Evidence map›Paper›PMID 31571907›Full record

ArticleOncoTargets and therapy2019

Up-regulated LncRNA-ATB regulates the growth and metastasis of cholangiocarcinoma via miR-200c signals.

Hai Lin, Lili Yang, Feng Tian, Shuang Nie, Hailang Zhou, Jun Liu, Weichang Chen

Open access · goldAbstract read
In one paragraph

Article in OncoTargets and therapy, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
1.5field-weighted citation impact, top 20% 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

19 citing papers in PubMed, 27 citations in OpenAlex.

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  16. Review
  17. LncRNA-ATB in cancers: what do we know so far?Molecular biology reports · 2020
    Review
  18. Cholangiocarcinoma: novel therapeutic targets.Expert opinion on therapeutic targets · 2020
    Review
  19. Review
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

7 authors at 3 institutions in 1 country.

Hai LinDepartment of Gastroenterology, The First Affiliated Hospital of Soochow University, Suzhou, Jiangsu 215006, People's Republic of China.
Lili YangDepartment of Gastroenterology, Lin Yi Central Hospital, Linyi, Shandong 276400, People's Republic of China.
Feng TianDepartment of Gastroenterology, Lin Yi Central Hospital, Linyi, Shandong 276400, People's Republic of China.
Shuang NieDepartment of Gastroenterology, Drum Tower Hospital, Medical School of Nanjing University, Nanjing, Jiangsu 210008, People's Republic of China.
Hailang ZhouDepartment of Gastroenterology, Lian Shui County People's Hospital, Huaian, Jiangsu 223400, People's Republic of China.
Jun LiuDepartment of Pathology, Lin Yi Central Hospital, Linyi, Shandong 276400, People's Republic of China.
Weichang ChenDepartment of Gastroenterology, The First Affiliated Hospital of Soochow University, Suzhou, Jiangsu 215006, People's Republic of China.
Linyi People's Hospital · CNSoochow University · CNNanjing Drum Tower Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

BACKGROUND AND

objectiveCholangiocarcinoma (CCA) is a highly aggressive neoplasm featured with regional invasiveness and distant metastasis, which often present a phenotype of epithelial-mesenchymal transition (EMT). Long non-coding RNAs (LncRNAs) are dysregulated during carcinogenesis, and up-regulated LncRNA-activated by TGF-β (Lnc-ATB) supports tumor growth and metastasis via tumor suppressor microRNA 200 (miR-200). However, the role of Lnc-ATB in CCA is unclear.

methodsCCA tissues and non-cancer tissues (n=30) were used to determine the Lnc-ATB and miR-200a/b/c levels. The functions and mechanisms of Lnc-ATB/miR-200 pathway were determined by knockdown of Lnc-ATB via siRNAs in vitro and in vivo.

resultsCCA tissues have increased Lnc-ATB and reduced miR-200a/b/c levels, but the down-regulated miR-200c was most prominent. Up-regulated Lnc-ATB significant negatively correlated with miR-200c and predicted advanced TNM stage and more lymph node metastasis of CCA patients. Knockdown of Lnc-ATB in two CCA cell lines HuCCT1 and RBE increased miR-200c levels. The luciferase reporter assay further confirmed the direct binding site of miR-200c in Lnc-ATB. Inhibition of Lnc-ATB significantly impaired cell vitality and induced apoptosis and G0/G1 arrest, which, however, was rescued by miR-200c inhibitor. The ability of migration of CCA cells was also up-regulated by Lnc-ATB but was suppressed by miR-200c. Mechanistically, the cell cycle-related CCND1/CDK2, apoptosis-related BCL-2/caspase-3 and EMT-related E-cadherin/ZEB1/2 were regulated by Lnc-ATB via miR-200c. Knockdown of Lnc-ATB in vivo up-regulated miR-200c signals to inhibit tumor growth with decreased PCNA expression in tumor tissues, which was restored by miR-200c inhibition.

conclusionOverexpressed Lnc-ATB functioned as an oncogene for CCA growth and metastasis via miR-200 signals.

Indexed as

cholangiocarcinomaEMTgrowthLnc-ATBmiR-200

Identifiers

PMID31571907
PMCPMC6750848
OpenAlexW2973159701

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.