"In the study, the scientists analyzed prostate cancer cells and observed that EZH2 doesn't simply modify histone H3; it also stabilizes another protein called FOXA1, which in turn boosts the transcriptional activity of YTHDF1, an m6A "reader" protein. That change sets off a chain reaction in which YTHDF1 increases the protein production of key enzymes (METTL14 and WTAP) that add m6A marks to RNA, raising m6A levels in prostate cancer cells."
"The consequence of this process is that higher m6A levels help cancer cells grow and survive, Yi said. Next, the investigators blocked EZH2's enzymatic activity and found that it disrupted the entire pathway, slowing protein production and weakening cancer cell growth. Even more promising, combining an EZH2-targeting drug with an m6A inhibitor significantly reduced tumor growth in lab models of prostate cancer, suggesting a powerful new therapeutic approach."
EZH2, beyond its role in histone modification, stabilizes FOXA1 leading to increased transcriptional activity of YTHDF1, an m6A reader. YTHDF1 elevates protein production of METTL14 and WTAP, the m6A methyltransferase components, increasing m6A RNA marks in prostate cancer cells. Elevated m6A enhances protein production that supports cancer cell growth and survival. Pharmacologic blockade of EZH2 enzymatic activity disrupts this pathway, slows protein synthesis, and weakens cancer cell proliferation. Combined treatment with an EZH2 inhibitor and an m6A inhibitor markedly reduces tumor growth in laboratory models, indicating a promising therapeutic strategy.
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