Evidence map›Paper›PMID 33683827›Full record

ArticleJournal of cellular and molecular medicine2021

LncRNA TP73-AS1 enhances the malignant properties of pancreatic ductal adenocarcinoma by increasing MMP14 expression through miRNA -200a sponging.

Haiyan Miao, Jingjing Lu, Yibing Guo, Hongquan Qiu, Yu Zhang, Xihao Yao, Xiaohong Li, Yuhua Lu

Open access · goldAbstract read
In one paragraph

Article in Journal of cellular and molecular medicine, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
5.9field-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

15 citing papers in PubMed, 29 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

8 authors at 2 institutions in 2 countries.

Haiyan MiaoResearch Center of Clinical Medical and Department of General Surgery, Affiliated Hospital of Nantong University, Nantong, China.ORCID 0000-0002-2741-1817
Jingjing LuResearch Center of Clinical Medical and Department of General Surgery, Affiliated Hospital of Nantong University, Nantong, China.
Yibing GuoResearch Center of Clinical Medical and Department of General Surgery, Affiliated Hospital of Nantong University, Nantong, China.
Hongquan QiuResearch Center of Clinical Medical and Department of General Surgery, Affiliated Hospital of Nantong University, Nantong, China.
Yu ZhangResearch Center of Clinical Medical and Department of General Surgery, Affiliated Hospital of Nantong University, Nantong, China.
Xihao YaoResearch Center of Clinical Medical and Department of General Surgery, Affiliated Hospital of Nantong University, Nantong, China.
Xiaohong LiResearch Center of Clinical Medical and Department of General Surgery, Affiliated Hospital of Nantong University, Nantong, China.
Yuhua LuResearch Center of Clinical Medical and Department of General Surgery, Affiliated Hospital of Nantong University, Nantong, China.
Nantong University · CNForest Institute · US

Funding

Jiangsu Provincial Commission of Health and Family Planning LGY2018080Nantong Municipal Commission of Health and Family Planning QA2020040Nantong Science and Technology Bureau GJZ17096Nantong Science and Technology Bureau JC2019141National Natural Science Foundation of China 81672903
6 · The paper itself

Abstract

Pancreatic ductal adenocarcinoma (PDAC) is an invasive and aggressive cancer that remains a major threat to human health across the globe. Despite advances in cancer treatments and diagnosis, the prognosis of PDAC patients remains poor. New and more effective PDAC therapies are therefore urgently required. In this study, we identified a novel host factor, namely the LncRNA TP73-AS1, as overexpressed in PDAC tissues compared to adjacent healthy tissue samples. The overexpression of TP-73-AS1 was found to correlate with both PDAC stage and lymph node metastasis. To reveal its role in PDCA, we targeted TP73-AS1 using LnRNA inhibitors in a range of pancreatic cancer (PC) cell lines. We found that the inhibition of TP73-AS1 led to a loss of MMP14 expression in PC cells and significantly inhibited their migratory and invasive capacity. No effects of TP73-AS1 on cell survival or proliferation were observed. Mechanistically, we found that TP73-AS1 suppressed the expression of the known oncogenic miR-200a. Taken together, these data highlight the prognostic potential of TP73-AS1 for PC patients and highlight it as a potential anti-PDAC therapeutic target.

Indexed as

Gene Expression Regulation, NeoplasticAnimalsApoptosisCarcinoma, Pancreatic DuctalCell Line, TumorCell MovementCell ProliferationFemaleHEK293 CellsHumansImmunohistochemistryLymphatic MetastasisMaleMatrix Metalloproteinase 14MiceMice, Inbred BALB CMatrix Metalloproteinase 14MicroRNAsMIRN200 microRNA, humanMMP14 protein, humanRNA, Long NoncodingceRNAmiR-200ammp14pancreatic ductal adenocarcinomaTP73-AS1

Identifiers

PMID33683827
PMCPMC8034458
OpenAlexW3134991285

What OpenQuestion holds

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LicenceCC BY
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.