Cancer capsaicin
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Capsaicin and Its Anticancer Properties
Capsaicin and Thyroid Cancer: Inhibition of Metastasis
Capsaicin, a potent agonist of the transient receptor potential vanilloid type 1 (TRPV1) channel, has shown significant anticancer effects against papillary thyroid carcinoma. Research indicates that capsaicin inhibits multiple steps of metastasis in BCPAP cells without affecting cell viability. This inhibition is mediated through the activation of TRPV1, which leads to a decrease in the expression of critical epithelial-mesenchymal transition (EMT) transcription factors such as Snail1 and Twist1, and an increase in E-cadherin levels. Additionally, capsaicin reduces the expression of matrix metalloproteinases MMP-2 and MMP-9, which are crucial for cancer cell invasion and migration.
Prostate Cancer: Capsaicin's Antiproliferative Effects
In prostate cancer, capsaicin has demonstrated profound antiproliferative effects, inducing apoptosis in both androgen receptor (AR)-positive and AR-negative cell lines. This effect is associated with increased levels of p53, p21, and Bax proteins. Capsaicin also downregulates prostate-specific antigen (PSA) and AR expression, inhibits NF-kappaB activation, and prevents the degradation of IkappaBalpha, thereby suppressing proteasome activity. These mechanisms collectively contribute to the significant slowing of tumor growth in prostate cancer xenografts.
Breast Cancer: Modulation of the EGFR/HER-2 Pathway
Capsaicin has been found to inhibit the growth of both estrogen receptor (ER)-positive and ER-negative breast cancer cells. This inhibition is linked to G0/G1 cell-cycle arrest, increased apoptosis, and reduced expression of EGFR, HER-2, and cyclin D1. Capsaicin also enhances caspase activity and poly-ADP ribose polymerase (PARP) cleavage, which are markers of apoptosis. Notably, capsaicin reduces breast cancer cell migration and significantly decreases tumor size in vivo without noticeable side effects.
Osteosarcoma: Reducing Cancer Stemness and Metastasis
In osteosarcoma, capsaicin has been shown to decrease cancer stemness and inhibit metastasis. This effect is dose-dependent and involves the downregulation of stemness factors SOX2 and EZH2. Capsaicin also modulates the expression of metastasis-related genes, reducing the overall survival and disease-free survival of cancer cells. These findings suggest that capsaicin can inhibit the migratory ability of osteosarcoma by suppressing its stemness.
Nasopharyngeal Carcinoma: Inducing Autophagy and Apoptosis
Capsaicin has potential as a chemotherapeutic agent for nasopharyngeal carcinoma (NPC). It inhibits cancer cell growth, induces G1 phase cell cycle arrest, and promotes autophagy and apoptosis. These effects are mediated through the downregulation of the PI3K/Akt/mTOR pathway, which is crucial for cell survival and proliferation. Capsaicin increases the levels of autophagy markers and enhances caspase-3 activity, further supporting its role in inducing apoptosis.
Colorectal Cancer: Suppression of β-Catenin Signaling
In colorectal cancer, capsaicin suppresses cell proliferation by altering β-catenin-dependent signaling. It decreases intracellular β-catenin levels and reduces the transcriptional activity of β-catenin/TCF. Capsaicin also enhances the proteasomal degradation of β-catenin and disrupts the interaction between TCF-4 and β-catenin, contributing to its anticancer activity.
Conclusion
Capsaicin exhibits significant anticancer properties across various types of cancer, including thyroid, prostate, breast, osteosarcoma, nasopharyngeal, and colorectal cancers. Its mechanisms of action include the modulation of key signaling pathways, induction of apoptosis, inhibition of metastasis, and reduction of cancer stemness. These findings highlight the potential of capsaicin as a therapeutic agent in cancer treatment. However, further clinical studies are necessary to fully understand its efficacy and safety in humans.
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