No abstract

T-box transcription factor 5 (TBX5), a member of the conserved T-box transcription factor family that functions in organogenesis and embryogenesis, has recently been identified as a critical player in cancer development. The aim of this study was to determine the role of TBX5 in non-small cell lung carcinoma (NSCLC). Immunohistochemistry was used to detect the correlation between levels of TBX5 and clinicopathological features of NSCLC patients in tissue microarray. Expression of TBX5 in NSCLC tissues and cell lines was evaluated by quantitative PCR and Western blot. The role of TBX5 in regulating proliferation, colony formation, invasion, and apoptosis of NSCLC cells was evaluated in vitro. Finally, a tumorigenicity assay was performed to determine the effect of TBX5 on tumor growth in vivo. The levels of TBX5 in NSCLC tissues were significantly correlated with the TNM stage (p = 0.016), histopathologic type (p = 0.029), and lymph node status (p = 0.035) of NSCLC. TBX5 overexpression markedly suppressed in vitro NSCLC cell proliferation, colony formation, and invasion and induced apoptosis. In vivo tumor growth was significantly suppressed by TBX5. TBX5 has a tumor-suppressing effect in NSCLC and may serve as a therapeutic target for diagnoses and treatment of NSCLC.

This study identifies the active ingredients of Ferula sinkiangensis and investigates the role and mechanism of episamarcandin in colon cancer cells. The silica gel column chromatography was utilized to separate the chemical components of Ferula sinkiangensis. Sephadex LH-20 and semipreparative HPLC were adopted for further separation and purification. The compound episamarcandin showed good anticolon cancer activity among the 13 monomeric compounds obtained. Its effects on the apoptosis, cell cycle, and invasion and migration of colon cancer HCT 116 cells and PI3K-Akt signaling pathway were further investigated. The results showed that, similar to positive control cisplatin, episamarcandin inhibited the proliferation, promoted the apoptosis, arrested cells at G0/G1 phase, and suppressed migration and invasion of HCT 116 cells. A large number of apoptotic HCT 116 cells were observed under a transmission electron microscope. Fluorescence real-time quantitative PCR and western blot analysis showed that episamarcandin increased the expression of PTEN, p53, and Bax and decreased the expression of P-Akt, Akt, mTOR, Bcl-xl, and Bcl-2. Conclusively, episamarcandin may inhibit cell proliferation, migration, and invasion and promote the apoptosis of human colon cancer HCT 116 cells possibly through the PI3K-Akt signaling pathway.

Ferula akitschkensis volatile oil (FAVO) has a good inhibitory activity on gastric cancer cell proliferation, but the mechanism of action is not yet clear. In this study, we tested the antigastric cancer efficacy and mechanism of FAVO using both in vivo and in vitro models. The results showed that FAVO effectively inhibited the proliferation, migration, and invasion of human gastric cancer SGC-7901 cells, the formation of small tubules of human umbilical vein endothelial cells as well as zebrafish intersegmental vessel and intestinal vein angiogenesis. In vivo experiments showed that FAVO significantly delayed the growth of SGC-7901 tumor-bearing nude mice and induced higher serum IL-2 and IFN-γ and reduced serum IL-6. Western blot results showed that FAVO reduced the expression of HIF-2α, VEGF, VEGFR2, P-VEGFR2, Akt, and P-Akt in SGC-7901 cells with CoCl2 induced hypoxia. We further clarified the main chemical components of FAVO through GC-MS analysis. In summary, FAVO may inhibit tumor growth and angiogenesis via inhibiting the HIF-2α/VEGF signaling pathway.