Evidence map›Paper›PMID 28591705›Full record

ArticleOncotarget2017

M2 tumor-associated macrophages produce interleukin-17 to suppress oxaliplatin-induced apoptosis in hepatocellular carcinoma.

Bin Guo, Leilei Li, Jiapei Guo, Aidong Liu, Jinghua Wu, Haixin Wang, Jun Shi, Dequan Pang, Qing Cao

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed
3.5field-weighted citation impact, top 7% 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

35 citing papers in PubMed, 65 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 2 institutions in 1 country.

Bin GuoNorth China University of Science and Technology Affiliated Hospital, Tangshan, Hebei, China.
Leilei LiNorth China University of Science and Technology Affiliated Hospital, Tangshan, Hebei, China.
Jiapei GuoNorth China University of Science and Technology Affiliated Hospital, Tangshan, Hebei, China.
Aidong LiuNorth China University of Science and Technology Affiliated Hospital, Tangshan, Hebei, China.
Jinghua WuNorth China University of Science and Technology Affiliated Hospital, Tangshan, Hebei, China.
Haixin WangHospital of Traditional Chinese Medicine of Tangshan City, Tangshan, Hebei, China.
Jun ShiNorth China University of Science and Technology Affiliated Hospital, Tangshan, Hebei, China.
Dequan PangNorth China University of Science and Technology Affiliated Hospital, Tangshan, Hebei, China.
Qing CaoHebei Medical University Second Hospital, Shijiazhuang, Hebei, China.
North China University of Science and Technology Affiliated Hospital · CNSecond Hospital of Hebei Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

M2 macrophages are a major component of the tumor microenvironment and are important promoters of tumor occurrence and progression. In this study, we detected large numbers of M2 macrophages in hepatocellular carcinoma tissues using immunohistochemistry and immunofluorescence. Moreover, upon oxaliplatin treatment, the M2 macrophages overexpressed interleukin-17, an important inflammatory cytokine, and thus inhibited oxaliplatin-induced apoptosis. By knocking down the interleukin-17 receptor and lysosome-associated membrane protein 2A (a key protein in chaperone-mediated autophagy) in hepatocellular carcinoma cells, we found that interleukin-17 stimulated chaperone-mediated autophagy, which further suppressed apoptosis upon oxaliplatin treatment. Chaperone-mediated autophagy induced tolerance to oxaliplatin treatment by reducing cyclin D1 expression; thus, cyclin D1 overexpression stimulated oxaliplatin-induced apoptosis. In addition, cyclin D1 expression was inhibited by interleukin-17, but increased when the interleukin-17 receptor was knocked down. Thus M2 macrophages in the hepatocellular carcinoma microenvironment generate large amounts of interleukin-17, which suppress oxaliplatin-induced tumor cell apoptosis by activating chaperone-mediated autophagy and in turn reducing cyclin D1 expression. These findings may facilitate the development of novel therapeutic strategies for chemorefractory liver cancer.

Indexed as

Antineoplastic AgentsApoptosisBiomarkersCarcinoma, HepatocellularCell Line, TumorCyclin D1Gene ExpressionHumansImmunohistochemistryInterleukin-17Liver NeoplasmsLysosomal-Associated Membrane Protein 2MacrophagesOrganoplatinum CompoundsOxaliplatinReceptors, Interleukin-17Antineoplastic AgentsBiomarkersCyclin D1Interleukin-17Lysosomal-Associated Membrane Protein 2Organoplatinum CompoundsOxaliplatinReceptors, Interleukin-17RNA, Small Interferingchaperone-mediated autophagycyclin D1hepatocellular carcinomainterleukin-17M2 tumor-associated macrophages

Identifiers

PMID28591705
PMCPMC5546494
OpenAlexW2614947170

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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.