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Context: Hydrogen sulfide gas poses significant risks to both human health and the environment, with the potential to induce respiratory and neurological effects, and a heightened fatality risk at elevated concentrations. This article investigates the catalytic decomposition of H2S on a Sc-Ti3C2O2 single-atom catalyst(SAC) using the density functional theory-based first-principles calculation approach. Initially, the adsorption behavior of H2S on Ti3C2O2-MXene was examined, revealing weak physical adsorption between them. Subsequently, the transition metal atom Sc was introduced to the Ti3C2O2 surface, and its stability was studied, demonstrating high stability. Further exploration of H2S adsorption on Sc-Ti3C2O2 revealed direct dissociation of H2S gas molecules into HS* and H*, with HS* binding to Sc and H* binding to O on the Ti3C2O2 surface, resulting in OH groups. Using the transition state search method, the dissociation of H2S molecules on the SAC's surface was investigated, revealing a potential barrier of 2.45 eV for HS* dissociation. This indicates that the H2S molecule can be dissociated into H2 and S with the action of the Sc-Ti3C2O2 SAC. Moreover, the S atom left on the catalyst surface can aggregate to produce elemental S8, desorbing on the catalyst surface, completing the catalytic cycle. Consequently, the Sc-Ti3C2O2 SAC is poised to be an efficient catalyst for the catalytic decomposition of H2S. Methods: The Dmol3 module in Materials Studio software based on density functional theory is used in this study. The generalized gradient approximation method GGA-PBE is used for the exchange–correlation function. The complete LST/QST and the NEB methods in the Dmol3 module were used to study the minimum energy path of the dissociation of hydrogen sulfide molecules on the catalyst surface. [ABSTRACT FROM AUTHOR]

Background: Endometrial carcinoma (EC) is one of the major gynecologic malignancy cancers affecting females with dismal prognosis and high mortality around the world. Numerous studies have proven that an aberrant level of long noncoding RNAs is present in many endometrial cancer patients, while the underlying molecular mechanism remains unclear.Method: The expression levels of lncRNA OIP5-AS1, miR200c-3p, and PTEN were measured by a quantitative real-time polymerase chain reaction in endometrial cancer tissue and endometrial cancer cells. CCK8 assay, wound-healing assay, and cell colony formation were applied to evaluate cell proliferation, cell migration, and cell colony formation ability. Cell cycle and cell apoptosis were detected by flow cytometry. The interactions between OIP5-AS1, miR200c-3p, and PTEN were explored by luciferase activity.Results: In the present study, we demonstrated that long noncoding RNA OIP5-AS1 was significantly reduced in EC tissue compared with normal tissue. The lower expression level of OIP5-AS1 was also confirmed in four kinds of EC cell lines compared with the normal endometrial cell line. Gain- and loss-of-function of experiments indicated that upregulation of OIP5-AS1 could inhibit the proliferation, migration, and invasion of EC cells in vitro. Meanwhile, overexpression of OIP5-AS1 could also suppress the growth of tumor in the xenograft model. Moreover, further study revealed that miR-200c-3p could bind to OIP5-AS1, and the loss function of miR-200c-3p could reverse the elevated OIP5-AS1's inhibitory effect on the progression of EC. Furthermore, we found that downregulation of miR-200c-3p was inversely correlated with PTEN expression in EC cells. Reduced OIP5-AS1 could lead to the accumulation of miR-200c-3p, which could induce the upregulation of PTEN indirectly.Conclusion: Our study demonstrated a novel molecular mechanism that lncRNA OIP5-AS1 could modulate the progression of EC by combining competitively with miR-200c-3p to control the PTEN/AKT pathway in EC cells, which might supply important information for developing novel therapeutic strategies for EC patients. [ABSTRACT FROM AUTHOR]

Endometrial cancer is a common gynaecological malignant tumour among women across the world. Circular RNAs (circRNAs) are a novel kind of non‐coding RNAs, and they can play a crucial role in multiple cancers. Nevertheless, the mechanisms of circRNAs in regulating gene expression in endometrial cancer are still unclear. Here, our work sought to focus on the role that circ_0067835 exert in progression and development of endometrial cancer cells. We observed circ_0067835 was markedly elevated in endometrial cancer. Then, changes in endometrial cancer cell (RL95‐2 and HEC‐1B) function were determined after circ_0067835 knockdown. Loss‐of‐functional assays revealed that circ_0067835 down‐regulation significantly repressed RL95‐1 and HEC‐1B cell proliferation, migration and invasion. Bioinformatics analysis, luciferase reporter experiment and RNA pull‐down assay were employed to predict and validate circ_0067835 can bind to miR‐324‐5p. Increase in miR‐324‐5p remarkably depressed the proliferation, migration and invasion of endometrial cancer cells via inhibiting high mobility group A1 (HMGA1). HMGA1 is identified as a vital prognostic biomarker in endometrial cancer. Currently, we reported circ_0067835 was positively correlated with HMGA1 in endometrial cancer. We implied that circ_0067835 was capable of sponging miR‐324‐5p and inducing its downstream target HMGA1 in vitro and in vivo. In conclusion, circ_0067835 can compete with miR‐324‐5p, resulting in HMGA1 up‐regulation, and therefore induce the development of endometrial cancer. [ABSTRACT FROM AUTHOR]

Purposes: To measure expression levels of CD47 during endometrial carcinoma development, and to determine specific modulatory effects. Methods: CD47 expression levels in endometrial carcinoma tissues and adjacent tissues were analyzed using qRT-PCR. CD47-overexpressed or downregulated cell models were established using CD47 plasmid or CD47 shRNA. The effects of CD47 on HEC-1A and Ishikawa cell growth were evaluated using CCK-8 assays. Migration ability of transfected HEC-1A and Ishikawa cells were examined using wound healing assays. Flow cytometry was used to measure the effects of CD47 on apoptosis and the cell cycle in HEC-1A and Ishikawa cells. Western blot was used to analyze the correlation between CD47 expression level and PI3K/Akt/mTOR signaling pathway. Results: Highly expressed CD47 was observed in endometrial carcinoma tissues, with higher levels in more advanced tissues than in early tissues. Upregulation of CD47 enhanced cell viability and migration ability in HEC-1A and Ishikawa cells, while silencing CD47 caused the opposite results. CD47 overexpression suppressed apoptosis and inhibited cell cycle arrest in HEC-1A and Ishikawa cells. CD47 upregulation contributes to the activation of PI3K/Akt/mTOR signaling pathway in endometrial carcinoma cells. Conclusion: CD47 exerts oncogenic functions in endometrial carcinoma by activating PI3K/Akt/mTOR signaling, suggesting it may be a novel immunotherapeutic target for therapeutic interventions. [ABSTRACT FROM AUTHOR]

The introduction also contains an annotated bibliography of Feng's writings, translations of his other works, and several translations of the key sources to which Feng referred. It is also regrettable that Milburn does not address how Feng reconciles inconsistencies among his sources or her reasons for selecting these nine stories from the text's forty or fifty. She showcases how Feng's hometown, scholarly background, and contemporary political events (e.g. the decline of the Ming dynasty) may have influenced the novel. [Extracted from the article]

• hsa_circ_0061140 was up-regulated in EC. • hsa_circ_0061140 induced EC progression via sponging miR-149-5p. • STAT3 acted as a target of miR-149-5p. Circular RNAs (circRNAs) are reported to participate in many diseases including tumorigenesis, which can modulate gene expression post-transcriptionally. Up to now, the detailed function of circRNAs in endometrial carcinoma (EC) progression are to be well established. hsa_circ_0061140 has been revealed to act as crucial regulators in several cancers. This current study was carried out to explore the function of hsa_circ_0061140 in EC development. Here, hsa_circ_0061140 expression was modulated using functional assays and we found loss of hsa_circ_0061140 significantly restrained EC cells progression. Moreover, we revealed hsa_circ_0061140 could act as a molecular sponge for miR-149-5p. STAT3 was predicted as a downstream target gene of miR-149-5p. As well known, miR-149-5p is reported to be involved in tumor growth and metastasis. Then, dual luciferase reporter experiment and RIP assay were carried out to evidence the direct binding association between hsa_circ_0061140 and miR-149-5p. miR-149-5p was able to negatively modulate STAT3 expression. Additionally, we proved hsa_circ_0061140 exhibited its oncogenic role due to the modulation of miR-149-5p and STAT3 axis. Taken these together, we suggested that hsa_circ_0061140 might act as an effective therapy to treat EC through functioning as a molecular sponge of miR-149-5p. [ABSTRACT FROM AUTHOR]