Evidence map›Paper›PMID 36793374›Full record

ArticleJournal of oncology2023

Effect of Exosomal lncRNA MALAT1/miR-370-3p/STAT3 Positive Feedback Loop on PI3K/Akt Pathway Mediating Cisplatin Resistance in Cervical Cancer Cells.

Yi Hu, Genlin Li, Yan Ma, Guifang Luo, Qian Wang, Shufen Zhang

Open access · hybridAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Journal of oncology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
4.5field-weighted citation impact, top 5% 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

16 citing papers in PubMed, 19 citations in OpenAlex.

  1. Therapy resistance-related ncRNAs in cervical cancer: biomarkers and therapeutic targets.Daru : journal of Faculty of Pharmacy, Tehran University of Medical Sciences · 2026
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  6. Exosomal microRNA as a key regulator of PI3K/AKT pathways in human tumors.Medical oncology (Northwood, London, England) · 2024
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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

6 authors at 1 institution in 1 country.

Yi HuDepartment of Obstetrics and Gynaecology, The First Affiliated Hospital of Hengyang Medical School, University of South China, Hengyang, Hunan 421001, China.
Genlin LiDepartment of Obstetrics and Gynaecology, The First Affiliated Hospital of Hengyang Medical School, University of South China, Hengyang, Hunan 421001, China.ORCID https://orcid.org/0000-0001-7524-4999
Yan MaDepartment of Obstetrics and Gynaecology, The First Affiliated Hospital of Hengyang Medical School, University of South China, Hengyang, Hunan 421001, China.
Guifang LuoDepartment of Obstetrics and Gynaecology, The First Affiliated Hospital of Hengyang Medical School, University of South China, Hengyang, Hunan 421001, China.
Qian WangDepartment of Obstetrics and Gynaecology, The First Affiliated Hospital of Hengyang Medical School, University of South China, Hengyang, Hunan 421001, China.
Shufen ZhangDepartment of Obstetrics and Gynaecology, The First Affiliated Hospital of Hengyang Medical School, University of South China, Hengyang, Hunan 421001, China.
University of South China · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Background: Exosomes can encapsulate lncRNA to mediate intercellular communication in cancer progression. Our study devoted to research the effect that long noncoding RNA Metastasis-associated lung adenocarcinoma transcript 1 (lncRNA MALAT1) influence on cervical cancer (CC). Methods: MALAT1 and miR-370-3p levels in CC was assessed using qRT-PCR. CCK-8 assay and flow cytometry were devoted to confirm the influence on MALAT1 influencing the proliferation in cisplatin-resistant CC cells. Futher more, MALAT1, combined with miR-370-3p was confirmed by dual-luciferase reporter assay and RNA immunoprecipitation assay. Results: In CC tissues, MALAT1 turned into substantially expressed, cisplatin-resistant cell lines, as well as exosomes. Cell proliferation was restrained and cisplatin-induced apoptosis was promoted by way of Knockout MALAT1. And promoted the miR-370-3p level, MALAT1 targeted miR-370-3p. Promoting effect of MALAT1 on cisplatin resistance of CC was partially reversed through miR-370-3p. In addition, STAT3 may induce up-regulation of MALAT1 expression in cisplatin-resistant CC cells. It was further confirmed that the effect of MALAT1 on cisplatin-resistant CC cells was achieved by activating PI3K/Akt pathway. Conclusion: The positive feedback loop of exosomal MALAT1/miR-370-3p/STAT3 mediates the cisplatin resistance of cervical cancer cells affecting PI3K/Akt pathway. Exosomal MALAT1 may become a promising therapeutic target for treating cervical cancer.

Identifiers

PMID36793374
PMCPMC9925267
OpenAlexW4319299655

What OpenQuestion holds

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LicenceCC BY
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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.