Evidence map›Paper›PMID 28901509›Full record

ArticleMolecular medicine reports2017

CT45A1 siRNA silencing suppresses the proliferation, metastasis and invasion of lung cancer cells by downregulating the ERK/CREB signaling pathway.

Feng Tang, Shengjun Tang, Xiaolong Guo, Chao Yang, Ke Jia

Open access · hybridAbstract read
In one paragraph

Article in Molecular medicine reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
1.2field-weighted citation impact, top 19% 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

17 citing papers in PubMed, 24 citations in OpenAlex.

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  14. Cadmium induces A549 cell migration and invasion by activating ERK.Experimental and therapeutic medicine · 2019
    Article
  15. ERK is a Pivotal Player of Chemo-Immune-Resistance in Cancer.International journal of molecular sciences · 2019
    Review
  16. Article
  17. Article
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

5 authors at 2 institutions in 1 country.

Feng TangDepartment of Thoracic Surgery, Three Gorges Center Hospital, Chongqing 404000, P.R. China.
Shengjun TangDepartment of Thoracic Surgery, Three Gorges Center Hospital, Chongqing 404000, P.R. China.
Xiaolong GuoDepartment of Thoracic Surgery, Three Gorges Center Hospital, Chongqing 404000, P.R. China.
Chao YangDepartment of Thoracic Surgery, Three Gorges Center Hospital, Chongqing 404000, P.R. China.
Ke JiaDepartment of Cardiothoracic Surgery, Affiliated Hospital of North Sichuan Medical College, Nanchong, Sichuan 637000, P.R. China.
Chongqing Three Gorges Central Hospital · CNAffiliated Hospital of North Sichuan Medical College · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The aim of the present study was to investigate the role of the cancer‑testis antigen family 45 member A1 (CT45A1) in the proliferation, apoptosis, invasion and metastasis of lung cancer cells, and the associated molecular mechanisms. Western blotting determined that the expression of CT45A1 in normal lung cells was far lower than that observed in lung cancer cells. Following the transfection of CT45A1 small (or short) interfering (si)RNA and its negative control into A549 cells using Lipofectamine 2000, the CT45A1 protein and mRNA levels were determined further by western blotting and reverse transcription‑polymerase chain reaction. Following CT45A1 siRNA transfection, the levels of CT45A1 in lung cancer cells were markedly reduced (P<0.01). Then, cell viability and apoptosis were investigated with a methyl thiazolyl tetrazolium assay and Annexin V‑FITC/propidium iodide staining, respectively. Transwell assays were employed to evaluate the migration and invasion of A549 cells. When compared with the negative control, the viability, migration and invasion of lung cancer cells treated with CT45A1 siRNA were suppressed and apoptosis was promoted (all P<0.01). In addition, the levels of B‑cell lymphoma‑2 (Bcl‑2), Bcl‑2 associated X (Bax), survivin, matrix metalloproteinase 2 (MMP2), MMP9, extracellular signal‑regulated kinase 1/2 (ERK1/2), phosphorylated ERK1/2 (p‑ERK1/2), cyclic AMP response element binding protein (CREB) and p‑CREB were assessed by western blotting. Following CT45A1 silencing, the expressions of Bcl‑2, survivin, MMP2, MMP9, p‑ERK1/2 and p‑CREB were downregulated and the expression of Bax was upregulated (all P<0.01). It was concluded that CT45A1 siRNA silencing suppressed the proliferation, metastasis and invasion of lung cancer cells by downregulating the ERK/CREB signalling pathway.

Indexed as

RNA InterferenceA549 CellsAntigens, NeoplasmApoptosisbcl-2-Associated X ProteinCell Line, TumorCell MovementCell ProliferationCyclic AMP Response Element-Binding ProteinDown-RegulationHumansLung NeoplasmsMatrix Metalloproteinase 2Matrix Metalloproteinase 9Mitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 3Antigens, Neoplasmbcl-2-Associated X ProteinCT45A1 protein, humanCyclic AMP Response Element-Binding ProteinMatrix Metalloproteinase 2Matrix Metalloproteinase 9Mitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 3Proto-Oncogene Proteins c-bcl-2RNA, MessengerRNA, Small Interfering

Identifiers

PMID28901509
PMCPMC5865787
OpenAlexW2754757241

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.