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ObjectiveThe aim of this study was to investigate whether evodiamine (EVO) could potentiate the antitumor activity of gemcitabine (GEM) in tongue cancer cells and determine its potential underlying mechanisms.Materials and methodsHuman Tca8113 and CAL-27 tongue squamous carcinoma cell lines were treated with EVO and GEM in different sequences and doses, after which cell proliferation was measured. Drug interactions were analyzed using the Chou–Talalay method with CompuSyn software. Clonality, apoptosis, and migration were measured using the plate clone formation assay, annexin V/propidium iodide (PI) staining, Hoechst 33342 staining, and the wound-healing test. The activity of the nuclear factor kappa light-chain enhancer of activated B cell (NF-κB) p65 subunit and its downstream proteins was quantified by Western blotting. The effects of the drug combination in vivo were assessed using a CAL-27 heterotopic xenograft model.ResultsEVO and GEM had synergistic effects on CAL-27 and Tca8113 cell lines in time- and concentration-dependent manners. Combination of drugs inhibited cell proliferation and migration and reduced the expression of NF-κB p65, B cell lymphoma 2 (Bcl-2), and B cell lymphoma extra large (Bcl-xl) compared with the control and either drug alone. In vivo, combination treatment of the xenograft model with EVO and GEM led to a significant reduction in tumor volume growth and inhibited the activation of NF-κB p65 with no obvious adverse reactions.ConclusionThe results of this study showed that EVO may inhibit cancer cells by suppressing NF-κB activity, and in combination with GEM, it may increase the chemosensitivity of tongue squamous cancer cells, thereby improving the treatment response.

LIRA can enhance the proliferation, migration, and osteogenic differentiation of hPDLCs and inhibit the inflammatory response. Thus, LIRA may have potential therapeutic use as an adjuvant treatment for human periodontitis, and this effect is independent of hypoglycemic activity.

The survival rates associated with Wilms tumour (WT) remain dismal despite advancements in detection and treatment strategies. Cancer stem cells (CSCs) are correlated with the initiation, recurrence and metastasis of tumours, but its impact on Wilms cancer stem cell (WCSC) maintenance remains unclear. In this study, CD133+ cells were successfully isolated from a single-cell suspension of the G401 Wilms tumour cell line using magnetic activated cell sorting (MACS). Signal transducers and activators of transcription 3 (STAT3) has been implicated in tumorigenesis, but its contribution to the metastatic progression of WCSCs has not been investigated. Here, we show that STAT3 is overexpressed in WCSCs. Activation of STAT3 in WCSCs initiated a forward feedback loop that was responsible for mediating the aggressive malignant character of Wilms tumour cells in vitro and in vivo. Treatment of CD133+ cells with stattic, a STAT3 inhibitor, also inhibited tumour formation and progression in xenograft animal models in vivo. Collectively, these studies revealed a critical role of STAT3 signalling in WCSC proliferation and motility and a role for CD133 in cancer stem-like cell function, providing evidence for CD133 as a potential therapeutic target in Wilms tumour.

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