Catalogue Number
BN-O1749
Analysis Method
HPLC,NMR,MS
Specification
98%(HPLC)
Storage
-20℃
Molecular Weight
552.5
Appearance
Yellow powder
Botanical Source
Leaf of Metasequoia glyptostroboides and from Cycas revoluta
Structure Type
Flavonoids
Category
Standards;Natural Pytochemical;API
SMILES
COC1=C(C2=C(C(=C1)O)C(=O)C=C(O2)C3=CC=C(C=C3)O)C4=C(C=CC(=C4)C5=CC(=O)C6=C(C=C(C=C6O5)O)O)O
Synonyms
4H-1-Benzopyran-4-one, 8-[5-(5,7-dihydroxy-4-oxo-4H-1-benzopyran-2-yl)-2-hydroxyphenyl]-5-hydroxy-2-(4-hydroxyphenyl)-7-methoxy-/8-[5-(5,7-Dihydroxy-4-oxo-4H-chromen-2-yl)-2-hydroxyphenyl]-5-hydroxy-2-(4-hydroxyphenyl)-7-methoxy-4H-chromen-4-one/8-[5-(5,7-Dihydroxy-4-oxo-4H-chromen-2-yl)-2-hydroxy-phenyl]-5-hydroxy-2-(4-hydroxy-phenyl)-7-methoxy-chromen-4-one/Sotetsuflavone
IUPAC Name
8-[5-(5,7-dihydroxy-4-oxochromen-2-yl)-2-hydroxyphenyl]-5-hydroxy-2-(4-hydroxyphenyl)-7-methoxychromen-4-one
Density
1.6±0.1 g/cm3
Solubility
Soluble in Chloroform,Dichloromethane,Ethyl Acetate,DMSO,Acetone,etc.
Flash Point
293.0±27.8 °C
Boiling Point
873.1±65.0 °C at 760 mmHg
Melting Point
InChl
InChI=1S/C31H20O10/c1-39-26-13-23(38)30-22(37)12-24(14-2-5-16(32)6-3-14)41-31(30)28(26)18-8-15(4-7-19(18)34)25-11-21(36)29-20(35)9-17(33)10-27(29)40-25/h2-13,32-35,38H,1H3
InChl Key
OIFVLHZEBAXHPM-UHFFFAOYSA-N
WGK Germany
RID/ADR
HS Code Reference
2932990000
Personal Projective Equipment
Correct Usage
For Reference Standard and R&D, Not for Human Use Directly.
Meta Tag
provides coniferyl ferulate(CAS#:2608-21-1) MSDS, density, melting point, boiling point, structure, formula, molecular weight etc. Articles of coniferyl ferulate are included as well.>> amp version: coniferyl ferulate
No Technical Documents Available For This Product.
30092797
BACKGROUND:
Sotetsuflavone is isolated from Cycas revoluta Thunb., which has biological activity against tumors. However, the anti-proliferative effects of sotetsuflavone on A549 cells and its mechanism are not fully elucidated.
METHODS:
This study investigated the mechanisms of growth inhibition, cell cycle arrest and apoptosis in non-small cell lung cancer A549 cells induced by sotetsuflavone and evaluated whether sotetsuflavone can be safely utilized by humans as therapeutic agent.
RESULTS:
We found that sotetsuflavone had significant antiproliferative activity against A549 cells. At the same time, the reactive oxygen species (ROS) content increased while the mitochondrial membrane potential and the ratio of Bcl-2/Bax decreased. Cleaved caspase-3, cleaved caspase-9, cytochrome C and Bax expression increased, and Cyclin D1, CDK4, cleaved caspase-8 and Bcl-2 expression decreased. Interestingly, we demonstrated that sotetsuflavone could effectively inhibit the G0/G1 cycle progression, and then induce the endogenous apoptosis pathway. Our results show that sotetsuflavone could inhibit the growth of A549 cells by up-regulating intracellular ROS levels and causing the mitochondrial membrane potential to collapse, inducing G0/G1 phase arrest and endogenous apoptosis.
CONCLUSIONS:
In short, we confirm that sotetsuflavone had an inhibitory effect on A549 cells and discovered that it causes apoptosis of A549 lung cancer cells. Sotetsuflavone may be used as a novel candidate for anti-tumor therapy in patients with lung cancer.
Apoptosis; Cycle arrest; Mitochondria-dependent pathway; Reactive oxygen species (ROS); Sotetsuflavone
Sotetsuflavone inhibits proliferation and induces apoptosis of A549 cells through ROS-mediated mitochondrial-dependent pathway.
Wang S1, Hu Y1, Yan Y1, Cheng Z1, Liu T2.
2018 Aug 9
29531823
Epithelial-mesenchymal transition (EMT) is associated with tumor invasion and metastasis, and offers insight into novel strategies for cancer treatment. Sotetsuflavone was isolated from Cycas revolute, which has excellent anticancer activity in the early stages. The present study aims to evaluate the anti-metastatic potential of sotetsuflavone in vitro. Our data demonstrated that sotetsuflavone inhibits metastasis of A549 cells, and EMT. This inhibition was reflected in the upregulation of E-cadherin, and downregulation of N-cadherin, vimentin, and Snail. Mechanistically, our study demonstrated that HIF-1α played an important role in the anti-metastatic effect of sotetsuflavone in non-small-cell lung cancer A549 cells. Sotetsuflavone not only mediated VEGF expression but also downregulated VEGF and upregulated angiostatin, and simultaneously affected the expression of MMPs and decreased MMP-9 and MMP-13 expression. More importantly, HIF-1α expression may be regulated by the inhibition of PI3K/AKT and TNF-α/NF-κB pathways. These results suggest that sotetsuflavone can reverse EMT, thereby inhibiting the migration and invasion of A549 cells. This process may be associated with both PI3K/AKT and TNF-α/NF-κB pathways, and sotetsuflavone may be efficacious in the treatment of non-small-cell lung cancer.
Sotetsuflavone suppresses invasion and metastasis in non-small-cell lung cancer A549 cells by reversing EMT via the TNF-α/NF-κB and PI3K/AKT signaling pathway.
Wang S1, Yan Y1, Cheng Z1, Hu Y1, Liu T1
018 Feb 14
31920653
Non-small cell lung cancer (NSCLC) is a globally scaled disease with a high incidence and high associated mortality rate. Autophagy is one of the important physiological activities that helps to control cell survival, influences the dynamics of cell death, and which plays a crucial role in the pathophysiology of NSCLC. Sotetsuflavone is a naturally derived and occurring flavonoid, and previous studies have demonstrated that sotetsuflavone possesses potential anti-cancer activities. However, whether or not sotetsuflavone induces autophagy, as well as has effects and influences cell death in NSCLC cells remains unclear. Thus, in our study, we examined and elucidated the roles and underlying mechanisms of sotetsuflavone upon the dynamics of autophagy in NSCLC in vivo and in vitro. The results indicated that sotetsuflavone was able to inhibit proliferation, migration, and invasion of NSCLC cells. Mechanistically, sotetsuflavone was able to induce apoptosis by increasing the levels of expression of cytochrome C, cleaved-caspase 3, cleaved-caspase 9, and Bax, and contrastingly decreased levels of expression of Bcl-2. In addition, we also found that decreased levels of expression of cyclin D1 and CDK4 caused arrest of the G0/G1 phases of the cell cycle. Furthermore, we also found that sotetsuflavone could induce autophagy which in turn can play a cytoprotective effect on apoptosis in NSCLC. Sotetsuflavone-induced autophagy appeared related to the blocking of the PI3K/Akt/mTOR pathway. Our in vivo study demonstrated that sotetsuflavone significantly inhibited the growth of xenograft model inoculated A549 tumor with high a degree of safety. Taken together, these findings suggest that sotetsuflavone induces autophagy in NSCLC cells through its effects upon blocking of the PI3K/Akt/mTOR signaling pathways. Our study may provide a theoretical basis for future clinical applications of sotetsuflavone and its use as a chemotherapeutic agent for treatment of NSCLC.
Copyright © 2019 Wang, Xu, Hu, Lei and Liu.
PI3K/Akt/mTOR signaling pathway; apoptosis; autophagy; non-small cell lung cancer; sotetsuflavone
Sotetsuflavone Induces Autophagy in Non-Small Cell Lung Cancer Through Blocking PI3K/Akt/mTOR Signaling Pathway in Vivo and in Vitro.
Wang S1,2,3, Xu X4, Hu Y1,3, Lei T4, Liu T1,3.
2019 Dec 5
