Evidence map›Paper›PMID 33510942›Full record

ArticleMolecular therapy. Nucleic acids2021

lncRNA-Xist/miR-101-3p/KLF6/C/EBPα axis promotes TAM polarization to regulate cancer cell proliferation and migration.

Yanyun Zhao, Zhaojin Yu, Rong Ma, Yifan Zhang, Lin Zhao, Yuanyuan Yan, Xuemei Lv, Liwen Zhang, Panpan Su, Jia Bi and 3 more

Open access · goldAbstract read
In one paragraph

Article in Molecular therapy. Nucleic acids, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 83 papers.

0numbers the graph read from it
0cells of the map it votes in
83citing papers in PubMed
6.2field-weighted citation impact, top 2% 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

83 citing papers in PubMed, 126 citations in OpenAlex.

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23 more citing papers are in PubMed but not listed here.

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

13 authors at 2 institutions in 1 country.

Yanyun ZhaoDepartment of Pharmacology, School of Pharmacy, China Medical University, Shenyang City, 110122 Liaoning Province, China.
Zhaojin YuDepartment of Pharmacology, School of Pharmacy, China Medical University, Shenyang City, 110122 Liaoning Province, China.
Rong MaDepartment of Pharmacology, School of Pharmacy, China Medical University, Shenyang City, 110122 Liaoning Province, China.
Yifan ZhangDepartment of Pharmacology, School of Pharmacy, China Medical University, Shenyang City, 110122 Liaoning Province, China.
Lin ZhaoDepartment of Pharmacology, School of Pharmacy, China Medical University, Shenyang City, 110122 Liaoning Province, China.
Yuanyuan YanDepartment of Pharmacology, School of Pharmacy, China Medical University, Shenyang City, 110122 Liaoning Province, China.
Xuemei LvDepartment of Pharmacology, School of Pharmacy, China Medical University, Shenyang City, 110122 Liaoning Province, China.
Liwen ZhangDepartment of Pharmacology, School of Pharmacy, China Medical University, Shenyang City, 110122 Liaoning Province, China.
Panpan SuDepartment of Pharmacology, School of Pharmacy, China Medical University, Shenyang City, 110122 Liaoning Province, China.
Jia BiDepartment of Pharmacology, School of Pharmacy, China Medical University, Shenyang City, 110122 Liaoning Province, China.
Hong XuDepartment of Breast Cancer, Cancer Hospital of China Medical University, Dadong District, 110042 Shenyang, China.
Miao HeDepartment of Pharmacology, School of Pharmacy, China Medical University, Shenyang City, 110122 Liaoning Province, China.
Minjie WeiDepartment of Pharmacology, School of Pharmacy, China Medical University, Shenyang City, 110122 Liaoning Province, China.
China Medical University · CNLiaoning Cancer Hospital & Institute · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The phenotypic switch in tumor-associated macrophages (TAMs) mediates immunity escape of cancer. However, the underlying mechanisms in the TAM phenotypic switch have not been systematically elucidated. In this study, long noncoding RNA (lncRNA)-Xist, CCAAT/enhancer-binding protein (C/EBP)α, and Kruppel-like factor 6 (KLF6) were upregulated, whereas microRNA (miR)-101 was downregulated in M1 macrophages-type (M1). Knockdown of Xist or overexpression of miR-101 in M1 could induce M1-to-M2 macrophage-type (M2) conversion to promote cell proliferation and migration of breast and ovarian cancer by inhibiting C/EBPα and KLF6 expression. Furthermore, miR-101 could combine with both Xist and C/EBPα and KLF6 through the same microRNA response element (MRE) predicted by bioinformatics and verified by luciferase reporter assays. Moreover, we found that miR-101 knockdown restored the decreased M1 marker and the increased M2 marker expression and also reversed the promotion of proliferation and migration of human breast cancer cells (MCF-7) and human ovarian cancer (OV) cells caused by silencing Xist. Generally, the present study indicates that Xist could mediate macrophage polarization to affect cell proliferation and migration of breast and ovarian cancer by competing with miR-101 to regulate C/EBPα and KLF6 expression. The promotion of Xist expression in M1 macrophages and inhibition of miR-101 expression in M2 macrophages might play an important role in inhibiting breast and ovarian tumor proliferation and migration abilities.

Indexed as

ceRNAlncRNA XistmiR-101polarizationtumor-associated macrophages

Identifiers

PMID33510942
PMCPMC7810606
OpenAlexW3113146690

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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.