Immune Infiltrates of m5C RNA Methylation-Related LncRNAs in Uterine Corpus Endometrial Carcinoma.

Aberrant 5-methylcytidine (m5C) modification plays an essential role in the progression of different cancers. More and more researchers are focusing on developing a lncRNA-based risk model to assess the clinical prognosis of cancer patients. However, the impact of m5C-related lncRNAs on the prognosis of patients with uterine corpus endometrial carcinoma (UCEC), as well as the immune microenvironment of UCEC, remains unclear. Here, we comprehensively analyzed the predictive value of m5C-associated lncRNAs in UCEC and their association with the tumor immune microenvironment, according to the information extracted from the TCGA-UCEC dataset. We identified a total of 32 m5C-associated lncRNAs that were significantly correlated with the prognosis of UCEC patients. Two molecular subtypes were determined by consensus clustering analysis of these 32 m5C-associated prognostic lncRNAs. Further data showed that cluster 1 was associated with poor clinical prognosis, advanced tumor grade, higher PD-L1 expression levels, higher ESTIMATEScore, and higher immuneScore, as well as the immune cell infiltration. Then, 17 m5C-associated lncRNAs with prognostic values were obtained using LASSO regression analysis. And a risk model was constructed based on these 17 lncRNAs. It was revealed that the risk model could be used as an independent factor for UCEC prognosis. In addition, patients with UCEC in the high-risk group had higher tumor grades and immune scores. The risk model based on m5C-related lncRNAs was also closely associated with infiltrating immune cells. In conclusion, our study elucidated the crucial roles of the identified m5C-related lncRNAs in the UCEC patients' prognoses, as well as in the immune microenvironment in UCEC. The results suggest that the components of risk models based on the m5C-related lncRNAs may serve as important mediators of the immune microenvironment in UCEC.

TBL1XR1 induces cell proliferation and inhibit cell apoptosis by the PI3K/AKT pathway in pancreatic ductal adenocarcinoma.

BACKGROUND: Pancreatic ductal adenocarcinoma (PDAC) is one of the deadliest solid tumors. Identification of diagnostic and therapeutic biomarkers for PDAC is urgently needed. Transducin (ß)-like 1 X-linked receptor 1 (TBL1XR1) has been linked to the progression of various human cancers. Nevertheless, the function and role of TBL1XR1 in pancreatic cancers are unclear. AIM: To elucidate the function and potential mechanism of TBL1XR1 in the development of PDAC. METHODS: Ninety patients with histologically-confirmed PDAC were included in this study. PDAC tumor samples and cell lines were used to determine the expression of TBL1XR1. CCK-8 assays and colony formation assays were carried out to assess PDAC cell viability. Flow cytometry was performed to measure the changes in the cell cycle and cell apoptosis. Changes in related protein expression were measured by western blot analysis. Animal analysis was conducted to confirm the impact of TBL1XR1 in vivo. RESULTS: Patients with TBL1XR1-positive tumors had worse overall survival than those with TBL1XR1-negative tumors. Moreover, we found that TBL1XR1 strongly promoted PDAC cell proliferation and inhibited PDAC cell apoptosis. Moreover, knockdown of TBL1XR1 induced G0/G1 phase arrest. In vivo animal studies confirmed that TBL1XR1 accelerated tumor cell growth. The results of western blot analysis showed that TBL1XR1 might play a key role in regulating PDAC cell proliferation and apoptosis via the PI3K/AKT pathway. CONCLUSION: TBL1XR1 promoted PDAC cell progression and might be an effective diagnostic and therapeutic marker for pancreatic cancer.

Catalytic conversion of cellulose to 5-hydroxymethyl furfural using acidic ionic liquids and co-catalyst.

Efficient catalytic conversion of microcrystalline cellulose (MCC) to 5-hydroxymethyl furfural (HMF), is achieved using acidic ionic liquids (ILs) as the catalysts and metal salts as co-catalysts in the solvent of 1-ethyl-3-methylimidazo-lium acetate ([emim][Ac]). A series of acidic ILs has been synthesized and tested in conversion of MCC to HMF. The effect of reaction conditions, such as reaction time, temperature, catalyst dosage, metal salts, water dosage, Cu(2+) concentration and various acidic ILs are investigated in detail. The results show that CuCl(2) in 1-(4-sulfonic acid) butyl-3-methylimidazolium methyl sulfate ([C(4)SO(3)Hmim][CH(3)SO(3)]), is found to be an efficient catalyst for catalytic conversion of MCC to HMF, and 69.7% yield of HMF is obtained. A mechanism to explain the high activity of CuCl(2) in [C(4)SO(3)Hmim][CH(3)SO(3)] is proposed. To the best of our knowledge, this report first proposes that the Cu(2+) and [C(4)SO(3)Hmim][CH(3)SO(3)] show better catalytic performance in catalytic conversion of MCC to HMF.

Theoretical and experimental investigation on dissolution and regeneration of cellulose in ionic liquid.

Density functional theory calculations and atoms in molecules theory were performed to investigate the mechanism of cellulose dissolution and regeneration in 1-ethyl-3-methylimidazolium acetate ([emim]Ac), and (1,4)-dimethoxy-ß-D-glucose (Glc) was chosen as the model for cellulose. The theoretical results show that the interaction of [emim]Ac with Glc is stronger than that of Glc with Glc. Further studies indicate that the anion acetate of [emim]Ac forms strong H-bonds with hydroxyl groups of Glc. It is also observed that the H-bonds between [emim]Ac and Glc are weakened or even destroyed by the addition of water. In addition, both the original and regenerated cellulose samples were characterized with FT-IR, XRD, TGA and SEM. The experimental results prove that cellulose can be readily reconstituted from the [emim]Ac-based cellulose solution by the addition of water and the crystalline structure of cellulose is converted to cellulose II from cellulose I in the original cellulose.