Evidence map›Paper›PMID 27391260›Full record

ArticleOncotarget2016

Adrenomedullin promotes the growth of pancreatic ductal adenocarcinoma through recruitment of myelomonocytic cells.

Min Xu, Feifei Qi, Shaosen Zhang, Xuhui Ma, Shan Wang, Chunying Wang, Yan Fu, Yongzhang Luo

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
0.2field-weighted citation impact, top 44% 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

12 citing papers in PubMed, 16 citations in OpenAlex.

  1. Adrenomedullin in Tumorigenesis and Cancer Progression.International journal of molecular sciences · 2025
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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

8 authors at 1 institution in 1 country.

Min XuThe National Engineering Laboratory for Anti-Tumor Protein Therapeutics, School of Life Sciences, Tsinghua University, Beijing, China.
Feifei QiThe National Engineering Laboratory for Anti-Tumor Protein Therapeutics, School of Life Sciences, Tsinghua University, Beijing, China.
Shaosen ZhangThe National Engineering Laboratory for Anti-Tumor Protein Therapeutics, School of Life Sciences, Tsinghua University, Beijing, China.
Xuhui MaThe National Engineering Laboratory for Anti-Tumor Protein Therapeutics, School of Life Sciences, Tsinghua University, Beijing, China.
Shan WangThe National Engineering Laboratory for Anti-Tumor Protein Therapeutics, School of Life Sciences, Tsinghua University, Beijing, China.
Chunying WangThe National Engineering Laboratory for Anti-Tumor Protein Therapeutics, School of Life Sciences, Tsinghua University, Beijing, China.
Yan FuThe National Engineering Laboratory for Anti-Tumor Protein Therapeutics, School of Life Sciences, Tsinghua University, Beijing, China.
Yongzhang LuoThe National Engineering Laboratory for Anti-Tumor Protein Therapeutics, School of Life Sciences, Tsinghua University, Beijing, China.
Tsinghua University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Stromal infiltration of myelomonocytic cells is a hallmark of pancreatic ductal adenocarcinoma (PDAC) and is related to a poor prognosis. However, the detailed mechanism for the recruitment of myelomonocytic cells to pancreatic cancer tissue remains unclear. In the present study, pancreatic cancer cells secreted high levels of adrenomedullin (ADM), and CD11b+ myelomonocytic cells expressed all components of ADM receptors, including GPR182, CRLR, RAMP2 and RAMP3. ADM enhanced the migration and invasion of myelomonocytic cells through activation of the MAPK, PI3K/Akt and eNOS signaling pathways, as well as the expression and activity of MMP-2. ADM also promoted the adhesion and trans-endothelial migration of myelomonocytic cells by increasing expression of VCAM-1 and ICAM-1 in endothelial cells. In addition, ADM induced macrophages and myeloid-derived suppressor cells (MDSCs) to express pro-tumor phenotypes. ADM knockdown in tumor-bearing mice or administration of AMA, an ADM antagonist, significantly inhibited the recruitment of myelomonocytic cells and tumor angiogenesis. Moreover, in vivo depletion of myelomonocytic cells using clodronate liposomes suppressed the progression of PDAC. These results reveal a novel function of ADM in PDAC, and suggest ADM is a promising target in the treatment of PDAC.

Indexed as

AdrenomedullinAdultAgedAged, 80 and overAnimalsCarcinoma, Pancreatic DuctalCell LineCell Line, TumorCell ProliferationFemaleGene Expression Regulation, NeoplasticHumansMaleMice, Inbred BALB CMice, Inbred C57BLMice, NudeAdrenomedullinadrenomedullincell recruitmentmyelomonocytic cellspancreatic ductal adenocarcinomatumor angiogenesis

Identifiers

PMID27391260
PMCPMC5342400
OpenAlexW2463245767

What OpenQuestion 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 OpenQuestion graph.