High miR-3650 expression in nasopharyngeal carcinoma and its clinical prognostic values.

BACKGROUND: A recent study has reported that miR-3650 expression was significant reduced in hepatocellular carcinoma and predicted poor prognosis. However, the role of miR-3650 in nasopharyngeal carcinoma (NPC) remains indefinite. METHODS: Total 140 cases of NPCs were included in this study. The expression of miR-3650 was determined in NPC tissues and adjacent nontumor tissues using qRT-PCR. Then the relationship between miR-3650 expression and clinicopathological features as well as survival were analyzed. RESULTS: The expression of miR-3650 was significant higher in NPC tissues than that in adjacent nontumor tissues (P < 0.001). High expression of miR-3650 was significant correlated with tumor progression and distant metastasis of NPC patients. And patients with high miR-3650 expression have much worse 5-year overall survival (OS) and 5-year progression-free survival (PFS) than those with low expression (all P < 0.0001). Furthermore, Cox regression analysis showed that miR-3650 was an independent risk predictor for OS and PFS in NPC patients (all P = 0.000). CONCLUSION: Our results demonstrated for the first time that miR-3650 was markedly upregulated in NPC tissues and positively associated with tumor progression and poor survival, suggesting that miR-3650 may be a potential novel prognostic biomarker and therapeutic target for NPC patients.

Discovery of dihydro-ß-agarofurans from Tripterygium wilfordii with their H2O2-induced SH-SY5Y cell protective effects.

Chemical investigations of the 75% EtOH extract of the leaves of Tripterygium wilfordii obtained five undescribed naturally occurring sesquiterpenes with dihydro-ß-agarofuran skeleton, tripteresters A-E (1-5), along with eight known analogues (6-13). Their chemical structures were elucidated by a combination of spectroscopic the comprehensive spectroscopic analyses, electronic circular dichroism (ECD) exciton chirality, and quantum chemical calculations ECD. In the bioactivity assay, their neuroprotective properties against hydrogen peroxide (H2O2)-induced oxidative damage in human neuroblastoma SH-SY5Y cells were investigated, and compounds 4, 8, and 12 revealed moderate protective activity at a concentration of 12.5 µM.

Dihydro-ß-agarofuran sesquiterpenoid derivatives with neuroprotective activity from the leaves of Tripterygium wilfordii.

A phytochemical investigation on the leaves of Tripterygium wilfordii Hook. F. was conducted, leading to the isolation of five undescribed dihydro-ß-agarofuran sesquiterpenoids (1-5) and one known analogue (6). Their structures were determined by comprehensive spectroscopic analyses. The absolute configurations of the compounds were determined by comparison of the experimental ECD with the calculated data. In addition, all the compounds were evaluated for their neuroprotective activities against H2O2-induced cell injury in human neuroblastoma SH-SY5Y cells, and 3 showed the better protective effect with 76.63% cell viability comparing with the positive control Trolox (69.84%) at 12.5 µM.

Tripterfordins A-O, Dihydro-ß-agarofuran Sesquiterpenoids from the Leaves of Tripterygium wilfordii.

Fifteen new dihydro-ß-agarofuran-type sesquiterpenoids, tripterfordins A-O, were obtained from the aqueous EtOH extracts of the leaves of Tripterygium wilfordii. These constituted a class of highly oxygenated tricyclic sesquiterpenoid polyesters with a cinnamoyloxy group at C-1. The assignments of their structures were conducted via extensive analyses of the spectroscopic data and comparison of experimental and calculated ECD data. The absolute configurations of compounds 1, 4, 9, and 10 were established via single-crystal X-ray diffraction data. Additionally, compounds 1, 4, 9, 10, and 13 exhibited pronounced inhibitory effects on nitric oxide production in RAW 264.7 murine macrophages stimulated by lipopolysaccharide with IC50 values ranging from 11.9 to 31.0 µM.

Dihydro-ß-agarofuran sesquiterpenoid derivatives with anti-inflammatory activity from the leaves of Tripterygium wilfordii.

Triptersinoids A-E (1-5), five undescribed highly oxygenated dihydro-ß-agarofuran type sesquiterpenoid polyesters, along with three known analogues were isolated from the aqueous EtOH extracts of the dried leaves of Tripterygium wilfordii. Spectroscopic techniques were used for the elucidation of their chemical structures, and the absolute configurations determined by means of electron circular dichroism (ECD) studies, including octant rule of saturated cyclohexanone and comparison between the experimental and calculated ECD data. These compounds were evaluated for the anti-inflammatory activities against lipopolysaccharide (LPS)-induced nitric oxide (NO) production in RAW 264.7 macrophages, and 1α,2α,8ß,15-tetraacetoxy-9α-benzoyloxyl-15-nicotinoyloxy-ß-dihydroagarofuran (7) and angulateoid B (8) showed potential inhibitory effects with IC50 values of 17.30 ±â€¯1.07 µM and 20.79 ±â€¯1.55 µM.

LINC01133 as ceRNA inhibits gastric cancer progression by sponging miR-106a-3p to regulate APC expression and the Wnt/ß-catenin pathway.

BACKGROUND: Gastric cancer (GC) is a common malignancy and frequent cause of cancer-related death. Long non-coding RNAs (lncRNAs) have emerged as important regulators and tissue-specific biomarkers of multiple cancers, including GC. Recent evidence has indicated that the novel lncRNA LINC01133 plays an important role in cancer progression and metastasis. However, its function and molecular mechanism in GC remain largely unknown. METHODS: LINC01133 expression was detected in 200 GC and matched non-cancerous tissues by quantitative reverse transcription PCR. Gain- and loss-of-function experiments were conducted to investigate the biological functions of LINC01133 both in vitro and in vivo. Insights into the underlying mechanisms of competitive endogenous RNAs (ceRNAs) were determined by bioinformatics analysis, dual-luciferase reporter assays, quantitative PCR arrays, TOPFlash/FOPFlash reporter assay, luciferase assay, and rescue experiments. RESULTS: LINC01133 was downregulated in GC tissues and cell lines, and its low expression positively correlated with GC progression and metastasis. Functionally, LINC01133 depletion promoted cell proliferation, migration, and the epithelial-mesenchymal transition (EMT) in GC cells, whereas LINC01133 overexpression resulted in the opposite effects both in vitro and in vivo. Bioinformatics analysis and luciferase assays revealed that miR-106a-3p was a direct target of LINC01133, which functioned as a ceRNA in regulating GC metastasis. Mechanistic analysis demonstrated that miR-106a-3p specifically targeted the adenomatous polyposis coli (APC) gene, and LINC01133/miR-106a-3p suppressed the EMT and metastasis by inactivating the Wnt/ß-catenin pathway in an APC-dependent manner. CONCLUSIONS: Our findings suggest that reduced expression of LINC01133 is associated with aggressive tumor phenotypes and poor patient outcomes in GC. LINC01133 inhibits GC progression and metastasis by acting as a ceRNA for miR-106a-3p to regulate APC expression and the Wnt/ß-catenin pathway, suggesting that LINC01133 may serve as a potential prognostic biomarker and anti-metastatic therapeutic target for GC.

Predictive Value of LINC01133 for Unfavorable Prognosis was Impacted by Alcohol in Esophageal Squamous Cell Carcinoma.

BACKGROUND/AIMS: Considerable evidence indicates that long noncoding RNAs (lncRNAs) exert importantly regulatory functions during human cancer initiation and progression and are promising biotargets in the flight against cancer. METHODS: In this study, we evaluated the role of the lncRNA LINC01133 in esophageal squamous cell carcinoma (ESCC). LINC01133 expression in ESCC was examined by quantitative real-time PCR. The correlations between LINC01133 expression and clinicopathological variables and survival were examined by the χ2 test, Kaplan-Meier method, log-rank test, and univariate Cox regression analysis. RESULTS: LINC01133 expression levels were frequently lower in ESCC tissues and cell lines than in paired normal tissues and an immortalized esophageal epithelial cell line, respectively. The expression of LINC01133 decreased in a TNM stage- and lifestyle-independent manner. LINC01133 was an independent protective factor and had an anti-tumor effect in the early stage of ESCC development. More importantly, we discovered that drinking status in our cohort impaired the predictive accuracy of LINC01133 for patients with ESCC. Furthermore, a new risk model combining LINC01133 expression, drinking status, and TNM stage provided better survival discrimination compared with three other predictors. CONCLUSIONS: Our data indicate that a loss of LINC01133 expression is a potential poor prognostic biomarker and therapeutic target for ESCC and provide additional prognostic information to improve the outcomes of ESCC patients.

Synergistic antitumor effects of liposomal honokiol combined with cisplatin in colon cancer models.

Honokiol, a novel antitumor agent, may induce apoptosis and inhibit the growth of vascular endothelium in a number of tumor cell lines and xenograft models. It has been proposed that the antitumor effects of chemotherapy may be increased in combination with an antiangiogenesis agent as an anticancer strategy. In the present study, we examined the potential of honokiol to increase the antitumor effect of cisplatin (DDP) when the agent and drug were combined in murine CT26 colon cancer models, and investigated the underlying mechanism. Liposomal honokiol (LH) was prepared, and female BALB/c mice were administered LH at various doses to determine the optimum doses for honokial. Evaluation of cell apoptosis was analyzed using flow cytometry. Honokiol was encapsulated with liposome to improve its water insolubility. In vitro, LH inhibited the proliferation of CT26 cells via apoptosis and significantly enhanced the DPP-induced apoptosis of CT26 cells. In vivo, the systemic administration of LH plus DDP resulted in the inhibition of subcutaneous tumor growth beyond the effects observed with either LH or DDP alone. This growth reduction was associated with elevated levels of apoptosis (TUNEL staining) and reduced endothelial cell density (CD31 staining) compared with either treatment alone. Collectively, these findings indicate that LH may augment the induction of apoptosis in CT26 cells in vitro and in vivo, and this combined treatment has exhibited synergistic suppression in tumor progression according to the synergistic analysis. The present study may be significant to future exploration of the potential application of the combined approach in the treatment of colon cancer.