Chromobox protein homolog 7 suppresses the stem-like phenotype of glioblastoma cells by regulating the myosin heavy chain 9-NF-?B signaling pathway
Chromobox protein homolog 7 (CBX7) can inhibit the progression of various tumors, but its impact on the stem cell-like properties of GBM cells remains unclear. Clinically, low levels of CBX7 are associated with poor prognosis and increased distant metastasis in GBM patients, and this low expression is caused by methylation of the CBX7 promoter. In this study, through bioinformatics analysis, we found that CBX7 is the most significantly downregulated member of the CBX family in GBM and is closely associated with the stem-like phenotype of GBM cells. Subsequent research showed that CBX7 promotes the degradation of myosin heavy chain 9 (MYH9) protein through the ubiquitin-proteasome pathway via the polycomb repressive complex (PRC1) and suppresses the stem-like phenotype of GBM cells by inhibiting the nuclear factor kappa-B (NF ?B) signaling pathway. Furthermore, overexpression of MYH9 in GBM cells can reverse the inhibitory effects of CBX7 on migration, proliferation, invasion, and stemness of GBM cells. In summary, CBX7 acts as a tumor suppressor by inhibiting the stem cell-like characteristics of GBM. The CBX7-MYH9-NF-?B signaling axis may serve as a potential therapeutic target for GBM. Overall design: CBX7 overexpression group, 3 replicate biosample; CBX7 wt group, 3 replicate biosamples. All samples were subjected to transcriptome sequencing.