Kun Cheng

Epithelial ovarian cancer (EOC) is a gynecological tumor with high mortality. Despite aggressive treatment, survival rates for patients with advanced EOC are low, and more effective methods of diagnosis and treatment are urgently needed. Inflammation and cancer are strongly associated; however, the mechanisms that mediate this relationship are not fully understood. In this study, we found that the expression of interleukin-1β (IL-1β), a proinflammatory cytokine, increased in an ovarian cancer tissue microarray (TMA) and inhibited A2780 and SKOV3 cell viability and metastasis. Recombinant IL-1β protein and the overexpression of IL-1β decreased the proliferation and metastasis of ovarian cancer cells. IL-1β deficiency promoted proliferation and metastasis. Moreover, transcriptome sequencing revealed that IL-1β downregulates the expression of matrix metalloproteinase 12 (MMP12). The signaling pathway involving MAPK/AP-1/MMP12 is involved in IL-1β-regulated ovarian cancer progression. Overall, we found that the proinflammatory cytokine IL-1β inhibits ovarian cancer cell viability and metastasis. These findings provided deeper insights into inflammation and cancer progression.

Aspergillus niger is an important lignocellulose-degrading enzyme-producing strain. Multiple regulatory factors regulate the synthesis of lignocellulose-degrading enzymes in A. niger. We previously found that A. niger possessed an intracellular β-glucosidase BGL1B, and the intracellular localization of BGL1B and its active transglycosylation action prompted us to explore whether BGL1B was involved in the regulation of the synthesis of lignocellulose-degrading enzymes in A. niger. In this study, by investigating the production of lignocellulose-degrading enzymes of bgl1B knockout strain (Δbgl1B) and overexpression strain (OE::bgl1B), it was found that BGL1B exhibited a repressive role on the expression of lignocellulose-degrading enzyme genes through carbon catabolite repression (CCR) way. On the other hand, BGL1B’s transglycosylation products sophorose and laminaribiose were proved to be able to induce the expression of lignocellulose-degrading enzyme genes, which explained why OE::bgl1B showed the same enhanced enzyme activity and gene expression as Δbgl1B strain compared to the starting strain (WT). The present study demonstrates that BGL1B plays dual regulatory roles in the regulation of the synthesis of lignocellulose-degrading enzymes in A. niger: the repressive role caused by BGL1B’s hydrolysis product glucose and the induction role caused by BGL1B’s transglycosylation products sophorose and laminaribiose. This study broadens the understanding of the regulatory network of the synthesis of lignocellulose-degrading enzymes in A. niger. Also, it provides a strategy to create an engineered strain with high production of lignocellulose-degrading enzymes.