AI Article Synopsis
- * Experiments demonstrate that nanaomycin K significantly inhibits cell proliferation and tumor growth, both in vitro and in vivo, particularly in TRAMP-C2 carcinoma-bearing mice.
- * The drug's mechanism involves the suppression of processes like epithelial-mesenchymal transition and the MAPK signaling pathway, leading to reduced tumor migration and enhanced apoptosis markers.
Article Abstract
Since castration-resistant prostate cancer (CRPC) acquires resistance to molecularly targeted drugs, discovering a class of drugs with different mechanisms of action is needed for more efficient treatment. In this study, we investigated the anti-tumor effects of nanaomycin K, derived from " subsp. " OS-3966. The cell lines used were LNCaP (non-CRPC), PC-3 (CRPC), and TRAMP-C2 (CRPC). Experiments included cell proliferation analysis, wound healing analysis, and Western blotting. In addition, nanaomycin K was administered intratumorally to TRAMP-C2 carcinoma-bearing mice to assess effects on tumor growth. Furthermore, immuno-histochemistry staining was performed on excised tissues. Nanaomycin K suppressed cell proliferation in all cell lines ( < 0.001) and suppressed wound healing in TRAMP-C2 ( = 0.008). Nanaomycin K suppressed or showed a tendency to suppress the expression of N-cadherin, Vimentin, Slug, and Ras in all cell lines, and suppressed the phosphorylation of p38, SAPK/JNK, and Erk1/2 in LNCaP and TRAMP-C2. In vivo, nanaomycin K safely inhibited tumor growth ( = 0.001). In addition, suppression of phospho-Erk1/2 and increased expression of E-cadherin and cleaved-Caspase3 were observed in excised tumors. Nanaomycin K inhibits tumor growth and suppresses migration by inhibiting epithelial-mesenchymal transition in prostate cancer. Its mechanism of action is related to the inhibition of phosphorylation of the MAPK signaling pathway.
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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC10216623 | PMC |
| http://dx.doi.org/10.3390/cancers15102684 | DOI Listing |
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