revealed that exendin-4-treated PSCs could suppress pancreatic cancer cell proliferation and invasion, offering a potential strategy for the treatment of pancreatic cancer.

Indexed as

exendin-4pancreatic cancerpancreatic stellate cellsSDF-1

Identifiers

PMID33061431
PMCPMC7522302
OpenAlexW3088800458

What OpenQuestion holds

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LicenceCC BY-NC
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.