Evidence map›Paper›PMID 31789397›Full record

ArticleInternational journal of oncology2020

Semaphorin 5A suppresses the proliferation and migration of lung adenocarcinoma cells.

Pin-Hao Ko, Govinda Lenka, Yu-An Chen, Eric Y Chuang, Mong-Hsun Tsai, Yuh-Pyng Sher, Liang-Chuan Lai

RetractedOpen access · hybridAbstract readRetracted Publication
In one paragraph

Article in International journal of oncology, 2020. 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 It has been retracted, and should not be counted.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 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
0.9field-weighted citation impact, top 30% 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

8 citing papers in PubMed, 19 citations in OpenAlex.

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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

7 authors at 2 institutions in 1 country.

Pin-Hao KoGraduate Institute of Physiology, College of Medicine, National Taiwan University, Taipei 10051, Taiwan, R.O.C.
Govinda LenkaGraduate Institute of Physiology, College of Medicine, National Taiwan University, Taipei 10051, Taiwan, R.O.C.
Yu-An ChenBioinformatics and Biostatistics Core, Center of Genomic and Precision Medicine, National Taiwan University, Taipei 10055, Taiwan, R.O.C.
Eric Y ChuangBioinformatics and Biostatistics Core, Center of Genomic and Precision Medicine, National Taiwan University, Taipei 10055, Taiwan, R.O.C.
Mong-Hsun TsaiBioinformatics and Biostatistics Core, Center of Genomic and Precision Medicine, National Taiwan University, Taipei 10055, Taiwan, R.O.C.
Yuh-Pyng SherGraduate Institute of Clinical Medical Science, China Medical University, Taichung 40402, Taiwan, R.O.C.
Liang-Chuan LaiGraduate Institute of Physiology, College of Medicine, National Taiwan University, Taipei 10051, Taiwan, R.O.C.
National Taiwan University · TWChina Medical University · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Semaphorin 5A (SEMA5A), a member of the semaphorin family, plays an important role in axonal guidance. Previously, the authors identified another possible role of SEMA5A as a prognostic biomarker for non‑smoking women with lung adenocarcinoma in Taiwan, and this phenomenon has been validated in other ethnic groups. However, the functional significance of SEMA5A in lung adenocarcinoma remains unclear. Therefore, we assessed the function of SEMA5A in three lung adenocarcinoma cell lines in this study. Kaplan‑Meier Plotter for lung cancer was conducted for survival analyses. Reverse transcription‑quantitative PCR (RT‑qPCR) and western blot analysis were performed to investigate the expression and post‑translational regulation of SEMA5A in lung adenocarcinoma cell lines. A pre‑designed PyroMark CpG assay and 5‑aza‑2'‑deoxycytidine treatment were used to measure the methylation levels of SEMA5A. The biological functions of lung adenocarcinoma cells overexpressing SEMA5A were investigated by microarrays, and validated both in vitro (proliferation, colony formation and migration assays) and in vivo (tumor xenografts) experiments. The results revealed that the hypermethylation of SEMA5A and the cleavage of the extracellular domain of SEMA5A were responsible for the downregulation of the SEMA5A levels in lung adenocarcinoma cells (A549 and H1299) as compared to the normal controls. Functional analysis of SEMA5A‑regulated genes revealed that they were involved in cellular growth and proliferation. The overexpression of SEMA5A in A549 and H1299 cells significantly decreased the proliferation (P<0.01), colony formation (P<0.001) and migratory ability (P<0.01) of the cells. The suppressive effects of SEMA5A on the proliferative and migratory ability of the cells were also observed in both in vitro and in vivo experiments using brain metastatic Bm7 lung adenocarcinoma cells. On the whole, the findings of this study suggest a suppressive role for SEMA5A in lung adenocarcinoma involving the inhibition of the proliferation and migration of lung transformed cells.

Indexed as

Cell MovementCell ProliferationGene Expression Regulation, NeoplasticAdenocarcinoma of LungAnimalsApoptosisBiomarkers, TumorDNA MethylationHumansLung NeoplasmsMaleMiceMice, Inbred BALB CMice, NudeNeoplasm InvasivenessPrognosisBiomarkers, TumorSEMA5A protein, humanSemaphorins

Identifiers

PMID31789397
PMCPMC6910195
OpenAlexW2992881214

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.