ArticleTumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine2012
The dual PI3K/mTOR inhibitor NVP-BGT226 induces cell cycle arrest and regulates Survivin gene expression in human pancreatic cancer cell lines.
Article in Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 40 citations in OpenAlex.
- NVP-BEZ235 or JAKi Treatment leads to decreased survival of examined GBM and BBC cells.Cancer treatment and research communications · 2021Article
- Quinoline-Based Molecules Targeting c-Met, EGF, and VEGF Receptors and the Proteins Involved in Related Carcinogenic Pathways.Molecules (Basel, Switzerland) · 2020Review
- Decrypting the Molecular Mechanistic Pathways Delineating the Chemotherapeutic Potential of Ruthenium-Phloretin Complex in Colon Carcinoma Correlated with the Oxidative Status and Increased Apoptotic Events.Oxidative medicine and cellular longevity · 2020Article
- Combined inhibition of the PI3K/mTOR/MEK pathway induces Bim/Mcl-1-regulated apoptosis in pancreatic cancer cells.Cancer biology & therapy · 2019Article
- Inhibition of Aurora Kinase A Induces Necroptosis in Pancreatic Carcinoma.Gastroenterology · 2017Article
- Co-targeting PI3K, mTOR, and IGF1R with small molecule inhibitors for treating undifferentiated pleomorphic sarcoma.Cancer biology & therapy · 2017Article
- The novel dual PI3K/mTOR inhibitor NVP-BGT226 displays cytotoxic activity in both normoxic and hypoxic hepatocarcinoma cells.Oncotarget · 2015Article
- The effect of tou nong san on transplanted tumor growth in nude mice.Evidence-based complementary and alternative medicine : eCAM · 2015Article
- mTOR ATP-competitive inhibitor INK128 inhibits neuroblastoma growth via blocking mTORC signaling.Apoptosis : an international journal on programmed cell death · 2015Article
- Differential regulatory functions of three classes of phosphatidylinositol and phosphoinositide 3-kinases in autophagy.Autophagy · 2015Review
- Mir-155 promotes cervical cancer cell proliferation through suppression of its target gene LKB1.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2014Article
- Overexpression of GOLPH3 protein is associated with worse prognosis in patients with epithelial ovarian cancer.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2014Article
- Neurogenin 3-directed cre deletion of Tsc1 gene causes pancreatic acinar carcinoma.Neoplasia (New York, N.Y.) · 2014Article
- Phosphatidylinositol 3-kinase (PI3K) inhibitors as cancer therapeutics.Journal of hematology & oncology · 2013Review
- Cell cycle-dependent activity of the novel dual PI3K-MTORC1/2 inhibitor NVP-BGT226 in acute leukemia.Molecular cancer · 2013Article
- Tandutinib inhibits the Akt/mTOR signaling pathway to inhibit colon cancer growth.Molecular cancer therapeutics · 2013Article
- CDK-4 inhibitor P276 sensitizes pancreatic cancer cells to gemcitabine-induced apoptosis.Molecular cancer therapeutics · 2012Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The phosphatidylinositol-3-kinase (PI3K) pathway is one of the most commonly activated signaling pathways in pancreatic cancer and is a target of interest for new therapeutic approaches. NVP-BGT226 is a novel dual class PI3K/mammalian target of rapamycin (mTOR) inhibitor that has entered Phase I/II clinical trials. We analyzed the effect of NVP-BGT226 (10-100 nM) on the pancreatic cell lines Panc-1, BxPc-3, AsPC-1 and MiaPaCa-2 in regard to cell viability, induction of apoptosis, cell cycle, and expression of the antiapoptotic genes Survivin, MCL-1, BCL-2 and BCL-xL. Cell viability decreased within 24-72 h after exposure to about 50% compared to untreated control cells in a concentration- but not time-dependent manner. Cell cycle analysis revealed that NVP-BGT226 induced predominantly G0/G1 cell cycle arrest. Additionally, real-time RT-PCR and Western blot analysis showed a remarkable decrease of Survivin expression. Originally designed as a dual inhibitor, there was only a significant inhibition of p-mTOR. In summary, the dual PI3K/mTOR inhibitor NVP-BGT226 induces G0/G1 arrest and acts, at least, partially via downregulation of Survivin.
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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.