Evidence map›Paper›PMID 31545478›Full record

ArticleOncology reports2019

lncRNA‑u50535 promotes the progression of lung cancer by activating CCL20/ERK signaling.

Wei Wei, Xiaoliang Zhao, Jianquan Zhu, Lianmin Zhang, Yulong Chen, Bin Zhang, Yue Li, Meng Wang, Zhenfa Zhang, Changli Wang

RetractedOpen access · hybridAbstract readRetracted Publication
In one paragraph

Article in Oncology reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
1.0field-weighted citation impact, top 29% 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

12 citing papers in PubMed, 22 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. The Vital Roles of LINC00662 in Human Cancers.Frontiers in cell and developmental biology · 2021
    Review
  9. Article
  10. Article
  11. Review
  12. The CCL20-CCR6 Axis in Cancer Progression.International journal of molecular sciences · 2020
    Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

10 authors at 1 institution in 1 country.

Wei WeiDepartment of Lung Cancer, Tianjin Medical University Cancer Institute and Hospital, National Clinical Research Center for Cancer, Key Laboratory of Cancer Prevention and Therapy, Tianjin's Clinical Research Center for Cancer, Tianjin Lung Cancer Center, Tianjin 300060, P.R. China.
Xiaoliang ZhaoDepartment of Lung Cancer, Tianjin Medical University Cancer Institute and Hospital, National Clinical Research Center for Cancer, Key Laboratory of Cancer Prevention and Therapy, Tianjin's Clinical Research Center for Cancer, Tianjin Lung Cancer Center, Tianjin 300060, P.R. China.
Jianquan ZhuDepartment of Lung Cancer, Tianjin Medical University Cancer Institute and Hospital, National Clinical Research Center for Cancer, Key Laboratory of Cancer Prevention and Therapy, Tianjin's Clinical Research Center for Cancer, Tianjin Lung Cancer Center, Tianjin 300060, P.R. China.
Lianmin ZhangDepartment of Lung Cancer, Tianjin Medical University Cancer Institute and Hospital, National Clinical Research Center for Cancer, Key Laboratory of Cancer Prevention and Therapy, Tianjin's Clinical Research Center for Cancer, Tianjin Lung Cancer Center, Tianjin 300060, P.R. China.
Yulong ChenDepartment of Lung Cancer, Tianjin Medical University Cancer Institute and Hospital, National Clinical Research Center for Cancer, Key Laboratory of Cancer Prevention and Therapy, Tianjin's Clinical Research Center for Cancer, Tianjin Lung Cancer Center, Tianjin 300060, P.R. China.
Bin ZhangDepartment of Lung Cancer, Tianjin Medical University Cancer Institute and Hospital, National Clinical Research Center for Cancer, Key Laboratory of Cancer Prevention and Therapy, Tianjin's Clinical Research Center for Cancer, Tianjin Lung Cancer Center, Tianjin 300060, P.R. China.
Yue LiDepartment of Lung Cancer, Tianjin Medical University Cancer Institute and Hospital, National Clinical Research Center for Cancer, Key Laboratory of Cancer Prevention and Therapy, Tianjin's Clinical Research Center for Cancer, Tianjin Lung Cancer Center, Tianjin 300060, P.R. China.
Meng WangDepartment of Lung Cancer, Tianjin Medical University Cancer Institute and Hospital, National Clinical Research Center for Cancer, Key Laboratory of Cancer Prevention and Therapy, Tianjin's Clinical Research Center for Cancer, Tianjin Lung Cancer Center, Tianjin 300060, P.R. China.
Zhenfa ZhangDepartment of Lung Cancer, Tianjin Medical University Cancer Institute and Hospital, National Clinical Research Center for Cancer, Key Laboratory of Cancer Prevention and Therapy, Tianjin's Clinical Research Center for Cancer, Tianjin Lung Cancer Center, Tianjin 300060, P.R. China.
Changli WangDepartment of Lung Cancer, Tianjin Medical University Cancer Institute and Hospital, National Clinical Research Center for Cancer, Key Laboratory of Cancer Prevention and Therapy, Tianjin's Clinical Research Center for Cancer, Tianjin Lung Cancer Center, Tianjin 300060, P.R. China.
Tianjin Medical University Cancer Institute and Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The ligand/receptor pair C‑C motif chemokine ligand 20 (CCL20)/C‑C motif chemokine receptor 6 (CCR6) is considered to be highly activated in lung cancer and significantly accelerates lung cancer progression through activation of ERK signaling. In addition, it has been shown that long non‑coding RNA‑u50535 (lncRNA‑u50535) upregulates CCL20 expression and facilitates cancer progression in colorectal cancer (CRC). However, the effects of lncRNA‑u50535 in lung cancer progression and whether lncRNA‑u50535 regulates CCL20/CCR6/ERK signaling in lung cancer remain ill‑defined. Therefore, the aim of the present study was to investigate the effects of lncRNA‑u50535 on CCL20/CCR6/ERK signaling in lung cancer progression. The results demonstrated that lncRNA‑u50535 expression was upregulated in lung cancer tissues and cell lines compared with normal tissues and cells. Knockdown of lncRNA‑u50535 decreased lung cancer cell proliferation and migration, induced G0/G1 phase arrest and promoted cell apoptosis. Western blot and luciferase reporter gene assays demonstrated that lncRNA‑u50535 overexpression increased the translation and transcription of CCL20. In addition, knockdown of lncRNA‑u50535 decreased CCL20, CCR6 and p‑ERK levels. The effects of lncRNA‑u50535 on cell proliferation and cell apoptosis were weakened when CCL20 was silenced. Overall, the present study demonstrated that lncRNA‑u50535 may function as an oncogene in lung cancer progression by regulating CCL20/ERK signaling.

Indexed as

MAP Kinase Signaling SystemUp-RegulationA549 CellsAgedAnimalsCell Line, TumorCell MovementCell ProliferationChemokine CCL20Disease ProgressionFemaleGene Expression Regulation, NeoplasticGene Knockdown TechniquesHumansLung NeoplasmsMaleCCL20 protein, humanCCR6 protein, humanChemokine CCL20Receptors, CCR6RNA, Long Noncoding

Identifiers

PMID31545478
PMCPMC6775802
OpenAlexW2971847599

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.