ArticleCancer chemotherapy and pharmacology2019
NO donor inhibits proliferation and induces apoptosis by targeting PI3K/AKT/mTOR and MEK/ERK pathways in hepatocellular carcinoma cells.
Article in Cancer chemotherapy and pharmacology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 7 papers.
What it found
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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
7 citing papers in PubMed, 12 citations in OpenAlex.
- MEK/ERK and PI3K/AKT pathway inhibitors affect the transformation of myelodysplastic syndrome into acute myeloid leukemia via H3K27me3 methylases and de‑methylases.International journal of oncology · 2023Article
- Antitumor efficacy of CHMFL-KIT-110 solid dispersion in mouse xenograft models of human gastrointestinal stromal tumors.Cancer chemotherapy and pharmacology · 2021Article
- Increase in NO causes osteoarthritis and chondrocyte apoptosis and chondrocyte ERK plays a protective role in the process.Molecular biology reports · 2021Article
- GlutathioneThe Journal of pharmacology and experimental therapeutics · 2021Article
- Phenotypic Modulation of Macrophages and Vascular Smooth Muscle Cells in Atherosclerosis-Nitro-Redox Interconnections.Antioxidants (Basel, Switzerland) · 2021Review
- Systems Pharmacology-Based Dissection of Anti-Cancer Mechanism of Traditional Chinese HerbFrontiers in pharmacology · 2021Article
- Role of lncRNA NR2F1-AS1 and lncRNA H19 Genes in Hepatocellular Carcinoma and Their Effects on Biological Function of Huh-7.Cancer management and research · 2021Article
Corrections and comments
- Retraction · 2024-10-16Concerns/Issues about Image · Duplication of/in Image · Euphemisms for Duplication · Investigation by Journal/Publisher · Objections by Author(s) · Unreliable Results and/or Conclusions ·
- Retracted
Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
backgroundPABA/NO, O PURPOSE: This study aimed to determine the effects of PABA/NO on hepatocellular carcinoma proliferation and apoptosis induction both in vitro and in vivo experiments.
resultsPABA/NO dramatically inhibited the growth of Bel-7402 hepatocellular carcinoma cells and significantly induced apoptosis in a concentration-dependent manner, accompanied by down-regulation of Bcl-2 and Bcl-xL, up-regulation of Bax and Bad, release of Cyt c and activation of cleaved-caspase-9/3 and cleaved-PARP, which were related to suppressing PI3K/AKT/mTOR and MEK/ERK signaling pathways. LY294002 (a PI3K inhibitor) and U0126 (an ERK inhibitor) prior to PABA/NO were found to synergistically enhance PABA/NO-induced apoptosis. Carboxy-PTIO as a NO scavenger obviously attenuated PABA/NO-induced apoptosis. Additionally, H22 tumor-bearing mice experiments demonstrated that PABA/NO exerted good anti-tumor effects via reducing tumor volume, tumor weight and decreasing the expression of CD34. Furthermore, PABA/NO treatment strongly inhibited the phosphorylation of PI3K/AKT/mTOR and MEK/ERK signaling pathways in H22 hepatocellular carcinoma tissues.
conclusionsPABA/NO induced apoptosis through inhibition of PI3K/Akt/mTOR and MEK/ERK pathway in hepatocellular carcinoma cells.
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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.