Garlic contains a variety of bioactive sulfur-containing compounds, such as allicin, diallyl sulfide, and diallyl disulfide, which have been found to have anticancer activity in both in vitro and in vivo studies.
Allicin has been found to induce apoptosis and inhibit tumor cell invasion, while diallyl sulfide and diallyl disulfide have been found to inhibit cancer cell proliferation and induce apoptosis.
Allicin and its derivatives have also been shown to induce reactive oxygen species production and to modulate signaling pathways involved in cell survival, proliferation and migration. Additionally, garlic extracts have been found to inhibit angiogenesis, which is necessary for cancer growth and metastasis. These compounds have been shown to have a synergistic effect with other anticancer agents, such as chemotherapy drugs and radiation therapy, suggesting that garlic may be an effective adjuvant therapy.
Allicin can promote Ferroptosis {ref}
Ornithine Decarboxylase Inhibitor {ref}
Synergy
→ Thymoquinone
→ Artesunate/Artemisinin
→ Ginger
→ Betulinic acid
Allicin inhibits the invasion of lung adenocarcinoma cells by altering tissue inhibitor of metalloproteinase/matrix metalloproteinase balance via reducing the activity of phosphoinositide 3-kinase/AKT signaling.
Allicin inhibits invasion and migration of breast cancer cells through the suppression of VCAM-1: Regulation of association between p65 and ER-Ξ±
Allicin induces apoptosis in gastric cancer cells through activation of both extrinsic and intrinsic pathways
"Allicin is an active compound derived from garlic that has been shown to have antitumor properties in vitro. The current study was designed to explore the effects and the underlying mechanism of allicin on gastric cancer cells. The MTT assay was used to detect cell viability. Transmission electron microscopy, Rh123 and propidium iodide staining, annexin V/FITC assay and the mitochondrial membrane potential were used to assess for the presence of apoptosis. Immunocytochemistry, western blot analysis, and Q-RT-PCR were used to detect gene expression. We found that allicin reduced cell viability in a dose- and time-dependent manner, partly through induction of apoptosis in gastric cancer cells. At the molecular level, allicin induced cytochrome c release from the mitochondria and increased caspase-3, -8, and -9 activation, with concomitant upregulation of bax and fas expression in the tumor cells. Allicin treatment inhibited proliferation and induced apoptosis in SGC-7901 cancer cells. Both intrinsic mitochondrial and extrinsic Fas/FasL-mediated pathways of apoptosis occur simultaneously in SGC-7901 cells following allicin treatment. Data from the current study demonstrated that allicin should be further investigated as a novel cancer preventive or therapeutic agent in control of gastric cancer, with potential uses in other tumor types."
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