Evidence map›Paper›PMID 35399101›Full record

ArticleCell death discovery2022

Silencing of lncRNA MALAT1 facilitates erastin-induced ferroptosis in endometriosis through miR-145-5p/MUC1 signaling.

Zongwen Liang, Qiong Wu, Honglin Wang, Jiahuan Tan, Han Wang, Yanling Gou, Yingying Cao, Zhi Li, Zongfeng Zhang

Open access · goldAbstract read
In one paragraph

Article in Cell death discovery, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.

0numbers the graph read from it
0cells of the map it votes in
46citing papers in PubMed
6.8field-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

46 citing papers in PubMed, 78 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 1 institution in 1 country.

Zongwen Liang *Department of Obstetrics and Gynecology, Second Affiliated Hospital of Harbin Medical University, 150086, Harbin, China.ORCID http://orcid.org/0000-0001-9387-6420
Qiong Wu *Department of Obstetrics and Gynecology, Second Affiliated Hospital of Harbin Medical University, 150086, Harbin, China.ORCID http://orcid.org/0000-0002-7147-4751
Honglin WangDepartment of Obstetrics and Gynecology, Second Affiliated Hospital of Harbin Medical University, 150086, Harbin, China.ORCID http://orcid.org/0000-0002-4718-9846
Jiahuan TanDepartment of Obstetrics and Gynecology, Second Affiliated Hospital of Harbin Medical University, 150086, Harbin, China.ORCID http://orcid.org/0000-0002-4670-5263
Han WangDepartment of Obstetrics and Gynecology, Second Affiliated Hospital of Harbin Medical University, 150086, Harbin, China.ORCID http://orcid.org/0000-0003-1842-2888
Yanling GouDepartment of Obstetrics and Gynecology, Second Affiliated Hospital of Harbin Medical University, 150086, Harbin, China.ORCID http://orcid.org/0000-0002-2950-9834
Yingying CaoDepartment of Obstetrics and Gynecology, Second Affiliated Hospital of Harbin Medical University, 150086, Harbin, China.ORCID http://orcid.org/0000-0002-2563-5227
Zhi LiDepartment of Obstetrics and Gynecology, Second Affiliated Hospital of Harbin Medical University, 150086, Harbin, China.
Zongfeng ZhangDepartment of Obstetrics and Gynecology, Second Affiliated Hospital of Harbin Medical University, 150086, Harbin, China. viaac1973@163.com.ORCID http://orcid.org/0000-0002-0159-1290
Harbin Medical University · CN

Funding

Department of Health of Zhejiang Province 2018KY520National Natural Science Foundation of China (National Science Foundation of China) 81671430National Natural Science Foundation of China (National Science Foundation of China) 82071619
6 · The paper itself

Abstract

Endometriosis is a chronic disorder characterized by the implantation of endometrial glands and stroma outside the uterus. However, the pathogenesis of endometriosis is still unclear. To date, there is no fully effective treatment without trauma because of various side effects. Recent data suggest that ferroptosis is a novel recognized form of nonapoptosis-regulated cell death characterized by iron-dependent and lethal lipid peroxidation accumulation, showing great promise in the treatment of many diseases. In the present study, we verified that erastin induced ferroptosis in ectopic endometrial stromal cells (EESCs). Furthermore, we found that the expression of metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) was decreased during erastin-induced ferroptosis. Knockdown of MALAT1 significantly aggravated the inhibition of cell viability and increased intracellular iron, Liperfluo, and MDA levels in EESCs upon erastin treatment. Mechanistically, we demonstrated that MALAT1 served as a competing endogenous RNA of miR-145-5p to regulate the expression of MUC1, a suppressor of ferroptosis. MALAT1 knockdown-mediated ferroptotic cell death and MUC1 downregulation could be abrogated by inhibition of miR-145-5p. In addition, miR-145-5p inhibition-mediated ferroptotic cell death could be abolished by MUC1 knockdown. Furthermore, erastin-induced ferroptosis shrunk endometriotic lesions via the MALAT1/miR-145-5p/MUC1 axis in vivo. Taken together, our data indicate that knockdown of MALAT1 facilitates ferroptosis upon erastin treatment via miR-145-5p/MUC1 signaling. The synergistic effect of MALAT1 knockdown and erastin induction in ferroptosis may be a new therapeutic strategy for endometriosis.

Identifiers

PMID35399101
PMCPMC8995383
OpenAlexW4223590848

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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.