The structural scaffold of PRC2: A new vulnerability in small cell lung cancer
A study published in *Communications Biology* reveals a critical dependency in small cell lung cancer (SCLC) tumorigenesis. Researchers found that SCLC cells rely on the structural, rather than the enzymatic, function of the Polycomb Repressive Complex 2 (PRC2). This discovery was leveraged to develop a novel therapeutic strategy: combining enzymatic inhibition of PRC2 with inhibition of the histone methyltransferases G9a and GLP. This dual approach induces significant oxidative stress, leading to the selective death of neuroendocrine SCLC cells. The findings highlight a non-canonical role for PRC2 and identify a promising synthetic lethal interaction for targeted cancer therapy.
Why it might matter to you: For pathologists focused on molecular diagnostics and tumor biology, this research underscores the importance of understanding non-enzymatic protein functions in cancer pathogenesis. It directly informs the interpretation of immunohistochemistry and molecular testing for epigenetic regulators like PRC2 in neuroendocrine tumors. The identified therapeutic axis could influence future biomarker development and guide the pathological assessment of treatment response in SCLC, moving beyond traditional genetic mutations to target structural dependencies.
Source →Stay curious. Stay informed — with Science Briefing.
Always double check the original article for accuracy.