446 results match your criteria treatment nvp-bez235


The oncogene AAMDC links PI3K-AKT-mTOR signaling with metabolic reprograming in estrogen receptor-positive breast cancer.

Nat Commun 2021 03 26;12(1):1920. Epub 2021 Mar 26.

Cancer Epigenetics Group, The Harry Perkins Institute of Medical Research, The University of Western Australia, Perth, WA, Australia.

Adipogenesis associated Mth938 domain containing (AAMDC) represents an uncharacterized oncogene amplified in aggressive estrogen receptor-positive breast cancers. We uncover that AAMDC regulates the expression of several metabolic enzymes involved in the one-carbon folate and methionine cycles, and lipid metabolism. We show that AAMDC controls PI3K-AKT-mTOR signaling, regulating the translation of ATF4 and MYC and modulating the transcriptional activity of AAMDC-dependent promoters. Read More

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Synergistic Inhibition of Drug-Resistant Colon Cancer Growth with PI3K/mTOR Dual Inhibitor BEZ235 and Nano-Emulsioned Paclitaxel via Reducing Multidrug Resistance and Promoting Apoptosis.

Int J Nanomedicine 2021 15;16:2173-2186. Epub 2021 Mar 15.

Department of Pathology, The First Affiliated Hospital, School of Medicine, Shihezi University, Key Laboratory of Xinjiang Endemic and Ethnic Diseases of the Ministry of Education of China, Xinjiang, 832002, People's Republic of China.

Background: Colon cancer is a top lethal cancer in man and women worldwide and drug resistance is the major cause of cancer-related death. Combinational therapy and drug delivery with nanoparticles have been shown to effectively overcome drug resistance in many cancers. We previously reported that nanoemulsion (NE) loaded paclitaxel (PTX) and BEZ235 could synergistically inhibit colon cancer cell growth. Read More

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Alterations in the global proteome and phosphoproteome in third-generation EGFR TKI resistance reveal drug targets to circumvent resistance.

Cancer Res 2021 Mar 16. Epub 2021 Mar 16.

Thoracic and Gastrointestinal Oncology Branch, Center for Cancer Research, National Cancer Institute

Lung cancer is the leading cause of cancer mortality worldwide. The treatment of lung cancer patients harboring mutant EGFR with orally administered EGFR tyrosine kinase inhibitors (TKIs) has been a paradigm shift. Osimertinib and rociletinib are third-generation irreversible EGFR TKIs targeting the EGFR T790M mutation. Read More

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NVP-BEZ235 or JAKi Treatment leads to decreased survival of examined GBM and BBC cells.

Cancer Treat Res Commun 2021 Feb 17;27:100340. Epub 2021 Feb 17.

Department of Biology, University of Texas- Rio Grande Valley, 1201 W. University Dr., Edinburg, TX 78539, United States. Electronic address:

Cancer cells almost universally harbor constitutively active Phosphatidylinositol-3 Kinase (PI3K) Pathway activity via mutation of key signaling components and/or epigenetic mechanisms. Scores of PI3K Pathway inhibitors are currently under investigation as putative chemotherapeutics. However, feedback and stem cell mechanisms induced by PI3K Pathway inhibition can lead to reduced treatment efficacy. Read More

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February 2021

Quinolines, a perpetual, multipurpose scaffold in medicinal chemistry.

Bioorg Chem 2021 Apr 8;109:104639. Epub 2021 Jan 8.

Institute of Pharmaceutical Research, GLA University, Mathura, UP 281406, India. Electronic address:

Quinoline is a versatile pharmacophore, a privileged scaffold and an outstanding fused heterocyclic compound with a wide range of pharmacological prospective such as anticancer, anti-inflammatory, antibacterial, antiviral drug and superlative moiety in drug discovery. The quinoline hybrids have already been shown excellent results with new targets with a different mode of actions as an inhibitor of cell proliferation by cell cycle arrest, apoptosis, angiogenesis, disruption of cell migration and modulation. This review emphasized the mode of action, structure activity relationship and molecular docking to reveal the various active pharmacophores of quinoline hybrids accountable for novel anticancer, anti-inflammatory, antibacterial and miscellaneous activities. Read More

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Harmine and Piperlongumine Revert TRIB2-Mediated Drug Resistance.

Cancers (Basel) 2020 Dec 9;12(12). Epub 2020 Dec 9.

Instituto de Investigaciones Biomédicas "Alberto Sols" (CSIC-UAM), Arturo Duperier 4, 28029 Madrid, Spain.

Therapy resistance is responsible for most relapses in patients with cancer and is the major challenge to improving the clinical outcome. The pseudokinase Tribbles homologue 2 (TRIB2) has been characterized as an important driver of resistance to several anti-cancer drugs, including the dual ATP-competitive PI3K and mTOR inhibitor dactolisib (BEZ235). TRIB2 promotes AKT activity, leading to the inactivation of FOXO transcription factors, which are known to mediate the cell response to antitumor drugs. Read More

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December 2020

Synergistic antitumor effect of dual PI3K and mTOR inhibitor NVP-BEZ235 in combination with cisplatin on drug-resistant non-small cell lung cancer cell.

Oncol Lett 2020 Dec 5;20(6):326. Epub 2020 Oct 5.

Department of Pharmacy, Shanghai Ninth People's Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 200011, P.R. China.

Cisplatin resistance is an obstacle for the effective treatment of non-small cell lung cancer (NSCLC). The combined use of two or more chemotherapeutic agents displays advantages for the clinical treatment of drug-resistant lung cancer. The present study aimed to assess the synergy of the dual PI3K/Akt/mTOR signaling pathway inhibitor NVP-BEZ235 and cisplatin, a chemotherapeutic agent, on proliferation, apoptosis, cell cycle arrest and protein expression in cisplatin-resistant NSCLC A549/diamminedichloroplatinum resistance (DDP) cells. Read More

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December 2020

Horizontal Combination of MEK and PI3K/mTOR Inhibition in BRAF Mutant Tumor Cells with or without Concomitant PI3K Pathway Mutations.

Int J Mol Sci 2020 Oct 16;21(20). Epub 2020 Oct 16.

2nd Department of Pathology, Semmelweis University, H-1091 Budapest, Hungary.

The RAS/RAF and PI3K/Akt pathways play a key regulatory role in cancer and are often hit by oncogenic mutations. Despite molecular targeting, the long-term success of monotherapy is often hampered by de novo or acquired resistance. In the case of concurrent mutations in both pathways, horizontal combination could be a reasonable approach. Read More

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October 2020

HPV-induced Nurr1 promotes cancer aggressiveness, self-renewal, and radioresistance via ERK and AKT signaling in cervical cancer.

Cancer Lett 2021 Jan 30;497:14-27. Epub 2020 Sep 30.

Department of Obstetrics and Gynaecology, LKS Faculty of Medicine, The University of Hong Kong, Pokfulam, Hong Kong Special Administrative Region of China. Electronic address:

Human papillomavirus (HPV) is the etiological agent of cervical cancer; however, the mechanisms underlying HPV-mediated carcinogenesis remain poorly understood. Here, we showed that nuclear receptor related-1 protein (Nurr1) was upregulated in primary cervical cancer tissue-derived spheroid cells and HPV-positive cell lines, and Nurr1 upregulation was correlated with cancer grade. Nurr1 promoted cell proliferation, migration, invasion, and anchorage-independent cell growth. Read More

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January 2021

Anti-GPC3 Antibody-Conjugated BEZ235 Loaded Polymeric Nanoparticles (Ab-BEZ235-NP) Enhances Radiosensitivity in Hepatocellular Carcinoma Cells by Inhibition of DNA Double-Strand Break Repair.

J Biomed Nanotechnol 2020 Apr;16(4):446-455

Aim: To assess AB-BEZ235-NP potential as a radio-sensitizer in hepatocellular carcinoma models.

Method: By comparing hepatocellular carcinoma cell with simple radiation or combined AB-BEZ235-NP therapy, the HCC apoptosis and self-repair level have significant differences in mortality rates and cell migration abilities.

Results: Cell proliferation and DNA damage increased by pretreatment with AB-BEZ235-NP after irradiation; further studies on the repair pathway indicated that AB-BEZ235-NP inhibited the important pathway of DSB repair. Read More

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Co-targeting PIM and PI3K/mTOR using multikinase inhibitor AUM302 and a combination of AZD-1208 and BEZ235 in prostate cancer.

Sci Rep 2020 09 1;10(1):14380. Epub 2020 Sep 1.

Molecular Diagnostics and Therapeutics Group, University College London, London, UK.

PIM and PI3K/mTOR pathways are often dysregulated in prostate cancer, and may lead to decreased survival, increased metastasis and invasion. The pathways are heavily interconnected and act on a variety of common effectors that can lead to the development of resistance to drug inhibitors. Most current treatments exhibit issues with toxicity and resistance. Read More

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September 2020

GOLPH3 inhibition reverses oxaliplatin resistance of colon cancer cells via suppression of PI3K/AKT/mTOR pathway.

Life Sci 2020 Nov 18;260:118294. Epub 2020 Aug 18.

Department of General Surgery, Beijing Hospital, National Center of Gerontology, Institute of Geriatric Medicine, Chinese Academy of Medical Sciences, Beijing 100730, PR China. Electronic address:

Objective: To explore whether GOLPH3 regulated oxaliplatin (L-OHP) resistance of colon cancer cells via PI3K/AKT/mTOR pathway.

Methods: HCT116/L-OHP cells were divided into Blank, Control/GOLPH3 shRNA, BEZ235 (a PI3K/AKT/mTOR inhibitor), and GOLPH3 + BEZ235 groups followed by the detection with MTT, soft agar colony formation, flow cytometry and TUNEL assays. Mice bearing HCT116/L-OHP xenografts were randomized into Control, L-OHP, NC/GOLPH3 shRNA, L-OHP + NC/GOLPH3 shRNA groups. Read More

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November 2020

Synergistic Antitumor Effects of Combined Treatment with HSP90 Inhibitor and PI3K/mTOR Dual Inhibitor in Cisplatin-Resistant Human Bladder Cancer Cells.

Yonsei Med J 2020 Jul;61(7):587-596

Department of Medicine, Graduate School of Yonsei University College of Medicine, Seoul, Korea.

Purpose: The current study aimed to investigate the synergistic antitumor effect of combined treatment with 17-DMAG (HSP90 inhibitor) and NVP-BEZ235 (PI3K/mTOR dual inhibitor) on cisplatin-resistant human bladder cancer cells.

Materials And Methods: Human bladder cancer cells exhibiting cisplatin resistance (T24R2) were exposed to escalating doses of 17-DMAG (2.5-20 nM) with or without NVP-BEZ236 (0. Read More

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Cotargeting BET proteins overcomes resistance arising from PI3K/mTOR blockade-induced protumorigenic senescence in colorectal cancer.

Int J Cancer 2020 11 29;147(10):2824-2837. Epub 2020 Jun 29.

Laboratory for Systems Biology and Bio-Inspired Engineering, Department of Bio and Brain Engineering, Korea Advanced Institute of Science and Technology (KAIST), Daejeon, South Korea.

Therapeutics targeting the phosphatidylinositol 3-kinase/mammalian target of rapamycin (PI3K/mTOR) pathway initially produce potent antitumor effects, but resistance frequently occurs. Using a phosphoproteome analysis, we found that colorectal cancer (CRC) cells exhibit resistance against PI3K/mTOR inhibition through feedback activation of multiple receptor tyrosine kinases, and their downstream focal adhesion kinase, Src and extracellular signal-regulated kinases signaling. Unexpectedly, PI3K/mTOR blockade causes senescence, mediated by the activation of the stress kinase p38. Read More

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November 2020

Electroacupuncture Inhibits Neuronal Autophagy and Apoptosis the PI3K/AKT Pathway Following Ischemic Stroke.

Front Cell Neurosci 2020 15;14:134. Epub 2020 May 15.

Department of Rehabilitation Medicine, The Third Hospital of Hebei Medical University, Shijiazhuang, China.

Electroacupuncture (EA) is a safe and effective therapy for ischemic stroke in both clinical and laboratory settings. However, the underlying mechanism behind EA treatment for stroke remains unclear. Here, we aimed to evaluate whether EA treatment at the acupoints of Zusanli (ST36) and Quchi (LI11) exerted a neuroprotective effect on ischemic stroke rats by modulating autophagy and apoptosis the PI3K/AKT/mTOR signaling pathway. Read More

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The Synergistic Anti-Cancer Effects of NVP-BEZ235 and Regorafenib in Hepatocellular Carcinoma.

Molecules 2020 May 25;25(10). Epub 2020 May 25.

Department of Research, Taichung Tzu Chi Hospital, Buddhist Tzu Chi Medical Foundation, Taichung 427213, Taiwan.

Hepatocellular carcinoma (HCC) is the most common type of liver cancer worldwide. Regorafenib is a multi-kinase inhibitor and the second-line treatment for HCC. Since the PI3K/Akt/mTOR signaling pathway is dysregulated in HCC, we evaluated the therapeutic effects of regorafenib combined with a dual PI3K/mTOR inhibitor BEZ235 in the human HCC cell lines ( = 3). Read More

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Enhanced Sensitivity to NVP-BEZ235 by Inhibition of p62/SQSTM1 in Human Bladder Cancer KoTCC-1 Cells Both and .

In Vivo 2020 May-Jun;34(3):1001-1008

Department of Urology, Hamamatsu University School of Medicine, Hamamatsu, Japan

Background/aim: The prognosis of patients with invasive bladder cancer remains poor. The objective of this study was to evaluate the efficacy of NVP-BEZ235 (NVP), a dual PI3K/mTOR inhibitor, combined with the inactivation of p62/SQSTM1 (p62) in a human bladder cancer KoTCC-1 model.

Materials And Methods: An expression plasmid with short hairpin RNA targeted against p62 was transfected into KoTCC-1 cells (KoTCC-1/sh-p62). Read More

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February 2021

In Vitro and in Vivo Activity of mTOR Kinase and PI3K Inhibitors Against and .

Molecules 2020 Apr 23;25(8). Epub 2020 Apr 23.

Leishmania Research Laboratory, Institut Pasteur Korea, 696 Sampyeong-dong, Bundang-gu, Seongnam-si, Gyeonggi-do 463-400, Korea.

Kinetoplastid parasites, including and spp., are life threatening pathogens with a worldwide distribution. Next-generation therapeutics for treatment are needed as current treatments have limitations, such as toxicity and drug resistance. Read More

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Synergistic Effects of Combination Therapy with AKT and mTOR Inhibitors on Bladder Cancer Cells.

Int J Mol Sci 2020 Apr 18;21(8). Epub 2020 Apr 18.

Division of Hematology-Oncology, Department of Medicine, Samsung Medical Center, Sungkyunkwan University School of Medicine, Seoul 06351, Korea.

Despite comprehensive genomic analyses, no targeted therapies are approved for bladder cancer. Here, we investigate whether a single and combination therapy with targeted agents exert antitumor effects on bladder cancer cells through genomic alterations using a three-dimensional (3D) high-throughput screening (HTS) platform. Seven human bladder cancer cell lines were used to screen 24 targeted agents. Read More

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Folate decorated polymeric micelles for targeted delivery of the kinase inhibitor dactolisib to cancer cells.

Int J Pharm 2020 May 8;582:119305. Epub 2020 Apr 8.

Department of Pharmaceutics, Utrecht Institute for Pharmaceutical Sciences, Utrecht University, the Netherlands. Electronic address:

One of the main challenges in clinical translation of polymeric micelles is retention of the drug in the nanocarrier system upon its systemic administration. Core crosslinking and coupling of the drug to the micellar backbone are common strategies to overcome these issues. In the present study, polymeric micelles were prepared for tumor cell targeting of the kinase inhibitor dactolisib which inhibits both the mammalian Target of Rapamycin (mTOR) kinase and phosphatidylinositol-3-kinase (PI3K). Read More

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Pretargeted delivery of PI3K/mTOR small-molecule inhibitor-loaded nanoparticles for treatment of non-Hodgkin's lymphoma.

Sci Adv 2020 04 1;6(14):eaaz9798. Epub 2020 Apr 1.

Lineberger Comprehensive Cancer Center, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599, USA.

Overactivation of the PI3K/mTOR signaling has been identified in non-Hodgkin's lymphoma. BEZ235 is an effective dual PI3K/mTOR inhibitor, but it was withdrawn from early-phase clinical trials owing to poor solubility and on-target/off-tumor toxicity. Here, we developed a nanoparticle (NP)-based pretargeted system for the therapeutic delivery of BEZ235 to CD20- and HLA-DR-expressing lymphoma cells for targeted therapy. Read More

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Differential Targeting of Gr-MDSCs, T Cells and Prostate Cancer Cells by Dactolisib and Dasatinib.

Int J Mol Sci 2020 Mar 27;21(7). Epub 2020 Mar 27.

Integrated Biomedical Sciences Graduate Program, University of Notre Dame, Notre Dame, IN 46556, USA.

Granulocytic myeloid-derived suppressor cells (Gr-MDSCs) promote immune evasion and resistance to immunotherapeutics in a variety of malignancies. Our previous study showed that dual PI3K/mTOR inhibitor Dactolisib impaired the viability and immunosuppressive function of Gr-MDSCs, and significantly synergized with immune checkpoint blockade (ICB) antibodies targeting PD1 and CTLA4 to eradicate metastatic castration-resistant prostate cancer (CRPC) in a preclinical transgenic mouse model. On the contrary, tyrosine kinase inhibitor Dasatinib diminished tumor-infiltrating T lymphocytes and showed no synergic activity with ICB. Read More

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Evolution of PIKK family kinase inhibitors: A new age cancer therapeutics.

Front Biosci (Landmark Ed) 2020 03 1;25:1510-1537. Epub 2020 Mar 1.

Discipline of Chemistry, Indian Institute of Technology Gandhinagar, Gujarat, India, 382355, Indian Institute of Technology Gandhinagar, Gujarat, India 382355,

Phosphatidylinositol-3 kinase-related kinases (PIKKs) belong to a family of atypical serine/threonine kinases in humans. They actively participate in a diverse set of cellular functions such as meiotic, V(D)J recombination, chromosome maintenance, DNA damage sensing and repair, cell cycle progression and arrest. ATR, ATM, DNA-PKcs, mTOR and hSMG are the members of the PIKK family that play an important role in in cancer cell proliferation, autophagy, and cell survival to radio and chemotherapy. Read More

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Dual PI3K/mTOR Inhibitor NVP-BEZ235 Enhances Radiosensitivity of Head and Neck Squamous Cell Carcinoma (HNSCC) Cell Lines Due to Suppressed Double-Strand Break (DSB) Repair by Non-Homologous End Joining.

Cancers (Basel) 2020 Feb 18;12(2). Epub 2020 Feb 18.

Department of Radiotherapy and Radiooncology, Philipps-University, University Hospital Giessen and Marburg, 35043 Marburg, Germany.

The PI3K/Akt/mTOR pathway is frequently altered in human papillomavirus (HPV)-positive and negative squamous cell carcinoma of the head and neck (HNSCC) and overstimulation is associated with poor prognosis. PI3K drives Akt activation and constitutive signaling acts pro-proliferative, supports cell survival, DNA repair, and contributes to radioresistance. Since the small molecule NVP-BEZ235 (BEZ235) is a potent dual inhibitor of this pathway, we were interested whether BEZ235 could be an efficient radiosensitizer. Read More

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February 2020

A dual PI3 kinase/mTOR inhibitor BEZ235 reverses doxorubicin resistance in ABCB1 overexpressing ovarian and pancreatic cancer cell lines.

Biochim Biophys Acta Gen Subj 2020 06 14;1864(6):129556. Epub 2020 Feb 14.

VCU Pauley Heart Center, Division of Cardiology, Virginia Commonwealth University, Richmond, VA 23298, United States. Electronic address:

Background: Multi-drug resistance (MDR) develops because cancer cells evade toxicity of several structurally unrelated drugs. Besides other mechanisms, MDR is linked to the overexpression of ATP Binding Cassette (ABC), transporters, among which ABCB1 is the best characterized one. Since overactivation of PI3K/Akt/mTOR plays a pivotal role in the growth of human cancers, we hypothesized whether dual PI3K and mTOR inhibitor, BEZ235 (BEZ, dactolisib) reverses resistance to doxorubicin (DOX). Read More

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Resistance of hepatocellular carcinoma to sorafenib can be overcome with co-delivery of PI3K/mTOR inhibitor BEZ235 and sorafenib in nanoparticles.

Expert Opin Drug Deliv 2020 04 23;17(4):573-587. Epub 2020 Feb 23.

Department of Hepatobiliary Surgery, The First Affiliated Hospital of Bengbu Medical College, Bengbu, China.

: The combination of BEZ235 with sorafenib (SFB) enhances anti-hepatocellular carcinoma (HCC) efficacy of the two agents. However, pharmacokinetic profiles in vivo and different endocytosis abilities of these two drugs hinder their therapeutic application.: In this work, we developed d-α-tocopheryl polyethylene glycol 1000 succinate - polycaprolactone polymer nanoparticles (NPs) for co-delivery of SFB and BEZ235 (SFB/BEZ235-NPs). Read More

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The PI3K pathway impacts stem gene expression in a set of glioblastoma cell lines.

J Cancer Res Clin Oncol 2020 Mar 6;146(3):593-604. Epub 2020 Feb 6.

Department of Biology, University of Texas-Rio Grande Valley, 1201 W. University Dr., Room: ESCNE 4.633, Edinburg, TX, 78539, USA.

Background: The PI3K pathway controls diverse cellular processes including growth, survival, metabolism, and apoptosis. Nuclear FOXO factors were observed in cancers that harbor constitutively active PI3K pathway output and stem signatures. FOXO1 and FOXO3 were previously published to induce stem genes such as OCT4 in embryonic stem cells. Read More

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The PI3K/mTOR dual inhibitor NVP-BEZ235 stimulates mutant p53 degradation to exert anti-tumor effects on triple-negative breast cancer cells.

FEBS Open Bio 2020 04 6;10(4):535-545. Epub 2020 Mar 6.

Department of Laboratory Medicine, Affiliated Hospital of North Sichuan Medical College, Nanchong, China.

Nearly half of human cancers harbor p53 mutations, and mutant p53 (mutp53) promotes carcinogenesis, metastasis, tumor recurrence and chemoresistance. mutp53 is observed in 30% of breast carcinomas, including triple-negative breast cancer (TNBC), and thus mutp53 is a promising target for treatment of TNBC. In this study, we investigated the effect of a phosphatidylinositide 3 kinase/mammalian target of rapamycin dual inhibitor, NVP-BEZ235 (BEZ235), on two TNBC cell lines with mutp53: MDA-MB-231 and MDA-MB-468. Read More

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NVP-BEZ235 inhibits thyroid cancer growth by p53- dependent/independent p21 upregulation.

Int J Biol Sci 2020 14;16(4):682-693. Epub 2020 Jan 14.

Department of Endocrinology, The First Affiliated Hospital of Xi'an Jiaotong University, Xi'an 710061, P.R. China.

NVP-BEZ235 is a novel dual PI3K/mTOR inhibitor, currently in phase 1/2 clinical trials, exhibiting clinical efficiency in treatment of numerous malignancies including thyroid cancer. Cancer cells harboring mutant p53 was widely reported to be blunt to pharmaceutical therapies. However, whether this genotype dependent effect also presents in thyroid cancer when treated with NVP-BEZ235 remains unknown. Read More

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February 2021

Blocking AMPK/ULK1-dependent autophagy promoted apoptosis and suppressed colon cancer growth.

Cancer Cell Int 2019 13;19:336. Epub 2019 Dec 13.

1College of Biology, Hunan University, Changsha, 410082 China.

Background: Autophagy is an evolutionarily conserved process through which cells degrade and recycle cytoplasm. The relation among autophagy, apoptosis and tumor is highly controversial until now and the molecular mechanism is poorly understood.

Methods: Cell viability and apoptosis were detected by CCK8, crystal violet staining, Hoechst333342 staining and flow cytometry. Read More

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December 2019