ArticleBritish journal of cancer2005
The Akt inhibitor KP372-1 suppresses Akt activity and cell proliferation and induces apoptosis in thyroid cancer cells.
Article in British journal of cancer, 2005. 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 It has been retracted, and should not be counted.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 30 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
30 citing papers in PubMed, 88 citations in OpenAlex.
- Trial
- Transcriptome analysis revealed the role of mTOR and MAPK signaling pathways in the white strain ofFrontiers in pharmacology · 2022Article
- DNA damage induced by KP372-1 hyperactivates PARP1 and enhances lethality of pancreatic cancer cells with PARP inhibition.Scientific reports · 2020Article
- CYP24A1 depletion facilitates the antitumor effect of vitamin D3 on thyroid cancer cells.Experimental and therapeutic medicine · 2018Article
- SoNar, a Highly Responsive NAD+/NADH Sensor, Allows High-Throughput Metabolic Screening of Anti-tumor Agents.Cell metabolism · 2015Article
- Δ(9) Tetrahydrocannabinol attenuates Staphylococcal enterotoxin B-induced inflammatory lung injury and prevents mortality in mice by modulation of miR-17-92 cluster and induction of T-regulatory cells.British journal of pharmacology · 2015Article
- The PI3K/Akt Pathway in Tumors of Endocrine Tissues.Frontiers in endocrinology · 2015Review
- Autophagy in thyroid cancer: present knowledge and future perspectives.Frontiers in endocrinology · 2015Review
- SASH1 inhibits proliferation and invasion of thyroid cancer cells through PI3K/Akt signaling pathway.International journal of clinical and experimental pathology · 2015Article
- Estrogen receptor alpha prevents bladder cancer via INPP4B inhibited akt pathway in vitro and in vivo.Oncotarget · 2014Article
- BI-69A11 enhances susceptibility of colon cancer cells to mda-7/IL-24-induced growth inhibition by targeting Akt.British journal of cancer · 2014Article
- Genetics and epigenetics of sporadic thyroid cancer.Molecular and cellular endocrinology · 2014Review
- PI3K-AKT-mTOR-signaling and beyond: the complex network in gastroenteropancreatic neuroendocrine neoplasms.Theranostics · 2014Review
- MK-2206 causes growth suppression and reduces neuroendocrine tumor marker production in medullary thyroid cancer through Akt inhibition.Annals of surgical oncology · 2013Article
- Akt-mediated phosphorylation of argonaute 2 downregulates cleavage and upregulates translational repression of MicroRNA targets.Molecular cell · 2013Article
- PI3K and Akt as molecular targets for cancer therapy: current clinical outcomes.Acta pharmacologica Sinica · 2012Review
- Antineoplastic effects of mammalian target of rapamycine inhibitors.World journal of transplantation · 2012Review
- c-Met inhibitor synergizes with tumor necrosis factor-related apoptosis-induced ligand to induce papillary thyroid carcinoma cell death.Molecular medicine (Cambridge, Mass.) · 2012Article
- Sphingosine kinase 1 is overexpressed and promotes proliferation in human thyroid cancer.Molecular endocrinology (Baltimore, Md.) · 2011Article
- Mammalian target of rapamycin: a central node of complex signaling cascades.International journal of clinical and experimental pathology · 2011Review
Corrections and comments
- Retraction · 2021-02-18Concerns/Issues about Data · Duplication of/in Image · Manipulation of Images · Original Data and/or Images not Provided and/or not Available · · see also: https://pubpeer.com/publications/E3B3931AD2953898295911E9B755DB;
- Retracted
Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The phosphatidylinositol 3' kinase (PI3K)/phosphatase and tensin homologue deleted on chromosome ten/Akt pathway, which is a critical regulator of cell proliferation and survival, is mutated or activated in a wide variety of cancers. Akt appears to be a key central node in this pathway and thus is an attractive target for targeted molecular therapy. We demonstrated that Akt is highly phosphorylated in thyroid cancer cell lines and human thyroid cancer specimens, and hypothesised that KP372-1, an Akt inhibitor, would block signalling through the PI3K pathway and inhibit cell proliferation while inducing apoptosis of thyroid cancer cells. KP372-1 blocked signalling downstream of Akt in thyroid tumour cells, leading to inhibition of cell proliferation and increased apoptosis. As thyroid cancer consistently expresses phosphorylated Akt and KP372-1 effectively blocks Akt signalling, further preclinical evaluation of this compound for treatment of thyroid cancer is warranted.
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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.