Division of Tumor Dynamics and Regulation, Cancer Research Institute, Kanazawa University, Kanazawa, 920-1192, Japan.
WPI-Nano Life Science Institute (WPI-NanoLSI), Kanazawa University, Kanazawa, 920-1192, Japan.
Sci Rep. 2020 Oct 7;10(1):16678. doi: 10.1038/s41598-020-72448-y.
The aggressive invasiveness of malignant mesothelioma limits cancer therapy, however, the molecular mechanisms underlying the invasiveness remain largely unknown. Here we found that the matrix metalloproteinase-2 (MMP-2) was required for the invasion of mesothelioma cells in the collagen matrix and the gene expression of MMP-2 was correlated with the invasive phenotype. The MMP-2 gene expression was regulated by DNA and histone methylation around the transcription start site, implicating the involvement of the polycomb repressive complex (PRC). Knockdown of PRC component chromobox 6 (CBX6) promoted MMP-2 expression and invasion of mesothelioma cells. Transcriptome analysis suggested that CBX6 regulates sets of genes involved in cancer cell migration and metastasis. In invasive but not non-invasive cells, CBX6 was constantly unstable owing to ubiquitination and protein degradation. In human tissues, CBX6 localized in the nuclei of normal mesothelium and benign mesothelioma, but the nuclear staining of CBX6 was lost in malignant mesothelioma. These results suggest involvement of proteasomal degradation of CBX6 in mesothelioma progression.
恶性间皮瘤的侵袭性限制了癌症治疗,然而,侵袭性背后的分子机制在很大程度上仍不清楚。在这里,我们发现基质金属蛋白酶-2(MMP-2)是间皮瘤细胞在胶原基质中侵袭所必需的,并且 MMP-2 的基因表达与侵袭表型相关。MMP-2 基因表达受转录起始位点周围的 DNA 和组蛋白甲基化调控,暗示多梳抑制复合物(PRC)的参与。PRC 成分盒蛋白 6(CBX6)的敲低促进了间皮瘤细胞的 MMP-2 表达和侵袭。转录组分析表明,CBX6 调节参与癌细胞迁移和转移的基因集。在侵袭性而非非侵袭性细胞中,由于泛素化和蛋白降解,CBX6 一直不稳定。在人体组织中,CBX6 定位于正常间皮和良性间皮瘤的核内,但恶性间皮瘤中 CBX6 的核染色消失。这些结果表明 CBX6 的蛋白酶体降解参与了间皮瘤的进展。