Bez235

Manufactured by Selleck Chemicals

Sourced in United States

BEZ235 is a laboratory equipment product designed for research purposes. It functions as a precise tool for various experimental and analytical tasks in a laboratory setting.

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Lab products found in correlation

Close spelling variants of this product

NVP-BEZ235 (51 citations) NVP-BEZ235 (S1009), (2 citations) BEZ235 (S1009), (2 citations)

98 protocols using bez235

Enhancing Chemotherapy Sensitivity in Ovarian Cancer

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Human ovarian cancer SKOV3, SW626, HO8910, A2780 and 3AO cell lines and CDDP-resistant SKOV3/CDDP cell lines were taken from the cell bank of the People's Hospital of Zhengzhou University and Henan Provincial People's Hospital and cultured by RPMI-1640 medium containing 10% fetal bovine serum (FBS). Cells were cultured in an incubator (Sanyo, Japan) at 37°C, 5% CO₂ and 90% relative humidity. Then, the cells were digested with 0.4% trypsin for passage. CDDP (1 μg/mL) was added in the medium of SKOV3/CDDP cell lines to maintain the chemoresistance of cells. SKOV3/CDDP cells were divided into the following four groups: (1) CDDP group (only treated with CDDP); (2) CDDP + tunicamycin group (treated with 1 mg/L tunicamycin, then with CDDP); (3) CDDP + BEZ235 (Selleck Chemicals, the United States) group (treated with CDDP, then with 5 μmol/L BEZ235); (4) CDDP + BEZ235 + tunicamycin group (treated with 1 mg/L tunicamycin, then with CDDP and 5 μmol/L BEZ235). Each index was measured at the 24th hour after drugs were added in each group. SKOV3 cells were used as the blank control group.

Hu J.L., Hu X.L., Guo A.Y., Wang C.J., Wen Y.Y, & Cang S.D. (2017). Endoplasmic reticulum stress promotes autophagy and apoptosis and reverses chemoresistance in human ovarian cancer cells. Oncotarget, 8(30), 49380-49394.

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Viability of BRAF-inhibitor combination

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Cells were cultured overnight under serum-free conditions in RPMI or 50% rat CSF and then treated with DMSO, dabrafenib (1 µM), BEZ235 (5 µM) or dabrafenib (1 µM) plus BEZ235 (5 µM) (Selleckchem) for 24 hours, at which point viability was measured by CellTiter-Glo assays (Promega). Relative survival was normalised to DMSO controls in either media or in the presence of CSF. Data from one representative experiment is shown.

Lee R.J., Khandelwal G., Baenke F., Cannistraci A., Macleod K., Mundra P., Ashton G., Mandal A., Viros A., Gremel G., Galvani E., Smith M., Carragher N., Dhomen N., Miller C., Lorigan P, & Marais R. (2020). Brain microenvironment-driven resistance to immune and targeted therapies in acral melanoma. ESMO Open, 5(4), e000707.

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Inhibition of Receptor Tyrosine Kinases

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The pan-FGFR inhibitor JNJ42756493 (erdafitinib) was supplied by Janssen Pharmaceuticals (Beerse, Belgium), the MDM2-TP53 interaction inhibitor RG7388 (idasanutlin) was supplied by Roche (Roche Pharma Research and Early Development, Basel, Switzerland), and the dual PI3K/mTOR inhibitor BEZ235 (dactolisib) was purchased from Selleckchem (Houston, TX, USA).

Dadone-Montaudié B., Laroche-Clary A., Mongis A., Chamorey E., Di Mauro I., Chaire V., Finetti P., Schiappa R., Le Loarer F., Birtwisle-Peyrottes I., Michiels J.F., Bertucci F., Pedeutour F., Italiano A, & Bianchini L. (2020). Novel Therapeutic Insights in Dedifferentiated Liposarcoma: A Role for FGFR and MDM2 Dual Targeting. Cancers, 12(10), 3058.

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High-Throughput Screening of Anticancer Agents

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Nocodozole, BEZ235, BKM120, AZD6244 and AKTViii were purchased from Selleck Chemicals LCC. Small interfering RNAs (siRNAs) were from Shanghai Gene Pharma. Dulbecco’s Modified Eagle’s Media (DMEM), Click-iT Alexa Fluor 488 EdU (5-ethynyl-2’-deoxyuridine) imaging kit and Lipofectamine RNAiMAX was purchased from Life Technologies. Foetal Bovine Serum (FBS) was purchased from SAFC Biosciences™, Lenexa, USA. CellTiter 96^® AQueous One Solution Cell Proliferation Assay and Dual-Glo® Luciferase Assay were purchased from Promega Corporation.

Sinha D., Nag P., Nanayakkara D., Duijf P.H., Burgess A., Raninga P., Smits V.A., Bain A.L., Subramanian G., Wall M., Finnie J.W., Kalimutho M, & Khanna K.K. (2020). Cep55 overexpression promotes genomic instability and tumorigenesis in mice. Communications Biology, 3, 593.

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Western Blot Antibody Dilutions and Reagents

Cited 2 times

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All antibodies used for western blot analysis were 1:1000 dilution except for CK2α (1:500) and GAP (1:2000) and are as follows: From Cell Signaling Technology (CST); BRD4 (13,440), AXL (8661S), E-cadherin (3195), N-cadherin (13,116), β-catenin (8480), Vimentin (5741), EGFR (2232S), Ras (8955S), EGFR (L858R mutant specific) (3197), MYC (5605), and FOSL1 (5281). From abcam; CK2α (ab137788), and from Santa Cruz; GAP (sc-47724). Lastly the pBRD4 antibody was a gift from C. M. Chiang with specificities as previously described^{44 (link)} and used to detect pBRD4 as described in^{19 (link)}. (+)-JQ1 (active enantiomer) (cat. # 4499) was purchased from TOCRIS. I-BET762 (cat. # 10676) was purchased from Caymen Chemical. Crizotinib (cat. # S1068) and CX-4945 (also known as Silmitasertib) (cat# S2248) were purchased from Selleck Chemical, and BEZ235 (cat. #CT-BEZ) was purchased from ChemieTEK. All drugs were suspended in DMSO. Recombinant human TGF-beta 1 (TGFβ1) protein was purchased from R & D Systems (cat. # 240-B-002) and resuspended in 4 mM HCl containing 1 mg/mL BSA to a final concentration of 10 μg/mL. This was then added to regular cultured media at 1:1000 to give a final concentration of 10 ng/mL.

Calder J., Nagelberg A., Luu J., Lu D, & Lockwood W.W. (2021). Resistance to BET inhibitors in lung adenocarcinoma is mediated by casein kinase phosphorylation of BRD4. Oncogenesis, 10(3), 27.

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Inhibiting PI3K Signaling in CTCL

Cited 1 time

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PIKP110a inhibitors, PIK75, A66, GDC0941, and BEZ235 are from Selleck (Houston, TX). Isolation of PBMCs or CD4⁺ T cells from both patients and healthy donors and culture of CTCL cell lines (Hut78, HH, and H9) were performed as previously described (Bliss-Moreau et al., 2015 (link)). All patient tissue collection and research use adhered to protocols approved by the institutional review and privacy boards at City of Hope, in accordance with the Declaration of Helsinki. All participants signed written informed consent.

Zhang X.H., Nam S., Wu J., Chen C.H., Liu X., Li H., McKeithan T., Gong Q., Chan W.C., Yin H.H., Yuan Y.C., Pillai R., Querfeld C., Horne D., Chen Y, & Rosen S.T. (2018). Multi-Kinase Inhibitor with Anti-p38γ Activity in Cutaneous T-Cell Lymphoma. The Journal of investigative dermatology, 138(11), 2377-2387.

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NSCLC Cell Line Characterization and Drug Testing

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The H23, H1703, A549, HCC827, H157, H460, H2228, H3122 and H322 NSCLC cell lines were obtained from American Type Tissue Collection (Manassas, VA), and were grown in RPMI 1640 supplemented with 10% FBS and 1× Antibiotic/Antimycotic (Invitrogen, Carlsbad, CA). Among them, Cell lines H23, HCC827, H1703 and A549 were tested and authenticated by short tandem repeat profiling in August, 2014 and 2015 and the rest were not authenticated. PC9 cells were a gift from Dr. Susumu Kobayashi, Harvard Medical School, Boston, MA. Ba/F3 cells were obtained from G. Gilliland (Brigham and Women's Hospital, Boston, Massachusetts, USA). RICTOR-dependent Ba/F3 cells were developed by transfecting Ba/F3 cells with a doxycycline-inducible plasmid for the overexpression of wild-type RICTOR in the presence of doxycycline (RICTOR-pTetOne, modified from Tet-One Systems, Clontech Laboratories, Inc, CA, US and generated by GENEWIZ, Inc, NJ, US). BEZ235, AZD2014, RAD001 (everolimus), erlotinib, MK2206 and LY294002 were obtained from Selleck Chemicals (Houston, TX); Cisplatin was obtained from Sigma-Aldrich (St. Louis, MO).

Cheng H., Zou Y., Ross J.S., Wang K., Liu X., Halmos B., Ali S.M., Liu H., Verma A., Montagna C., Chachoua A., Goel S., Schwartz E.L., Zhu C., Shan J., Yu Y., Gritsman K., Yelensky R., Lipson D., Otto G., Hawryluk M., Stephens P.J., Miller V.A., Piperdi B, & Perez-Soler R. (2015). RICTOR amplification defines a novel subset of lung cancer patients who may benefit from treatment with mTOR1/2 inhibitors. Cancer discovery, 5(12), 1262-1270.

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Isolating and Authenticating GBM Neurospheres

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The GIC lines were established by isolating neurosphere-forming cells from fresh surgical specimens of human GBM tissue between the years of 2005 through 2008, as described previously (18 (link)). Cells were authenticated by testing short tandem repeats (STR) using the Applied Biosystems AmpFISTR Identifier kit (Foster City, CA). The last authentication testing was done in March 2014. This study was approved by the institutional review board of The University of Texas MD Anderson Cancer Center (Houston, Texas). These GBM neurospheres were cultured in DMEM/F12 medium containing B27 supplement (Invitrogen, Carlsbad, CA), basic fibroblast growth factor, and epidermal growth factor (20 ng/ml each). The PI3K/mTOR dual inhibitor BEZ235 was from Selleck (Houston, Texas), DS-7423 was provided by Daiichi Sankyo Co., Ltd. (Tokyo, Japan), and PD-0325901 was from Selleck (Houston, Texas). For in vitro use, all inhibitors were dissolved in dimethyl sulfoxide (Sigma-Aldrich, St. Louis, MO).

Wu S., Wang S., Zheng S., Verhaak R., Koul D, & Yung W.K. (2016). MSK1-mediated β-catenin phosphorylation confers resistance to PI3K/mTOR inhibitors in glioblastoma. Molecular cancer therapeutics, 15(7), 1656-1668.

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Inhibitor Treatment of Cultured Cells

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BEZ235 (dual PI3K/mTOR inhibitor), BKM120 (PI3K inhibitor), everolimus (mTOR inhibitor) and GSK1120212 (MEK inhibitor) were purchased from Selleck Chemicals (Houston, TX, USA) and were prepared as 2.1 mmol/L, 24 mmol/L, 10 mmol/L and 14 mmol/L stock solutions, respectively, in DMSO and stored at −80°C. Cultured cells were treated for 72 hours with a medium changes and fresh drug additions as indicated in the figure legends.

Fourneaux B., Chaire V., Lucchesi C., Karanian M., Pineau R., Laroche-Clary A, & Italiano A. (2016). Dual inhibition of the PI3K/AKT/mTOR pathway suppresses the growth of leiomyosarcomas but leads to ERK activation through mTORC2: biological and clinical implications. Oncotarget, 8(5), 7878-7890.

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Glutamine Metabolism Regulation Protocols

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L-Glutamine, L-glutamine-¹³C₅, D-glucose, dimethyl α-KG and AOA were purchased from Sigma. Inhibitors LY294002 (pan-PI3K inhibitor), BYL-719 (p110α-specific inhibitor), BEZ235 (PI3K/mTOR dual-specificity inhibitor), GSK2334470 (PDK1 inhibitor), GSK690693 (AKT inhibitor), CHIR-99021 (GSK3β inhibitor), rapamycin (mTOR inhibitor), BI-D1870 (pan-RSK inhibitor), FMK (RSK2 inhibitor) and MG132 (proteasome inhibitor) were purchased from Selleck Chemicals. siRNAs for ATF4 (SI03019345 and SI04236337) and PDK1 (SI00301140 and SI00301154) were purchased from Qiagen. siRNAs for RSK2 (J-003026-10 and J-003026-12) were purchased from Dharmacon. siRNAs for USP8 (SR306014A and SR306014B) were purchased from Origene. shRNAs for GPT2 (TRCN0000035025 and TRCN0000035026) were purchased from Sigma. Antibodies used in this study are listed in Supplementary Table 1.

Hao Y., Samuels Y., Li Q., Krokowski D., Guan B.J., Wang C., Jin Z., Dong B., Cao B., Feng X., Xiang M., Xu C., Fink S., Meropol N.J., Xu Y., Conlon R.A., Markowitz S., Kinzler K.W., Velculescu V.E., Brunengraber H., Willis J.E., LaFramboise T., Hatzoglou M., Zhang G.F., Vogelstein B, & Wang Z. (2016). Oncogenic PIK3CA mutations reprogram glutamine metabolism in colorectal cancer. Nature Communications, 7, 11971.

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