ArticlePharmacognosy magazine2017
Chalepin: A Compound from
Article in Pharmacognosy magazine, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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16 citing papers in PubMed, 21 citations in OpenAlex.
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- [Research Advances of JAK/STAT Signaling Pathway in Lung Cancer].Zhongguo fei ai za zhi = Chinese journal of lung cancer · 2019Review
- Mechanisms of Compound Kushen Injection for the Treatment of Lung Cancer Based on Network Pharmacology.Evidence-based complementary and alternative medicine : eCAM · 2019Article
- Silence of Stomatin-Like Protein 2 Represses Migration and Invasion Ability of Human Liver Cancer Cells via Inhibiting the Nuclear Factor Kappa B (NF-κB) Pathway.Medical science monitor : international medical journal of experimental and clinical research · 2018Article
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundPlants have been a major source of inspiration in developing novel drug compounds in the treatment of various diseases that afflict human beings worldwide.
objectiveA dihydrofuranocoumarin named chalepin, which was isolated from the chloroform extract of the plant, was tested on its ability to inhibit molecular pathways of human lung carcinoma (A549) cells. MATERIALS AND
methodsCell cycle analysis and caspase 8 activation were conducted using a flow cytometer, and protein expressions in molecular pathways were determined using Western blot technique.
resultsCell cycle analysis showed that cell cycle was arrested at the S phase. Further studies using Western blotting technique showed that cell cycle-related proteins such as cyclins, cyclin-dependent kinases (CDKs), and inhibitors of CDKs correspond to a cell cycle arrest at the S phase. Chalepin also showed inhibition in the expression of inhibitors of apoptosis proteins. Nuclear factor-kappa B (NF-κB) pathway, signal transducer and activation of transcription 3 (STAT-3), cyclooxygenase-2, and c-myc were also downregulated upon treatment with chalepin. Chalepin was found to induce extrinsic apoptotic pathway. Death receptors 4 and 5 showed a dramatic upregulation at 24 h. Analysis of activation of caspase 8 with the flow cytometer showed an increase in activity in a dose- and time-dependent manner. Activation of caspase 8 induced cleavage of BH3-interacting domain death agonist, which initiated a mitochondrial-dependent or -independent apoptosis.
conclusionChalepin causes S phase cell cycle arrest, NF-κB pathway inhibition, and STAT-3 inhibition, induces extrinsic apoptotic pathway, and could be an excellent chemotherapeutic agent. SUMMARY: This study reports the capacity of an isolated bioactive compound known as chalepin to suppress the nuclear factor kappa-light-chain-enhancer of activated B cells pathway, signal transducer and activation of transcription 3, and extrinsic apoptotic pathway and also its ability to arrest cell cycle in S phase. This compound was from the leaves of
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