ArticleMolecular biology reports2020
Nitric oxide induces HepG2 cell death via extracellular signal-regulated protein kinase activation by regulating acid sphingomyelinase.
Article in Molecular biology reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 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
3 citing papers in PubMed, 3 citations in OpenAlex.
- Euphol from Tapinanthus sp. Induces Apoptosis and Affects Signaling Proteins in Glioblastoma and Prostate Cancer CellsAsian Pacific journal of cancer prevention : APJCP · 2022Article
- Engineered lanthanide-doped upconversion nanoparticles for biosensing and bioimaging application.Mikrochimica acta · 2022Review
- Acid Sphingomyelinase, a Lysosomal and Secretory Phospholipase C, Is Key for Cellular Phospholipid Catabolism.International journal of molecular sciences · 2021Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Nitric oxide (NO) plays a vital role in the occurrence and development of tumours. Acid sphingomyelinase (ASM) participates in cell apoptosis, cell proliferation, metabolism and other biological processes. However, whether ASM has an effect on NO-treated HepG2 cells remains unknown, and the role of the extracellular signal-regulated protein kinase (ERK) pathway is also unclear. In the present study, the effects of NO on cell viability and apoptosis were assayed, followed by investigating the mRNA and protein levels of ASM and ERK phosphorylation in NO-treated HepG2 cells. The results showed that diethylenetriamine/NO (DETA-NO), an NO donor, promoted HepG2 cell death and apoptosis in a concentration-dependent manner and that the mRNA and protein expression levels of ASM were significantly decreased in DETA-NO-treated HepG2 cells. Moreover, ERK phosphorylation was significantly increased in DETA-NO-treated HepG2 cells. The inhibition of ERK phosphorylation increased DETA-NO-induced cell apoptosis. In summary, DETA-NO can promote HepG2 cell death in a concentration-dependent manner by activating ERK and NO might activate ERK by regulating ASM and then inducing HepG2 cell death.
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.