ArticleOncology letters2018
Role of Kruppel-like factor 4 in regulating inhibitor of apoptosis-stimulating protein of p53 in the progression of gastric cancer.
Article in Oncology letters, 2018. 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, 6 citations in OpenAlex.
- KLF4: a multifunctional nexus connecting tumor progression and immune regulation.Frontiers in immunology · 2025Review
- Depletion of microRNA-92a Enhances the Role of Sevoflurane Treatment in Reducing Myocardial Ischemia-Reperfusion Injury by Upregulating KLF4.Cardiovascular drugs and therapy · 2023Review
- Krüppel-like factors in tumors: Key regulators and therapeutic avenues.Frontiers in oncology · 2023Review
- SAMHD1, positively regulated by KLF4, suppresses the proliferation of gastric cancer cells through MAPK p38 signaling pathway.Cell cycle (Georgetown, Tex.) · 2022Article
- Recent Discoveries on the Involvement of Krüppel-Like Factor 4 in the Most Common Cancer Types.International journal of molecular sciences · 2020Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Gastric cancer (GC) remains one of the leading causes of cancer-associated mortality. The overexpression of inhibitor of apoptosis-stimulating protein of p53 (iASPP) has been detected in GC tissues but the function of iASPP in the viability of GC cells and its underlying molecular mechanism remains unknown. Kruppel-like factor 4 (KLF4) is a tumor suppressor gene in GC and it may interact with p53. iASPP is an evolutionarily conserved inhibitor of p53, whereas KLF4 may be negatively associated with iASPP in GC. However, whether KLF4 has regulatory effects on iASPP remains to be investigated. The objective of the present study was to examine the function of iASPP and KLF4 in the proliferation of GC cells and to determine whether KLF4 has regulatory effects on iASPP. It was demonstrated that iASPP was upregulated and KLF4 was downregulated in GC cell lines. Downregulation of iASPP inhibited the proliferation and colony formation ability, and promoted the apoptosis of GC cells. Additionally, upregulation of KLF4 inhibited the proliferation and colony formation ability, and promoted apoptosis of GC cells. Furthermore, upregulation of KLF4 inhibited the expression of iASPP. Upregulation of iASPP following overexpression of KLF4 reversed the KLF4-mediated effects in GC cells.
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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.