Evidence map›Paper›PMID 27121073›Full record

ArticleTechnology in cancer research & treatment2017

Gelsolin Promotes Radioresistance in Non-Small Cell Lung Cancer Cells Through Activation of Phosphoinositide 3-Kinase/Akt Signaling.

Ru-Sen Zhao, Wei Wang, Jun-Ping Li, Chun-Mei Liu, Liya He

Open access · bronzeAbstract read
In one paragraph

Article in Technology in cancer research & treatment, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
0.8field-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

8 citing papers in PubMed, 14 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Review
  5. Article
  6. Review
  7. Article
  8. 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 3 institutions in 1 country.

Ru-Sen Zhao1 Department of Oncology, People's Hospital of Linzi District, Binzhou Medical College, Zibo, People's Republic of China.
Wei Wang1 Department of Oncology, People's Hospital of Linzi District, Binzhou Medical College, Zibo, People's Republic of China.
Jun-Ping Li1 Department of Oncology, People's Hospital of Linzi District, Binzhou Medical College, Zibo, People's Republic of China.
Chun-Mei Liu2 Department of Radiotherapy, The Second Hospital of Hebei Medical University, Shijiazhuang, People's Republic of China.
Liya He3 Department of Oncology, Hebei General Hospital, Shijiazhuang, People's Republic of China.
Binzhou Medical University · CNHebei General Hospital · CNSecond Hospital of Hebei Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Gelsolin is an actin-binding protein and acts as an important regulator of cell survival. This study aimed to determine the function of gelsolin in the radioresistance of non-small cell lung cancer cells. We examined the expression of gelsolin in radioresistant A549 and H460 cells and their parental cells. The effects of gelsolin overexpression and knockdown on the clonogenic survival and apoptosis of non-small cell lung cancer cells after irradiation were studied. The involvement of phosphoinositide 3-kinase/Akt signaling in the action of gelsolin was checked. We found that gelsolin was significantly upregulated in radioresistant A549 and H460 cells. Overexpression of gelsolin significantly ( P < .05) increased the number of colonies from irradiated A549 and H460 cells compared to transfection of empty vector. In contrast, knockdown of gelsolin significantly ( P < .05) suppressed colony formation after irradiation. Gelsolin-overexpressing cells displayed reduced apoptosis in response to irradiation, which was coupled with decreased levels of cleaved caspase-3 and poly adenosine diphosphate-ribose polymerase. Ectopic expression of gelsolin significantly ( P < .05) enhanced the phosphorylation of Akt compared to nontransfected cells. Pretreatment with the phosphoinositide 3-kinase inhibitor LY294002 (20 μmol/L) significantly decreased clonogenic survival and enhanced apoptosis in gelsolin-overexpressing A549 and H460 cells after irradiation. Taken together, gelsolin upregulation promotes radioresistance in non-small cell lung cancer cells, at least partially, through activation of phosphoinositide 3-kinase/Akt signaling.

Indexed as

Radiation ToleranceSignal TransductionA549 CellsApoptosisCarcinoma, Non-Small-Cell LungGelsolinGene ExpressionHumansLung NeoplasmsPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktUp-RegulationGelsolinPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktgelsolinlung cancerradiotherapyresistancesignaling pathway

Identifiers

PMID27121073
PMCPMC5616058
OpenAlexW2343579072

What OpenQuestion holds

Textmetadata
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.