Tanshinlactone
Tanshinlactone is a compound found in Salvia miltiorrhiza with anti-coronavirus (CoV) and anti-tumor activities. Tanshinlactone induces methuocytic cell death (methuosis) by activating the NRF2 pathway, and selectively kills ER+, HER2+/EGFR+ breast cancer cells. Tanshinlactone is applicable to research related to breast cancer and coronavirus infections.
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- CAS No.: 105351-70-0
- Formule: C17H12O3
- Masse moléculaire:264.28
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Stockage:
Please store the product under the recommended conditions in the Certificate of Analysis.
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Activité biologique
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Chemical Information
- Protocole
- Pureté et documentation
- Références
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Help & FAQs
Activité biologique
Description
In Vitro
Tanshinlactone (0.1-10 μM; 72 h) selectively inhibits the proliferation of ER+, HER2+ and EGFR+ human breast cancer cells, but shows no activity against triple-negative breast cancer cells, normal cells or other types of cancer cells[2].
Tanshinlactone (0-2 μM; 7-14 days) reduces the colony-forming ability of ER+, HER2+ and EGFR+ human breast cancer cells in a dose-dependent manner, but exerts no effect on the colony formation of triple-negative breast cancer cells[2].
Tanshinlactone (0-6.32 μM; 0-64 h) induces dose- and time-dependent cytoplasmic vacuolization in ER+ and HER2+ human breast cancer cells, which further leads to cell rupture, but exerts no such effect in triple-negative breast cancer cells[2].
Treatment of human breast cancer cells SK-BR-3 and ZR-75-1 with Tanshinlactone (6.32 μM; 24 h) upregulates the mRNA expression of genes that promote macropinocytosis, while downregulating the mRNA expression of genes involved in the transport of macropinosomes to lysosomes and the plasma membrane[2].
Tanshinlactone (6.32 μM; 24-48 h) induces vesicular cell death (a non-apoptotic, non-ferroptotic, non-necrotic form of cell death) in human breast cancer cell lines SK-BR-3 and ZR-75-1, and this process depends on macropinocytosis[2].
Tanshinlactone (0-20 μM; 48 h) induces vacuolar cell death in human breast cancer cell lines SK-BR-3 and ZR-75-1 by activating the NRF2 signaling pathway[2].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only. Further protocols information, click here.
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Cell Line:human ER+, HER2+, EGFR+ breast cancer cells, normal cells, other cancer cells
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Concentration:0.1, 1, 10 μM
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Incubation Time:72 h
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Result:Inhibited growth of HER2+ (SK-BR-3: IC50 1.91 μM), HER2+/ER+ (BT-474: IC50 5.50 μM), ER+ (ZR-75-1: IC50 6.92 μM; MCF7: IC50 1.51 μM; T-47D: IC50 3.98 μM), and EGFR+ (MDA-MB-468: IC50 4.47 μM) breast cancer cells in a dose-dependent manner.
Did not affect triple-negative breast cancer cells (MDA-MB-231, BT-549, HCC1937: IC50 >20.0 μM), normal cells (MCF10A, WPMY-1, CCD841CoN, HUVECs), or other cancer cell lines.
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Cell Line:human HER2+ (SK-BR-3) and ER+ (ZR-75-1) breast cancer cells
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Concentration:6.32 μM
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Incubation Time:24 h
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Result:Significantly upregulated mRNA levels of macropinocytosis-related genes including RAB5, RAB7, RAC1, CDC42, EGF, EPGN, AREG, HBEGF, EGFR, PIK3CA, PAK1, NHE1, and SDC1 in SK-BR-3 and ZR-75-1 cells.
Downregulated mRNA levels of SEPT6 and ARF6 in these cells.
Chemical Information
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CAS No. 105351-70-0
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Masse moléculaire 264.28
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Formule C17H12O3
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SMILES
O=C1C2=C3C=CC=C(C)C3=CC=C2C(OC=C4C)=C4O1
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Structure Classification
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Initial Source
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Livraison
Room temperature in continental US; may vary elsewhere.
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Stockage
Please store the product under the recommended conditions in the Certificate of Analysis.
Protocole
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Cell Cytotoxicity Assay
Cytotoxicity assays are usually based on the assessment of cell membrane damage, which can also be indirectly detected by measuring cell viability. Detection methods include MTT assay, CKK-8 assay, LDH assay and ATP assay, etc.
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Mammalian live/dead viability and cytotoxicity staining
Live/dead viability and cytotoxicity staining assays are based on the simultaneous detection of intracellular esterase activity in metabolically active (viable) cells and membrane integrity loss in non-viable cells. In commonly used dual-staining approaches, membrane-permeant fluorogenic substrates are converted by intracellular esterases into fluorescent products in live cells, while impermeant DNA-binding dyes selectively enter cells with compromised plasma membranes and label nucleic acids in dead or dying cells, enabling discrimination between viable and non-viable populations by fluorescence microscopy or flow cytometry.
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Apoptosis Solutions
Apoptosis is a regulated, generally non-lytic cell-death pathway that removes unwanted, damaged, infected, or abnormal cells through coordinated morphological changes, caspase activation, DNA fragmentation, and membrane remodeling. The intrinsic apoptosis pathway is controlled mainly by mitochondrial outer membrane permeabilization, BCL-2 family proteins, cytochrome c release, apoptosome formation, caspase-9 activation, and downstream executioner caspase-3/7 activation. The extrinsic apoptosis pathway is initiated by death receptors such as Fas, TNFR, and TRAIL receptors, which recruit adaptor proteins and activate caspase-8 before engaging executioner caspases or mitochondrial amplification through BID cleavage. Apoptosis is linked to many phenotypes, including cancer cell killing, tissue homeostasis, immune regulation, neurodegeneration, infection response, and treatment-induced cytotoxicity; unresolved questions include how apoptosis interacts with necroptosis, pyroptosis, ferroptos
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Breast Cancer Modeling
Breast cancer is a heterogeneous cancer, and it has been distinguished into four subtypes: luminal A, luminal B, HER2-positive and basal-like. Molecular mutations, epigenetic alterations, hormone exposure and immune microenvironment are related to the progression of breast cancer.
Pureté et documentation
Références
[1]. Lin W, et al. Tanshinlactone triggers methuosis in breast cancer cells via NRF2 activation. Front Pharmacol. 2025;15:1534217. Published 2025 Jan 21. [Content Brief]
[2]. Rodrigues GCS, et al. Ligand and Structure-based Virtual Screening of Lamiaceae Diterpenes with Potential Activity against a Novel Coronavirus (2019-nCoV). Curr Top Med Chem. 2020;20(24):2126-2145. [Content Brief]
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)
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