Therapeutic potential of ethoxy mansonone G: A comprehensive exploration of its anticancer actions in breast cancer, colorectal cancer, and non-small cell lung carcinoma.
Amna FayyazMahnoor BasitAndleeb FarooqTooba KhanUmama AyubSomia KhanMuhammad Armaghannull Mati-Ur-RahmanMuhammad AmmadDietrich BüsselbergKhushbukhat KhanSolomon HabtemariamJavad Sharifi RadPublished in: Cell biology international (2024)
Mansonone G (MG), a 1,2-naphthoquinones with antiestrogenic, antimicrobial, and anti-adipogenic activities, is derived from the heartwood of Mansonia gagei Drumm. Ethoxy mansonone G (EMG), an essential derivative of MG, has anticancer and antioxidant agent. EMG also has antiestrogen activity and is demonstrated to lower estrogen receptor expression in endocrine-resistant cells. EMG significantly inhibits cell division, invasion, and anchorage-dependent growth in all cancer types. Through the stimulation of the tumor protein (p53) and extracellular signal-regulated kinase (ERK) signaling cascades, it also causes apoptosis. Moreover, it manifests its anti-cancerous effects in toll-like receptor pathways, c-Jun N-terminal kinase (c-JNK), and nuclear factor kappa B (NF-κB). EMG inhibits the phosphorylation of glycogen synthase kinase (GSK3), Erk, protein kinase B (Akt), and mammalian target of rapamycin (mTOR). By interfering with molecular cascades, EMG significantly reduces the metabolism of cancer cells. This paper focuses on the potential use of EMG in cancer treatment. Moreover, it states the methodology by which specific assays establish the anti-cancerous role of EMG. Breast cancer, non-small cell lung cancer, and colorectal cancer are only a few of the cancers for which EMG was shown to be effective. Through further research, EMG may be developed as a therapeutic solution to complications caused by cancer. This study presents EMG as a novel candidate for cancer therapy, offering a unique combination of pharmacological advantages and mechanistic insights that warrant further exploration and development toward addressing the complexities of cancer treatment.
Keyphrases
- nuclear factor
- high density
- toll like receptor
- signaling pathway
- protein kinase
- upper limb
- pi k akt
- cell proliferation
- cell cycle arrest
- cancer therapy
- oxidative stress
- cell death
- inflammatory response
- papillary thyroid
- immune response
- tyrosine kinase
- stem cells
- high throughput
- staphylococcus aureus
- small molecule
- mesenchymal stem cells
- risk factors
- lps induced
- young adults
- squamous cell
- cell migration