ArticleCancer reports (Hoboken, N.J.)2024
Anti-Cancer Effect of Sulforaphane in Human Pancreatic Cancer Cells Mia PaCa-2.
Article in Cancer reports (Hoboken, N.J.), 2024. 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.
- Sulforaphane in Cancer Prevention and Therapy: A State-of-the-Art Review of Epidemiological Evidence, Molecular Mechanisms, and Translational Challenges.International journal of molecular sciences · 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
backgroundPancreatic cancer is difficult to treat early as it has no early symptoms. The presence of sulforaphane (SFN) in cruciferous vegetables has been found to possess anti-cancer effects in gastric and colon cancers. Glycogen synthase kinase-3 beta (GSK-3β), a serine/threonine kinase, plays a significant role in pancreatic cancer progression, influencing tumor growth, metastasis, and treatment resistance. Targeting GSK-3β has shown potential to enhance the efficacy of chemotherapy. However, the mechanism underlying the anticancer effects of SFN on pancreatic cancer through GSK-3β is unclear.
aimsIn this study, we examined the anticancer effects of SFN in human pancreatic cancer cell line Mia PaCa-2 and evaluated its molecular mechanisms with respect to the GSK-3β-related pathway. METHODS AND
resultsSFN increased the protein expression of the phosphorylated form of GSK3β (Ser9). In the Wingless Int-1 homolog/β-catenin pathway, GSK3β induced apoptosis by phosphorylating β-catenin. However, in mutant Kirsten rat sarcoma viral oncogene homolog-like-dependent cells such as Mia PaCa-2, GSK3β was suppressed and the β-catenin level was increased, thus inducing apoptosis. Indeed, SFN increased the protein expression of β-catenin in the cytoplasm and nucleus. Subsequently, we measured the level of cMyc, the target gene of β-catenin. SFN decreased cMyc expression despite an increase in the β-catenin. We measured the expression of nuclear factor (NF)-κB, a downstream factor of GSK3β and an upstream factor of cMyc. SFN decreased the expression of NF-κB and cMyc, indicating that SFN inhibits cell proliferation by suppressing the GSK3β/NF-κB/cMyc pathway. As the suppression of NF-κB results in a decrease in B-cell lymphoma 2 (BCL-2) which is the anti-apoptotic gene, we tested the effect of SFN in the expression of BCL-2. SFN inhibited the expression of BCL-2 and increased the ratio of the apoptotic regulator gene BCL-2 associated X (BAX), where SFN induced the cleaved cysteine aspartase-3 and poly-adenosine diphosphate ribose polymerase.
conclusionThese results indicate that SFN may have therapeutic potential in the inhibition of pancreatic cancer.
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.