Evidence map›Paper›PMID 32194726›Full record

ArticleOncology letters2020

MARCKSL1 promotes the proliferation, migration and invasion of lung adenocarcinoma cells.

Wenjun Liang, Ruichen Gao, Mingxia Yang, Xiaohua Wang, Kewei Cheng, Xuejun Shi, Chen He, Yemei Li, Yuying Wu, Lei Shi and 2 more

Open access · diamondAbstract read
In one paragraph

Article in Oncology letters, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
2.1field-weighted citation impact, top 13% 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

32 citing papers in PubMed, 40 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 1 institution in 1 country.

Wenjun LiangDepartment of Respiratory Medicine, Affiliated Changzhou Second Hospital of Nanjing Medical University, Changzhou, Jiangsu 213000, P.R. China.
Ruichen GaoDepartment of Respiratory Medicine, Affiliated Changzhou Second Hospital of Nanjing Medical University, Changzhou, Jiangsu 213000, P.R. China.
Mingxia YangDepartment of Respiratory Medicine, Affiliated Changzhou Second Hospital of Nanjing Medical University, Changzhou, Jiangsu 213000, P.R. China.
Xiaohua WangDepartment of Respiratory Medicine, Affiliated Changzhou Second Hospital of Nanjing Medical University, Changzhou, Jiangsu 213000, P.R. China.
Kewei ChengDepartment of Respiratory Medicine, Affiliated Changzhou Second Hospital of Nanjing Medical University, Changzhou, Jiangsu 213000, P.R. China.
Xuejun ShiDepartment of Respiratory Medicine, Affiliated Changzhou Second Hospital of Nanjing Medical University, Changzhou, Jiangsu 213000, P.R. China.
Chen HeDepartment of Respiratory Medicine, Affiliated Changzhou Second Hospital of Nanjing Medical University, Changzhou, Jiangsu 213000, P.R. China.
Yemei LiDepartment of Respiratory Medicine, Affiliated Changzhou Second Hospital of Nanjing Medical University, Changzhou, Jiangsu 213000, P.R. China.
Yuying WuDepartment of Respiratory Medicine, Affiliated Changzhou Second Hospital of Nanjing Medical University, Changzhou, Jiangsu 213000, P.R. China.
Lei ShiDepartment of Respiratory Medicine, Affiliated Changzhou Second Hospital of Nanjing Medical University, Changzhou, Jiangsu 213000, P.R. China.
Jingtao ChenDepartment of Respiratory Medicine, Affiliated Changzhou Second Hospital of Nanjing Medical University, Changzhou, Jiangsu 213000, P.R. China.
Xiaowei YuDepartment of Respiratory Medicine, Affiliated Changzhou Second Hospital of Nanjing Medical University, Changzhou, Jiangsu 213000, P.R. China.
Nanjing Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Lung cancer is the most common cancer in males and females and ~40% of lung cancer cases are adenocarcinomas. Previous studies have demonstrated that myristoylated alanine rich protein kinase C substrate (MARCKS) is upregulated in several types of cancer and is associated with poor prognosis in patients with breast cancer. However, its expression level and role in lung adenocarcinoma remain unknown. Therefore, the aim of the present study was to investigate the expression level and biological functions of MARCKS like 1 (MARCKSL1), a member of the MARCKS family, in lung adenocarcinoma. The expression level of MARCKSL1 was examined in human lung adenocarcinoma tissues and cell lines. MARCKSL1-specific small interfering RNAs effectively suppressed its expression level and significantly inhibited the proliferation, migration and invasion of lung adenocarcinoma cells. Additionally, the role of MARCKSLI in the regulation of metastasis was examined. Silencing MARCKSL1 decreased the expression of the epithelial-mesenchymal transition (EMT)-associated proteins E-cadherin, N-cadherin, vimentin and snail family transcriptional repressor 2, and decreased the phosphorylation level of AKT. The results obtained in the current study suggested that MARCKSL1 promoted the progression of lung adenocarcinoma by regulating EMT. MARCKSLI may have prognostic value and serve as a novel therapeutic target in lung adenocarcinoma.

Indexed as

epithelial-mesenchymal transitionlung adenocarcinomametastasismyristoylated alanine rich protein kinase C substrate like 1protein kinase B

Identifiers

PMID32194726
PMCPMC7039154
OpenAlexW3000324032

What OpenQuestion holds

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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.