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The tumour microenvironment (TME) is crucial for tumour development and progression. Tumour-associated macrophages (TAMs) in the TME can promote tumour progression and metastasis by releasing cytokines, such as IL-6. Calycosin, a phytoestrogen that is one of the active compounds in Radix Astragali, has been shown to inhibit tumour growth and metastasis. However, the underlying mechanism by which calycosin inhibits tumour growth remains unclear. Thus, this study aimed to investigate the effect of calycosin on IL-6 production in peripheral blood mononuclear cell (PBMC)- and THP-1-derived macrophages and explore its potential mechanisms using co-immunoprecipitation, western blotting, immunofluorescence, chromatin immunoprecipitation and luciferase assays. We found that calycosin treatment substantially upregulated the expression of ER-α36, a variant of the ER, and reduced IL-6 production in macrophages. Mechanistically, ER-α36 physically interacted with NF-κBp65 and retained p65 in the cytoplasm to attenuate NF-κB function as an IL-6 transcriptional inducer. In conclusion, our result indicated that calycosin inhibited IL-6 production by enhancing ER-α36 expression and its interaction with p65, which attenuated NF-κB function as an IL-6 inducer. Therefore, calycosin can be developed as an effective agent for cancer therapy by targeting TAMs.
Background: Although poly (ADP-ribose) polymerase family member 10 (PARP10) has been implicated in the progression of multiple cancer types, its role in oral squamous cell carcinoma (OSCC) remains unknown. This study aimed to examine the function of PARP10 in OSCC and investigate the underlying mechanisms. Methods: The expression of PARP10 in OSCC was investigated in OSCC patient cohorts. Kaplan-Meier curve analysis was performed to assess the association between PARP10 and prognosis in OSCC. Correlation between PARP10 expression and the related variables was analyzed by χ2 test. CKK-8, transwell assay, western blot, immunohistochemistry, immunofluorescence, and bioinformatic analysis, were applied to clarify the role of PARP10 in OSCC. Results: PARP10 was found to be markedly elevated in OSCC tissues. The upregulation of PARP10 predicted shorter overall survival and disease-specific survival and was significantly correlated with several malignant features. Moreover, depletion of PARP10 markedly inhibited the proliferation, migration, and invasion of OSCC cells, and promoted OSCC cell apoptosis, and resulted in alterations of relevant proteins. Furthermore, a positive correlation was observed between the expression of PARP10 and Ki67, PARP1, MMP2, and VEGF. In addition, depletion of PARP10 impaired the PI3K-AKT and MAPK signaling pathways. Conclusion: PARP10 is involved in the progression of OSCC via regulation of PI3K-AKT and MAPK signaling pathways.
Cancer cell stemness (CCS) plays critical roles in both malignancy maintenance and metastasis, yet the underlying molecular mechanisms are far from complete. Although the importance of SOX2 in cancer development and CCS are well recognized, the role of MTA3 in these processes is unknown. In this study, we used esophageal squamous cell carcinoma (ESCC) as a model system to demonstrate that MTA3 can repress both CCS and metastasis in vitro and in vivo. Mechanistically, by forming a repressive complex with GATA3, MTA3 downregulates SOX2OT, subsequently suppresses the SOX2OT/SOX2 axis, and ultimately represses CCS and metastasis. More importantly, MTA3low/SOX2high is associated with poor prognosis and could serve as an independent prognostic factor. These findings altogether indicate that MTA3/SOX2OT/SOX2 axis plays an indispensable role in CCS. Therefore, this axis could be potentially used in cancer stratification and serves as a therapeutic target.
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