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Abt 263

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ABT-263 is a small molecule that inhibits the anti-apoptotic proteins Bcl-2 and Bcl-xL. It functions by disrupting the interaction between these proteins and pro-apoptotic Bcl-2 family members, thereby promoting apoptosis or programmed cell death.

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Lab products found in correlation

Abt 199, by Active Motif (3 mentions) P egfr y1068, by Abcam (2 mentions) E cadherin, by BD (2 mentions) Vimentin, by BD (2 mentions) Pakt t308, by Cell Signaling Technology (2 mentions) Wz4002, by Selleck Chemicals (2 mentions) Neurod, by Cell Signaling Technology (2 mentions) Gefitinib, by Selleck Chemicals (2 mentions) Total egfr, by Santa Cruz Biotechnology (2 mentions) Synaptophysin, by Cell Signaling Technology (2 mentions) Perk t202 y204, by Cell Signaling Technology (2 mentions) Chromogranin a, by Abcam (2 mentions) Gdc 0941, by Chemietek (1 mentions) Nvp bez235, by Novartis (1 mentions) On targetplus smartpool, by Thermo Fisher Scientific (1 mentions) Alexa fluor 546 phalloidin, by Thermo Fisher Scientific (1 mentions) Anti integrin β1 antibody, by Merck Group (1 mentions) 4 6 diamidino 2 phenylindole (dapi), by Thermo Fisher Scientific (1 mentions) α sma 1a4, by Merck Group (1 mentions) S63845, by Apexbio (1 mentions)

9 protocols using abt 263

1

Radiation-Induced Injury: ABT-263 Treatment

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Mice were exposed to a single dose of 17 Gy of radiation on the right side of the thorax, and 16 weeks after IR, they were treated with vehicle (ethanol/polyethylene glycol 400/Phosal 50 PG (Fisher, MA, USA) at 10:30:60) or ABT-263 (Active Biochem, Maplewood, NJ) (50 mg/kg per day for 5 days per cycle for 2 cycles, with a 2-week interval between cycles) by gavage, as we reported recently (19 (link)) and as described in Appendix E1 (available online at www.redjournal.org).
Pan J., Li D., Xu Y., Zhang J., Wang Y., Chen M., Lin S., Huang L., Chung E.J., Citrin D.E., Wang Y., Hauer-Jensen M., Zhou D, & Meng A. (2017). Inhibition of Bcl-2/xl With ABT-263 Selectively Kills Senescent Type II Pneumocytes and Reverses Persistent Pulmonary Fibrosis Induced by Ionizing Radiation in Mice. International journal of radiation oncology, biology, physics, 99(2), 353-361.
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2

Characterization of KRAS/EGFR Mutant NSCLC Cell Lines

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Human KRAS mutant and EGFR mutant NSLCLC cell lines were obtained from the Center for Molecular Therapeutics at the MGH Cancer Center which performs routine SNP and STR authentication (21 (link)); cell lines were passaged for less than 6 months following receipt. A427-R and DV-90-R resistant cell lines were generated by exposing parental cell lines to 1 μM AZD6244/GDC-0941 for three days followed by drug washout for 3 days. Cells were treated for 5-10 cycles, followed by maintenance in the continuous presence of drug. The N1, N2 (treatment naïve) and R1, R2, R3 (AZD6244/BEZ235 resistant) lines are tumor-derived cell lines from Kras p53L/L mice. For cell culture studies, AZD6244 (Otava), GDC-0941 (Chemietek), ABT-263 (Active Biochem), ABT-199 (Active Biochem), NVP-BEZ235 (kindly provided by Novartis) were dissolved in DMSO to a final concentration of 10 mmol/l and stored at −20°C. Antibodies utilized for western blotting are listed in Supplementary Materials and Methods.
Hata A.N., Yeo A., Faber A.C., Lifshits E., Chen Z., Cheng K.A., Walton Z., Sarosiek K.A., Letai A., Heist R.S., Mino-Kenudson M., Wong K.K, & Engelman J.A. (2014). Failure to induce apoptosis via BCL-2 family proteins underlies lack of efficacy of combined MEK and PI3K inhibitors for KRAS mutant lung cancers. Cancer research, 74(11), 3146-3156.
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3

Investigating Cell Apoptosis Pathways

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Antibodies used were as follows: α-SMA (1A4, Sigma-Aldrich); cleaved caspase-3 (5A1E, Cell Signaling); MCL-1, BCL-XL, BAK, BAK, BIM, BID, tubulin, and GAPDH (glyceraldehyde-3-phosphate dehydrogenase) (Cell Signaling); and BCL-2 (Bcl-2-100, Life Technologies). Secondary antibodies were obtained from Invitrogen [Alexa Fluor 488 goat anti-mouse immunoglobulin G2a (IgG2a) and Alexa Fluor 555 goat anti-rabbit IgG1]. F-actin and nuclei were stained with Alexa Fluor 546–phalloidin and 4′,6-diamidino-2-phenylindole (DAPI) (Invitrogen), respectively.
Reagents used included PF-562,271 (Selleckchem), S63845 (ApexBio), ABT-263 (Active Biochem), ABT-199 (Active Biochem), and Y-27632, RGD peptide, CCG-1423, and anti–integrin β1 antibody (Sigma). siRNA duplexes targeting human BCL-2, human BCL-XL, human MCL-1, human BIM, human YAP, and human TAZ were obtained from Dharmacon Inc. using ON-TARGETplus SMARTpool (Thermo Scientific).
Nonreplicative recombinant adenovirus expressing human α-SMA fused to red fluorescent protein (Ad-α-SMA-RFP) or shRNA against α-SMA and GFP (Ad-GFP-U6-α-SMA-shRNA) were generated, amplified, and purified by Vector Biolabs. Table S1 lists the primer and siRNA sequences used in this study.
Lagares D., Santos A., Grasberger P.E., Liu F., Probst C.K., Rahimi R.A., Sakai N., Kuehl T., Ryan J., Bhola P., Montero J., Kapoor M., Baron M., Varelas X., Tschumperlin D.J., Letai A, & Tager A.M. (2017). Targeted apoptosis of myofibroblasts with the BH3 mimetic ABT-263 reverses established fibrosis. Science translational medicine, 9(420), eaal3765.
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4

Apoe-/- Mice Western Diet Treatment

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ApoE−/− mice were weaned at 3 weeks, and fed a high fat (Western diet) at 8 weeks. Mice were administered vehicle (ethanol/polyethylene glycol 400 (Sigma, MO, USA)/Phosal 50PG (Lipoid GmbH, Ludwigshafen, Germany) at 10:30:60, or ABT-263 (Active Biochem, Kowloon, HK) at 50 mg/kg/day for 5 days for 3 cycles by gavage,16 (link),17 (link) each cycle separated by 3 weeks.
Garrido A.M., Kaistha A., Uryga A.K., Oc S., Foote K., Shah A., Finigan A., Figg N., Dobnikar L., Jørgensen H, & Bennett M. (2021). Efficacy and limitations of senolysis in atherosclerosis. Cardiovascular Research, 118(7), 1713-1727.
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5

Optimized Nanoparticle Drug Delivery

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In vitro experimental calculations indicated that approximately ~30 mg of drug, both Doxorubicin and navitoclax, are deliverable per g of GalNPs (see Appendix Table S3). GalNPs were weighted in 8 ml Wheaton glass vials (Sigma, Z256161) at 4 mg/ml in DMEM supplemented with 10% FBS and stirred with a magnetic stir bar for 1 h. Mice were i.v. injected as indicated, with 200 μl of a nanoparticle solution containing 4 mg/ml (equivalent to 1 mg/kg of deliverable drug). Doxorubicin (Sigma, #D1515) was dissolved in 7% saline/DMEM solution at 1 mg/kg and administered by daily i.v. (tail vein) injection as indicated. Navitoclax, also known as ABT263 (Active Biochem, #A‐100), was administered by daily oral gavage, for 13 days, at 25 mg/kg, dissolved in 15% DMSO/PEG400. Palbociclib (Pfizer Inc.) was dissolved in 50 mM sodium lactate at 12.5 mg/ml and administered by daily oral gavage at the indicated doses. Palbociclib treatment started 1 day before GalNPs or free drugs administration.
Muñoz‐Espín D., Rovira M., Galiana I., Giménez C., Lozano‐Torres B., Paez‐Ribes M., Llanos S., Chaib S., Muñoz‐Martín M., Ucero A.C., Garaulet G., Mulero F., Dann S.G., VanArsdale T., Shields D.J., Bernardos A., Murguía J.R., Martínez‐Máñez R, & Serrano M. (2018). A versatile drug delivery system targeting senescent cells. EMBO Molecular Medicine, 10(9), e9355.
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6

Pharmacological Inhibitor Acquisition Protocol

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We obtained rapamycin, MLN0128, GDC-0941, and NVP-BEZ235 from LC Laboratories (Woburn, MA, USA); ABT-263, ABT-199, MK2206 and GDC-0980 from Active Biochem (Wan Chai, Hong Kong), and AKT inhibitor VIII from Chemdea (Ridgewood, NJ, USA). InSolution Q-VD-OPh was obtained from EMD Millipore (Billerica, MA, USA), vincristine was obtained from Sigma-Aldrich (St. Louis, MO), dimethyl sulfoxide (DMSO) from Fisher Scientific (Waltham, MA, USA) and doxycycline from Sigma-Aldrich (St. Louis, MO).
Lee J.S., Tang S.S., Ortiz V., Vo T.T, & Fruman D.A. (2015). MCL-1-independent mechanisms of synergy between dual PI3K/mTOR and BCL-2 inhibition in diffuse large B cell lymphoma. Oncotarget, 6(34), 35202-35217.
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7

Characterization of Lung Cancer Cell Lines

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PC9, HCC827, MGH119, MGH119-R, MGH121, MGH134, MGH141, MGH157, NCI-H446, NCI-H196 and NCI-H82 cells were cultured in RPMI 1640 supplemented with 10% fetal bovine serum. MGH125, MGH126, MGH131-1 and MGH131-2 cells were cultured in ACL4 supplemented with 10% fetal bovine serum. NCI-H446, NCI-H196 and NCI-H82 cells were obtained from the Center for Molecular Therapeutics at MGH. PC9 and HCC827 cells were a gift from Pasi Jänne. Gefitinib and WZ4002 were purchased from Selleck, Abt-263 was purchased from Active Biochem. All compounds were reconstituted in dimethylsulphoxide for cell culture experiments. Antibodies for RB, actin, NCAM, synaptophysin, NeuroD, pAkt T308, pERK T202/Y204 and total Akt were purchased from Cell Signaling Technology. pEGFR Y1068 and chromogranin A were purchased from Abcam, E-cadherin and Vimentin from BD and total EGFR from Santa Cruz Biotechnology. All antibodies were used at a dilution of 1:1,000. Uncropped scans of the western blots from the main figures can be found in Supplementary Fig. 9.
Niederst M.J., Sequist L.V., Poirier J.T., Mermel C.H., Lockerman E.L., Garcia A.R., Katayama R., Costa C., Ross K.N., Moran T., Howe E., Fulton L.E., Mulvey H.E., Bernardo L.A., Mohamoud F., Miyoshi N., VanderLaan P.A., Costa D.B., Jänne P.A., Borger D.R., Ramaswamy S., Shioda T., Iafrate A.J., Getz G., Rudin C.M., Mino-Kenudson M, & Engelman J.A. (2015). RB loss in resistant EGFR mutant lung adenocarcinomas that transform to small-cell lung cancer. Nature Communications, 6, 6377.
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8

Lung Cancer Cell Lines Characterization

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The lung cancer cell lines A549, NCI-H358, NCI-H1792, NCI-H23, SW900 and SW1573 were purchased from the American Type Culture Collection. SK-LU-1, Calu-1, Calu-6 and NCI-H460 were provided by Takashi Takahashi (Nagoya University, Japan). RERF-LC-AD2, LU-65 and LU-99 cells were obtained from the Japanese Cell Research Bank (Osaka, Japan). HCC2108 cells were obtained from Korean Cell Line Bank (Seoul, South Korea). The NCI-H1573 and NCI-H2030 cells were provided from Massachusetts General Hospital Cancer Center. Cells were cultured in RPMI1640 (Invitrogen) with 10% FBS. Characteristic of cell lines used in this study were summarized in Supplementary Table S4. Cells were obtained between 2012 and 2016. Experiments using A549, SW900, LU-65 and HCC2108 cells were done within 6 months from the acquisition of these cells from cell banks. All other cell lines were tested and authenticated by short tandem repeat (STR) analysis with GenePrint 10 System (Promega) by the Japanese Cell Research Bank at the time of submission. Cells were regularly screened for Mycoplasma using a MycoAlert Mycoplasma Detection Kit (Lonza). NVP-BGJ398, GDC-0941, ABT-263, selumetinib, afatinib, and trametinib were obtained from Active Biochem. Compounds were dissolved in DMSO to a final concentration of 10 mmol/l and stored at −20°C when not in use.
Kitai H., Ebi H., Tomida S., Floros K.V., Kotani H., Adachi Y., Oizumi S., Nishimura M., Faber A.C, & Yano S. (2016). Epithelial-to-mesenchymal transition defines feedback activation of receptor tyrosine kinase signaling induced by MEK inhibition in KRAS mutant lung cancer. Cancer discovery, 6(7), 754-769.
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9

Cell Culture and Compound Treatments

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PC9, HCC827, MGH119, MGH119-R, MGH121, MGH134, MGH141, MGH157, NCI-H446, NCI-H196 and NCI-H82 cells were cultured in RPMI 1640 supplemented with 10% fetal bovine serum (FBS). MGH125, MGH126, MGH131-1, MGH131-2 cells were cultured in ACL4 supplemented with 10% FBS. NCI-H446, NCI-H196, and NCI-H82 cells were obtained from the Center for Molecular Therapeutics at MGH. PC9 and HCC827 cells were a gift from Pasi Jänne. Gefitinib and WZ4002 were purchased from Selleck, Abt-263 was purchased from Active Biochem. All compounds were reconstituted in DMSO for cell culture experiments. Antibodies for RB, actin, NCAM, synaptophysin, NeuroD, pAkt T308, pERK T202/Y204, and total Akt were purchased from Cell Signaling Technology. pEGFR Y1068 and chromogranin A were purchased from Abcam, E-cadherin and Vimentin from BD and total EGFR from Santa Cruz Biotechnology. All antibodies were used at a dilution of 1:1000). Uncropped scans of the Western blots from the main figures are can be found in Supplementary Fig. 9.
Niederst M.J., Sequist L.V., Poirier J.T., Mermel C.H., Lockerman E.L., Garcia A.R., Katayama R., Costa C., Ross K.N., Moran T., Howe E., Fulton L.E., Mulvey H.E., Bernardo L.A., Mohamoud F., Miyoshi N., VanderLaan P.A., Costa D.B., Jänne P.A., Borger D.R., Ramaswamy S., Shioda T., Iafrate A.J., Getz G., Rudin C.M., Mino-Kenudson M, & Engelman J.A. (2015). RB loss in resistant EGFR mutant lung adenocarcinomas that transform to small-cell lung cancer. Nature Communications, 6, 6377.
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