ArticleMolecular medicine reports2019
BP‑1‑102 exerts an antitumor effect on the AGS human gastric cancer cell line through modulating the STAT3 and MAPK signaling pathways.
Article in Molecular medicine reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 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
5 citing papers in PubMed, 12 citations in OpenAlex.
- BP‑1‑102 exerts antitumor effects on T‑cell acute lymphoblastic leukemia cells by suppressing the JAK2/STAT3/c‑Myc signaling pathway.Experimental and therapeutic medicine · 2023Article
- Discovery of potent STAT3 inhibitors using structure-based virtual screening, molecular dynamic simulation, and biological evaluation.Frontiers in oncology · 2023Article
- Sodium propionate exerts anticancer effect in mice bearing breast cancer cell xenograft by regulating JAK2/STAT3/ROS/p38 MAPK signaling.Acta pharmacologica Sinica · 2021Article
- STAT3 Pathway in Gastric Cancer: Signaling, Therapeutic Targeting and Future Prospects.Biology · 2020Review
- A Sesquiterpenoid from Farfarae Flos Induces Apoptosis of MDA-MB-231 Human Breast Cancer Cells through Inhibition of JAK-STAT3 Signaling.Biomolecules · 2019Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
BP‑1‑102, a novel inhibitor of signal transducer and activator of transcription 3 (STAT3), exhibits significant antitumor effects in several malignancies in vitro and in vivo. However, its role in gastric cancer (GC) remains to be elucidated. In the present study, the effect and potential molecular mechanisms of BP‑102 in human GC cell lines were investigated. The results showed that BP‑1‑02 dose‑dependently inhibited the proliferation of AGS cells, whereas it had little effect on HGC‑27 cells. Flow cytometric analysis indicated that BP‑1‑102 induced apoptosis, but had minimal effect on cell cycle distribution. In addition, cells treated with BP‑1‑102 demonstrated markedly suppressed migration and invasion capacities. Western blot analysis revealed that BP‑1‑102 inhibited the phosphorylation of STAT3 and its target genes, including c‑Myc, cyclin D1 and survivin, in a time‑ and dose‑dependent manner. Furthermore, it was found that BP‑1‑102 induced the phosphorylation of c‑Jun N‑terminal kinase and p38 mitogen‑activated protein kinase (MAPK) and inhibited the activation of extracellular signal‑related kinases. Taken together, these results demonstrated that BP‑1‑102 may be a potent antitumor agent that acts through modulating the STAT3 and MAPK signaling pathways in GC cells.
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.