Evidence map›Paper›PMID 32924881›Full record

ArticleTechnology in cancer research & treatment

MiR-331-3p Links to Drug Resistance of Pancreatic Cancer Cells by Activating WNT/β-Catenin Signal via ST7L.

Ting Zhan, Xiaoli Chen, Xia Tian, Zheng Han, Meng Liu, Yanli Zou, Shasha Huang, Aifang Chen, Xueting Cheng, Junsheng Deng and 2 more

Open access · goldAbstract read
In one paragraph

Article in Technology in cancer research & treatment. 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
1.7field-weighted citation impact, top 16% 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, 34 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

12 authors at 2 institutions in 1 country.

Ting ZhanDepartment of Gastroenterology, Wuhan Third Hospital, 89674Tongren Hospital of Wuhan University, Wuhan, China.ORCID 0000-0003-0622-7890
Xiaoli ChenDepartment of Gastroenterology, Wuhan Third Hospital, 89674Tongren Hospital of Wuhan University, Wuhan, China.
Xia TianDepartment of Gastroenterology, Wuhan Third Hospital, 89674Tongren Hospital of Wuhan University, Wuhan, China.
Zheng HanDepartment of Gastroenterology, Wuhan Third Hospital, 89674Tongren Hospital of Wuhan University, Wuhan, China.
Meng LiuDepartment of Gastroenterology, Wuhan Third Hospital, 89674Tongren Hospital of Wuhan University, Wuhan, China.
Yanli ZouDepartment of Gastroenterology, Wuhan Third Hospital, 89674Tongren Hospital of Wuhan University, Wuhan, China.
Shasha HuangDepartment of Gastroenterology, Wuhan Third Hospital, 89674Tongren Hospital of Wuhan University, Wuhan, China.
Aifang ChenDepartment of Gastroenterology, Wuhan Third Hospital, 89674Tongren Hospital of Wuhan University, Wuhan, China.
Xueting ChengDepartment of Gastroenterology, 89674Zhongnan Hospital of Wuhan University, Wuhan, China.
Junsheng DengDepartment of Gastroenterology, 89674Zhongnan Hospital of Wuhan University, Wuhan, China.
Jie TanDepartment of Gastroenterology, Wuhan Third Hospital, 89674Tongren Hospital of Wuhan University, Wuhan, China.
Xiaodong HuangDepartment of Gastroenterology, Wuhan Third Hospital, 89674Tongren Hospital of Wuhan University, Wuhan, China.
Tongren Hospital · CNWuhan University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundPancreatic cancer is an aggressive type of cancer with poor prognosis, short survival rate, and high mortality. Drug resistance is a major cause of treatment failure in the disease. MiR-331-3p has been reported to play an important role in several cancers. We previously showed that miR-331-3p is upregulated in pancreatic cancer and promotes pancreatic cancer cell proliferation and epithelial-to-mesenchymal transition-mediated metastasis by targeting ST7L. However, it is uncertain whether miR-331-3p is involved in drug resistance.

methodsWe investigated the relationship between miR-331-3p and pancreatic cancer drug resistance. As part of this, microRNA mimics or inhibitors were transfected into pancreatic cancer cells. Quantitative polymerase chain reaction was used to detect miR-331-3p expression, and flow cytometry was used to detect cell apoptosis. The Cell Counting Kit-8 assay was used to measure the IC50 values of gemcitabine in pancreatic cancer cells. The expression of multidrug resistance protein 1, multidrug resistance-related protein 1, breast cancer resistance protein, β-Catenin, c-Myc, Cyclin D1, Bcl-2, and Caspase-3 was evaluated by Western blotting.

resultsWe confirmed that miR-331-3p is upregulated in gemcitabine-treated pancreatic cancer cells and plasma from chemotherapy patients. We also confirmed that miR-331-3p inhibition decreased drug resistance by regulating cell apoptosis and multidrug resistance protein 1, multidrug resistance-related protein 1, and breast cancer resistance protein expression in pancreatic cancer cells, whereas miR-331-3p overexpression had the opposite effect. We further demonstrated that miR-331-3p effects in drug resistance were partially reversed by ST7L overexpression. In addition, overexpression of miR-331-3p activated Wnt/β-catenin signaling in pancreatic cancer cells, and ST7L overexpression restored activation of Wnt/β-catenin signaling.

conclusionsTaken together, our data demonstrate that miR-331-3p contributes to drug resistance by activating Wnt/β-catenin signaling via ST7L in pancreatic cancer cells. These data provide a theoretical basis for new targeted therapies in the future.

Indexed as

Gene Expression Regulation, NeoplasticWnt Signaling PathwayCell Line, TumorCell ProliferationDrug Resistance, NeoplasmHumansMicroRNAsPancreatic NeoplasmsRNA InterferenceTumor Suppressor ProteinsMicroRNAsMIRN331 microRNA, humanST7L protein, humanTumor Suppressor Proteinsdrug resistancemiR-331-3pWNT

Identifiers

PMID32924881
PMCPMC7493267
OpenAlexW3086621057

What OpenQuestion holds

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LicenceCC BY-NC
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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.