Evidence map›Paper›PMID 31746376›Full record

ArticleInternational journal of molecular medicine2020

Apoptotic SKOV3 cells stimulate M0 macrophages to differentiate into M2 macrophages and promote the proliferation and migration of ovarian cancer cells by activating the ERK signaling pathway.

Qun Zhang, Hui Li, Yiqing Mao, Xi Wang, Xuehui Zhang, Xiuyan Yu, Junrui Tian, Zhen Lei, Chang Li, Qing Han and 6 more

Open access · hybridAbstract read
In one paragraph

Article in International journal of molecular medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed
2.0field-weighted citation impact, top 12% 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

36 citing papers in PubMed, 42 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

16 authors at 3 institutions in 2 countries.

Qun ZhangDepartment of Pharmacology, School of Basic Medical Sciences, Peking University Health Science Center, Beijing 100191, P.R. China.
Hui LiDepartment of Pharmacology, School of Basic Medical Sciences, Peking University Health Science Center, Beijing 100191, P.R. China.
Yiqing MaoDepartment of Pharmacology, School of Basic Medical Sciences, Peking University Health Science Center, Beijing 100191, P.R. China.
Xi WangDepartment of Pharmacology, School of Basic Medical Sciences, Peking University Health Science Center, Beijing 100191, P.R. China.
Xuehui ZhangDepartment of Pharmacology, School of Basic Medical Sciences, Peking University Health Science Center, Beijing 100191, P.R. China.
Xiuyan YuDepartment of Pharmacology, School of Basic Medical Sciences, Peking University Health Science Center, Beijing 100191, P.R. China.
Junrui TianDepartment of Pharmacology, School of Basic Medical Sciences, Peking University Health Science Center, Beijing 100191, P.R. China.
Zhen LeiBeijing N&N Genetech Company, Beijing 100082, P.R. China.
Chang LiDepartment of Pharmacology, School of Basic Medical Sciences, Peking University Health Science Center, Beijing 100191, P.R. China.
Qing HanDepartment of Pharmacology, School of Basic Medical Sciences, Peking University Health Science Center, Beijing 100191, P.R. China.
Liping SuoDepartment of Pharmacology, School of Basic Medical Sciences, Peking University Health Science Center, Beijing 100191, P.R. China.
Yan GaoDepartment of Obstetrics and Gynecology, Peking University Third Hospital, Beijing 100191, P.R. China.
Hongyan GuoDepartment of Obstetrics and Gynecology, Peking University Third Hospital, Beijing 100191, P.R. China.
David M IrwinDepartment of Laboratory Medicine and Pathobiology, University of Toronto, Toronto, ON M5S 1A8, Canada.
Gang NiuBeijing N&N Genetech Company, Beijing 100082, P.R. China.
Huanran TanDepartment of Pharmacology, School of Basic Medical Sciences, Peking University Health Science Center, Beijing 100191, P.R. China.
Peking University · CNPeking University Third Hospital · CNUniversity of Toronto · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Ovarian cancer has a high rate of recurrence, with M2 macrophages having been found to be involved in its progression and metastasis. To examine the relationship between macrophages and ovarian cancer in the present study, M0 macrophages were stimulated with apoptotic SKOV3 cells and it was found that these macrophages promoted tumor proliferation and migration. Subsequently, the mRNAs and proteins expressed at high levels in these M2 macrophages were examined by RNA‑Seq and quantitative proteomics, respectively, which revealed that M0 macrophages stimulated by apoptotic SKOV3 cells also expressed M2 markers, including CD206, interleukin‑10, C‑C motif chemokine ligand 22, aminopeptidase‑N, disabled homolog 2, matrix metalloproteinase 1 and 5'‑nucleotidase. The abundance of phosphorylated Erk1/2 in these macrophages was increased. The results indicate that apoptotic SKOV3 cells stimulate M0 macrophages to differentiate into M2 macrophages by activating the ERK pathway. These results suggest possible treatments for patients with ovarian cancer who undergo chemotherapy; inhibiting M2 macrophage differentiation during chemotherapy may reduce the rate of tumor recurrence.

Indexed as

ApoptosisCell DifferentiationMAP Kinase Signaling SystemCell Line, TumorCell MovementCell ProliferationComputational BiologyFemaleGene Expression ProfilingGene Regulatory NetworksHigh-Throughput Nucleotide SequencingHumansMacrophagesOvarian NeoplasmsProteomeProteomicsProteomeapoptotic SKOV3ERK pathwayM2 macrophagequantitative proteomicsRNA-Seq

Identifiers

PMID31746376
PMCPMC6889918
OpenAlexW2990647996

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.