ArticleScientific reports2025
Study on the regulation of gastric cancer cell apoptosis by LACTB through mitochondrial autophagy pathway.
Article in Scientific reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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
4 citing papers in PubMed.
- Mitophagy interacts with mitochondrial dynamics and biogenesis, acting as a double-edged sword in digestive cancer.iScience · 2026Review
- New Functions of Mitochondrial Dysfunction in Gastric Cancer: From Molecular Processes to Potential Treatments.International journal of molecular sciences · 2026Review
- Reprogramming oncogenic mitochondria in pancreatic adenocarcinoma through BRD4 inhibition leads to programmed cell death.The Journal of pharmacology and experimental therapeutics · 2025Article
- Mitophagy in gastrointestinal tumors: mechanisms and new targets for immunotherapy.Frontiers in oncology · 2025Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors.
Funding
Abstract
This study aimed to determine whether β-lactamase-like protein (Lactamase-β, LACTB) influences apoptosis in gastric cancer cells by modulating mitochondrial autophagy through the PTEN-induced putative kinase 1 (PINK1) or Parkin pathway. Firstly, the expression level of LACTB in gastric cancer tissues was detected by immunohistochemistry, and the survival data of patients were used to explore the relationship between LACTB expression level and patient prognosis. Secondly, LACTB overexpression (+ LACTB) and knockdown (sh-LACTB) AGS gastric cancer cell lines were constructed; flow cytometry and other experiments were used to detect the effect of LACTB on AGS cell apoptosis; Western Blot was used to detect the expression of PINK1/Parkin mitochondrial autophagy pathway-related proteins and lysosome-related proteins in + LACTB and sh-LACTB gastric cancer cells; kits and electron microscopy were used to detect changes in the number of reactive oxygen species (ROS) and autophagosomes. Finally, Western blot was used to detect the expression of apoptotic proteins Bcl-2 associated x protein (Bax) and B-cell lymphoma-2 (Bcl-2) in + LACTB and sh-LACTB gastric cancer cells treated with mitochondrial autophagy inhibitor 3-methyladenine (3-MA). Immunohistochemistry analysis revealed that LACTB expression in gastric cancer tissues was higher than in adjacent non-cancerous tissues, for patients with tumor diameters exceeding 4.5 cm, high LACTB expression was associated with a poor prognosis (P < 0.05). LACTB overexpression reduced apoptosis in gastric cancer cells. It downregulated the pro-apoptotic protein Bax, while LACTB knockdown promoted apoptosis, upregulated Bax, the expression of pro-apoptotic protein Bax, and downregulated the expression of anti-apoptotic protein Bcl-2. In LACTB overexpressing cell lines, protein sequestosome 1 (P62) protein levels were elevated, lysosomal-associated membrane protein 2 (LAMP2) expression was decreased, Reactive oxygen species (ROS) levels remained significantly stable, and autophagosome counts were reduced. Conversely, LACTB knockdown cells, PINK1, Parkin, protein light chain 3II/I (LC3II/I), LAMP2, cathepsin B (CTSB), continuous traumatic stress disorder (CTSD), and other related proteins, downregulated P62 expression, increased ROS accumulation, and higher number of autophagosomes. In LV-LACTB and sh-LACTB gastric cancer cells treated with the mitochondrial autophagy inhibitor 3-methyladenine (3-MA), apoptotic protein Bax is downregulated, and anti-apoptotic protein Bcl-2 is upregulated. In summary, the LACTB protein may regulate the apoptosis in gastric cancer cells by modulating mitochondrial autophagy through the PINK1/Parkin pathway.
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.