Lovastatin

Manufactured by Selleck Chemicals

Sourced in United States

Lovastatin is a chemical compound used as a laboratory reagent. It functions as an inhibitor of 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase, an enzyme involved in the biosynthesis of cholesterol.

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Lab products found in correlation

Simvastatin, by Selleck Chemicals (4 mentions) Penicillin streptomycin, by Thermo Fisher Scientific (4 mentions) Fluvastatin, by Selleck Chemicals (3 mentions) Simvastatin, by Merck Group (3 mentions) Mevalonate, by Merck Group (3 mentions) Atorvastatin, by Selleck Chemicals (3 mentions) Doxycycline, by Takara Bio (3 mentions) Olaparib, by Selleck Chemicals (3 mentions) Nu7441, by GeneTex (2 mentions) Decitabine, by Merck Group (2 mentions) Roscovitine, by Merck Group (2 mentions) Mycoalert mycoplasma detection kit, by Lonza (2 mentions) Lipofectamine 2000 reagent, by Thermo Fisher Scientific (2 mentions) Opti mem, by Thermo Fisher Scientific (2 mentions) Dulbecco s modified eagle medium, by Thermo Fisher Scientific (2 mentions) Docetaxel, by LC Laboratories (1 mentions) Rneasy mini kit, by Qiagen (1 mentions) Erastin, by Bio-Techne (1 mentions) Verdinexor, by Cayman Chemical (1 mentions) Tipifarnib, by MedChemExpress (1 mentions)

24 protocols using lovastatin

Docetaxel and Lovastatin Treatment Effects

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MDA-231 and PC3-ML parental cells were plated for plated for 24 hours to a final confluency of 90%. MDA-231 cells were treated with 100 nM docetaxel (LC Laboratories) for 5 days, with fresh docetaxel-containing media added at day 3 of treatment. PC3-ML cells were treated with 20 nM docetaxel for 10 days, with fresh docetaxel-containing media added every 3 days. Following treatment, cells were washed twice with PBS to remove dead cells prior to RNA isolation or flow cytometry, conducted as described elsewhere. For Lovastatin treatment, MDA-231 and PC3-ML cells were stained for CX3CR1 cell-surface expression and CX3CR1^High cells were sorted, using ultra-purity sorting mode, into DMEM supplemented with 10% FBS. Cells were plated for both control and Lovastatin treatment for collection at days 0 and 7. Cells were allowed to attach overnight prior to treatment. Lovastatin (Selleckchem) was used at a concentration of 10 μM, with fresh Lovastatin-containing media added every 3 days. Cells were lysed with buffer RLT directly in the culture dish, and RNA was isolated using the RNeasy Mini Kit (Qiagen).

DiNatale A., Kaur R., Qian C., Zhang J., Marchioli M., Ipe D., Castelli M., McNair C.M., Kumar G., Meucci O, & Fatatis A. (2022). Subsets of cancer cells expressing CX3CR1 are endowed with metastasis-initiating properties and resistance to chemotherapy. Oncogene, 41(9), 1337-1351.

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Ferroptosis Inducers and Inhibitors Screening

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erastin (Bio-techne, 5449); SAS (MedchemExpress, HY-14655); RSL3 (Cayman, 19288); FIN56 (Cayman, 25180); FINO2 (MedchemExpress, HY-129457); PANKi (Cayman, 31002); BSO (Sigma, B2515); DEM (Sigma, D97703); etomoxir sodium salt (Selleckchem, S8244); lovastatin (Selleckchem, S2061); TOFA (Selleckchem, S6690); dorsomorphin (Selleckchem, S7306); alisertib (Selleckchem, S1133); verdinexor (Cayman, 26171); leptomycin B (Cayman, 10004976); tipifarnib (MedchemExpress, HY-10502); methotrexate (Selleckchem, S1210); pitstop2 (Sigma, SML1169); EML425 (Selleckchem, S2977); C646 (Selleckchem, S7152); brequinar (Selleckchem, S3565); elamipretide (Selleckchem, S9803)

Chen S.Y., Lin C.C., Wu J., Chen Y., Wang Y.E., Setayeshpour Y., Mestre A, & Chi J.T. (2024). NINJ1 regulates ferroptosis via xCT antiporter interaction and CoA modulation. bioRxiv.

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Statin Efficacy in Renal Cancer

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All cell lines used in this study were grown in Dulbecco’s Modified Eagle’s Medium (DMEM; Caisson Labs #25-500, North Logan, UT) + 10% Fetal Bovine Serum (FBS; Omega Scientific #FB-12, Tarzana, CA) + 1% Penicillin/Streptomycin (Caisson Labs #25-512) in 5%CO₂, 21%O₂ at +37°C. The cell lines used in this study were a gift from Dr. Giaccia (Stanford). The identities of RCC4, RCC10, and 786-O were confirmed via STR analysis through the University of Arizona Genetics Core.786-OT1 cells are a sub-line of 786-O described in (5 ). Simvastatin, Pravastatin, mevalonate, GGPP, squalene (Sigma-Aldrich, St. Louis, MO), Fluvastatin, Lovastatin (Selleck Chemicals, Houston, TX), and Arachidonic acid (MP Biomedicals, Santa Ana, CA). Fluvastatin and Pravastatin were diluted in Dimethyl Sulfoxide (DMSO) and serially diluted for each experiment. Simvastatin and Lovastatin were dissolved in ethanol and activated in 0.1N NaOH by incubation at 50°C for 2 hours, followed by neutralization with 1N HCl, and dilution to 20mM in DMSO. The vehicle control was subjected to the same process and is approximately 20% ethanol and 80% DMSO.

Thompson J.M., Alvarez A., Singha M.K., Pavesic M.W., Nguyen Q.H., Nelson L.J., Fruman D.A, & Razorenova O.V. (2018). Targeting the mevalonate pathway suppresses VHL-deficient CC-RCC through a HIF-dependent mechanism. Molecular cancer therapeutics, 17(8), 1781-1792.

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Statin Compounds Assay Protocol

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Simvastatin (purity ≥97%), mevalonate (Me) (purity ≥96%), geranylgeranyl pyrophosphate (GGPP) (purity ≥95%) and farnesyl pyrophosphate (FPP) (purity ≥95%) were obtained from Sigma-Aldrich (Sigma, USA). The concentration of Simvastatin was chosen based on previous experiments (Gopalan et al., 2013 (link); Zongping et al., 2015 (link)). ROCK inhibitor Y27632 (purity ≥98%) was obtained from Enzo Life Sciences (Enzo Life Sciences, NY, USA). Lovastatin (purity ≥99%) and mevastatin (purity ≥99%) were obtained from Selleck (Selleck, Houston, TX, USA), fluvastatin (purity ≥98%) and pravastatin ((purity ≥99%) were obtained from MedChemExpress (MCE, NJ, USA).

Yin L., He Z., Yi B., Xue L, & Sun J. (2020). Simvastatin Suppresses Human Breast Cancer Cell Invasion by Decreasing the Expression of Pituitary Tumor-Transforming Gene 1. Frontiers in Pharmacology, 11, 574068.

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Lipid Metabolism Regulation Assays

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The chemical reagents atorvastatin, lovastatin, fluvastatin, simvastatin, MF-438, diltiazem, carfilzomib, ispinesib, and selinexor were purchased from Selleckchem (Houston, TX, USA). These chemicals were dissolved in DMSO (Calbiochem, San Diego, CA, USA) and diluted to their final concentrations. Mevalonolactone, cholesterol, and oleic acid–albumin were purchased from Sigma-Aldrich; these reagents were dissolved in distilled water.

Song M., Lee H., Nam M.H., Jeong E., Kim S., Hong Y., Kim N., Yim H.Y., Yoo Y.J., Kim J.S., Kim J.S., Cho Y.Y., Mills G.B., Kim W.Y, & Yoon S. (2016). Loss-of-function screens of druggable targetome against cancer stem–like cells. The FASEB Journal, 31(2), 625-635.

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Vitamin D Compound Cell Culture Study

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Almost all compounds were purchased from Selleck (Shanghai, China), including vitamin D3 (S4063), vitamin D2 (S4035), calcitriol (S1466), calcifediol (S1469), calcipotriene (S3739), doxercalciferol (S1467), lithocholic acid (S4003), lovastatin (S2061) and cholesterol (S4154). Tacalcitol (HY‐32337) was purchased from MedChemExpress (Shanghai, China). These compounds were added to the cell culture medium at the concentrations indicated, as appropriate. If not labeled, the concentrations of vitamin D3, calcifediol and calcitriol used for BNI274 were 5 μm, and for BNI423 were 2.5 μm.

Yuan R., Zhang W., You Y., Cui G., Gao Z., Wang X, & Chen J. (2023). Vitamin D3 suppresses the cholesterol homeostasis pathway in patient‐derived glioma cell lines. FEBS Open Bio, 13(9), 1789-1806.

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Cell Cycle Analysis by Flow Cytometry

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Cells were harvested using 0.25% trypsin-EDTA and resuspended in 300 μl of PBS at 4 °C. Ice-cold methanol:acetone (1 (link):1 (link)) was added dropwise with intermittent vortexing and cells were stored overnight at −20 °C. Cells were washed with cold PBS and incubated with 0.25 ml of 5 μg/ml RNase A for 15 minutes at 37 °C. 0.25 ml of 100 μg/ml propidium iodide was added for 1 hour at room temperature and protected from light. DNA content was measured using a FACSCalibur flow cytometer and analyzed using Cell Quest software (BD Biosciences). Doublet discrimination was accomplished by gating on forward scatter-H v. FL3A and FL3A v. FL3-H. At least 10,000 events were analyzed in each sample and samples were run in triplicate. EdU (5-ethynyl-2’-deoxyuridine) incorporation was measured according to the manufacturer’s specifications (Life Technologies). EdU was visualized using a FACSCalibur flow cytometer (BD Biosciences) and propidium iodide was included as a DNA counterstain. At least 10,000 events were analyzed in each sample and samples were run in triplicate. For pharmacological cell cycle arrest experiments, cells were treated with 50 μM Lovastatin (Selleck Chem, Houston, TX) for 36h prior the androgen stimulation experiments.

Hedayati M., Haffner M.C., Coulter J.B., Raval R.R., Zhang Y., Zhou H., Mian O., Knight E.J., Razavi N., Dalrymple S., Isaacs J.T., Santos A., Hales R., Nelson W.G., Yegnasubramanian S, & DeWeese T.L. (2016). Androgen deprivation followed by acute androgen stimulation selectively sensitizes AR-positive prostate cancer cells to ionizing radiation. Clinical cancer research : an official journal of the American Association for Cancer Research, 22(13), 3310-3319.

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Investigating DNA Damage Response Modulators

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The following drugs and chemicals were used: DNA-PKcs inhibitor (NU7441; Genetex) at 10 µM, lovastatin (S2061; Selleck Chemicals) at 40 µM, doxycycline (#8634-1; Clontech), SCR7 (M60082-2; Xcessbio) at 1 µM. Olaparib was purchased from Selleck Chemicals.

Canny M.D., Moatti N., Wan L.C., Fradet-Turcotte A., Krasner D., Mateos-Gomez P.A., Zimmermann M., Orthwein A., Juang Y.C., Zhang W., Noordermeer S.M., Seclen E., Wilson M.D., Vorobyov A., Munro M., Ernst A., Ng T.F., Cho T., Cannon P.M., Sidhu S.S., Sicheri F, & Durocher D. (2017). Inhibition of 53BP1 favors homology-dependent DNA repair and increases CRISPR-Cas9 genome-editing efficiency. Nature biotechnology, 36(1), 95-102.

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Metabolic Stress and Signaling Pathways

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Unless otherwise indicated, cancer cells were cultured in complete RPMI 1640 medium with 2 g/L glucose and 10% fetal bovine serum at 37°C under 5% CO₂. To apply metabolic stress, cells were cultured in glucose-free RPMI 1640 medium. To block RhoA, ROCK or JNK, cells were respectively cultured with CCG1423 (300 nM), Y27632 (10 μM) or SP600125 (5 μM) (Selleck Chemicals, Houston, TX, US) for 24 hours. Lovastatin (Selleck) was added into medium as indicated. MKN45 cells were from Japanese Collection of Research Bioresources Cell Bank, and BGC823 cells were from the KeyGene Biotech (Nanjing, China).

Lin L., Liu Y., Pan C., Zhang J., Zhao Y., Shao R., Huang Z., Su Y., Shi M., Bin J., Liao Y., Li N., Wang C, & Liao W. (2019). Gastric cancer cells escape metabolic stress via the DLC3/MACC1 axis. Theranostics, 9(7), 2100-2114.

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Cytokine and Kinase Inhibition Assay

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Cells were treated with 100 ng/mL recombinant human IFN-α 1a (Prospec: cyt-520). Lovastatin (Selleck Chemicals, S2061) was used at 5 μM and Roscovitine (Sigma-Aldrich, R7772) was used at 5 μM. Decitabine (Sigma-Aldrich, A3656) was used at 100 μM. We note that we did not observe any cell death in the Decitabine experiments. In our system, Decitabine at 100 μM slowed down cell growth, but did not cause apoptosis at least during the time scales of our experiments. However, we did observe cell death at 200 μM Decitabine.

Mudla A., Jiang Y., Arimoto K.I., Xu B., Rajesh A., Ryan A.P., Wang W., Daugherty M.D., Zhang D.E, & Hao N. (2020). Cell-cycle-gated feedback control mediates desensitization to interferon stimulation. eLife, 9, e58825.

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