Evidence map›Paper›PMID 25811929›Full record

ArticleInternational journal of molecular sciences2015

Long noncoding RNA MALAT-1 enhances stem cell-like phenotypes in pancreatic cancer cells.

Feng Jiao, Hai Hu, Ting Han, Cuncun Yuan, Lei Wang, Ziliang Jin, Zhen Guo, Liwei Wang

Open access · goldAbstract read
In one paragraph

Article in International journal of molecular sciences, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 95 papers.

0numbers the graph read from it
0cells of the map it votes in
95citing papers in PubMed
9.1field-weighted citation impact, top 1% 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

95 citing papers in PubMed, 161 citations in OpenAlex.

  1. Article
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  5. LncRNAs in modulating cancer cell resistance to paclitaxel (PTX) therapy.Medical oncology (Northwood, London, England) · 2024
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35 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

8 authors at 3 institutions in 1 country.

Feng JiaoDepartment of Medical Oncology and Pancreatic Cancer Center, Shanghai General Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 201620, China. jiao_f@outlook.com.
Hai HuDepartment of Medical Oncology and Pancreatic Cancer Center, Shanghai General Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 201620, China. huhai87@126.com.
Ting HanDepartment of Medical Oncology and Pancreatic Cancer Center, Shanghai General Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 201620, China. yyhanwh@163.com.
Cuncun YuanDepartment of Pathology, Shanghai General Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 201620, China. blkcun@126.com.
Lei WangDepartment of Medical Oncology and Pancreatic Cancer Center, Shanghai General Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 201620, China. wang_lei744@hotmail.com.
Ziliang JinShanghai Key Laboratory of Pancreatic Diseases, Shanghai 201620, China. jzl920222@126.com.
Zhen GuoShanghai Key Laboratory of Pancreatic Diseases, Shanghai 201620, China. guozhenzhen@126.com.
Liwei WangDepartment of Medical Oncology and Pancreatic Cancer Center, Shanghai General Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 201620, China. yzwlw@hotmail.com.
Shanghai Jiao Tong University · CNShanghai First People's Hospital · CNShanghai Chest Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cancer stem cells (CSCs) play a vital role in tumor initiation, progression, metastasis, chemoresistance, and recurrence. The mechanisms that maintain the stemness of these cells remain largely unknown. Our previous study indicated that MALAT-1 may serve as an oncogenic long noncoding RNA in pancreatic cancer by promoting epithelial-mesenchymal transition (EMT) and regulating CSCs markers expression. More significantly, there is emerging evidence that the EMT process may give rise to CSCs, or at least cells with stem cell-like properties. Therefore, we hypothesized that MALAT-1 might enhance stem cell-like phenotypes in pancreatic cancer cells. In this study, our data showed that MALAT-1 could increase the proportion of pancreatic CSCs, maintain self-renewing capacity, decrease the chemosensitivity to anticancer drugs, and accelerate tumor angiogenesis in vitro. In addition, subcutaneous nude mouse xenografts revealed that MALAT-1 could promote tumorigenicity of pancreatic cancer cells in vivo. The underlying mechanisms may involve in increased expression of self-renewal related factors Sox2. Collectively, we for the first time found the potential effects of MALAT-1 on the stem cell-like phenotypes in pancreatic cancer cells, suggesting a novel role of MALAT-1 in tumor stemness, which remains to be fully elucidated.

Indexed as

AnimalsCell Line, TumorCell MovementEpithelial-Mesenchymal TransitionFemaleGene Expression Regulation, NeoplasticHumansHuman Umbilical Vein Endothelial CellsMiceNeoplasm TransplantationNeoplastic Stem CellsPancreatic NeoplasmsRNA, Long NoncodingSOXB1 Transcription FactorsUp-RegulationMALAT1 long non-coding RNA, humanMalat1 long non-coding RNA, mouseRNA, Long NoncodingSOXB1 Transcription Factors

Identifiers

PMID25811929
PMCPMC4424983
OpenAlexW1978546305

What OpenQuestion holds

Textmetadata
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.