ArticleTranslational cancer research2019
Up-regulated GGA3 promotes non-small cell lung cancer proliferation by regulating TrkA receptor.
Article in Translational cancer research, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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.
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.
Who cites it
1 citing paper in PubMed.
- GGAs: Regulation of Multiple Sorting Pathways and Potential Association With Human Diseases.Journal of cellular and molecular medicine · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundGGA3 has been reported to be related to cellular events such as cell survival, cell migration and cell apoptosis through different molecular mechanisms, which imply the potential role in tumorigenesis. However, the function of GGA3 in non-small cell lung cancer (NSCLC) is not clear. This research aims to reveal the effect of GGA3 on NSCLC proliferation and its underlying mechanisms.
methodsThe mRNA expression of GGA3 and TrkA, and association between GGA3 and TrkA in NSCLC tissues were analyzed based on data from TCGA database. And the mRNA expression level of GGA3 in NSCLC cell lines was determined by qRT-PCR. Expression level of GGA3 in A549 cell was detected by qRT-PCR and western blot after transfected with pcDNA3.1-GGA3. Cell counting kit 8, transwell, and flow cytometry assays were performed to detect A549 cell proliferation, aggressiveness, and apoptosis. Western blot was applied to assess the protein expression during apoptosis and TrkA-AKT/ERK signaling pathway.
resultsHigh expression of GGA3 was presented in NSCLC tissues and cell lines. In addition, overexpression of GGA3 could promote proliferation, invasion, and migration of A549 cell, but inhibit the apoptosis of A549 cell. After depletion of GGA3, the expression of anti-apoptotic protein Bcl-2 was increased, and the expression of pro-apoptotic protein Bax and Active Caspase 3 were reduced. Moreover, we found the expression of TrkA, p-AKT and p-ERK in pcDNA3.1-GGA3 group were obviously up-regulated in contrast with the sham group, which suggested that the induced effect of GGA3 on NSCLC cells might be performed via the TrkA-AKT/ERK signaling pathway.
conclusionsTaken together, overexpressed GGA3 in NSCLC could promote the A549 cells tumorigenesis partly through TrkA-AKT/ERK signaling pathway, supplying a theoretical basis for revealing the mechanism for NSCLC.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.