Novel MoS2/montmorillonite hybrid aerogel encapsulated PEG as composite phase change materials with superior solar-thermal energy harvesting and storage.

Phase change materials (PCMs) offer significant advantages in energy conversion and storage by facilitating the storage and release of thermal energy during phase transition processes. However, challenges such as leakage during PCM phase transitions and poor light absorption properties have constrained their application in the field of photothermal energy storage. In this study, Montmorillonite (Mt) and molybdenum disulfide (MoS2) has been used to design and synthesize hybrid aerogels (MoS2/Mt) boasting high mechanical strength and excellent photothermal conversion performance. These aerogels are then used to encapsulate polyethylene glycol (PEG) to prepare composite PCMs with outstanding solar-thermal conversion and storage performances. The results show that the synthesized MoS2/Mt-PEG composite PCMs exhibit high enthalpies of melting and solidification of 169.16 J/g and 170.78 J/g, respectively, while the aerogel supporting material has a high compressive modulus of 1.96 MPa. Moreover, the composite material displayed excellent thermal stability and leakage resistance after undergoing 30 melting-cooling cycles. Furthermore, the incorporation of MoS2 imparted outstanding light absorption properties to the MoS2/Mt-PEG composite, resulting in a high light absorption and photothermal conversion-storage efficiency of 93.4 % and 96.47 %, respectively. Synthesized composite PCMs also demonstrate outstanding performance in solar-thermal-electricity conversion, achieving a voltage output of 458 mV under illumination conditions and maintaining a sustainable voltage output even after removing the light source. Thus, the composite PCMs prepared in this work can meet the requirements of high enthalpy, effective leakage prevention, efficient solar-thermal conversion and solar-thermal-electricity conversion performance, thereby presenting potential applications in practical solar energy collection, conversion, and storage.

Crocin Combined With Cisplatin Regulates Proliferation, Apoptosis And Emt Of Gastric Cancer Cells Via The Fgfr3/Mapk/Erk Pathway In Vitro And In Vivo.

INTRODUCTION: Cisplatin (DDP)-based chemotherapy remains the main therapeutic strategy for human gastric cancer (GC). Combination therapy with Chinese medicine monomers and DDP has been investigated as a means to enhance the anti-tumor effect of DDP while reducing toxicity. METHOD: Previous studies have shown that crocin combined with DDP can inhibit the apoptosis of BG-823 GC cells; however, the mechanism of this combination therapy in inhibiting GC is not fully unclear. In this study, we measured the IC50 values of crocin combined with DDP in AGS cells and assessed its effect on cell proliferation using an MTT assay. Furthermore, we assessed apoptosis, cell migration, and EMT-related protein levels by using flow cytometry, scratch assay, and Western blotting, respectively. Our results showed that crocin combined with DDP inhibited the proliferation, induced apoptosis, and inhibited invasion and EMT. Next, we performed RNA sequence and KEGG enrichment analysis on GC cells treated with Crocin+DDP. RESULTS: The results showed that the most significant factor down-regulated by this combination therapy was Fibroblast growth factor receptor 3 (FGFR3) expression and that a differential gene was enriched in the MAPK/ERK pathway. We further constructed an FGFR3 OE transfection plasmid to overexpress FGFR3 and evaluate its effects on proliferation, apoptosis, migration, EMT, and MAPK/ERK pathway proteins in GC cells. We also conducted subcutaneous tumorigenesis experiments in nude mice to evaluate the effects of crocin and DDP on the progression of GC xenografts in vivo. Finally, we performed a rescue experiment using the MAPK/ERK pathway inhibitor PD184352. CONCLUSION: Our results showed that up-regulation of FGFR3 reversed the inhibitory effect of crocin+DDP on the MAPK/ERK signaling pathway. Still, this effect could be counteracted by PD184352, which simultaneously regulated the proliferation, apoptosis, and EMT of AGS cells. In conclusion, crocin, combined with DDP, inhibits proliferation, apoptosis, and EMT of GC through the FRFR3/MAPK/ERK pathway.

Integrated pan-cancer analysis and experimental verification of the roles of tropomyosin 4 in gastric cancer.

Objective: To investigate the function of tropomyosin 4 (TPM4) using pan-cancer data, especially in gastric cancer (GC), using comprehensive bioinformatics analysis and molecular experiments. Methods: We used UCSC Xena, The Cancer Genome Atlas (TCGA), Genotype-Tissue Expression Project (GTEx), TIMER2.0, GEPIA, cBioPortal, Xiantao tool, and UALCAN websites and databases for the extraction of pan-cancer data on TPM4. TPM4 expression was investigated with respect to prognosis, genetic alterations, epigenetic alterations, and immune infiltration. RNA22, miRWalk, miRDB, Starbase 2.0, and Cytoscape were used for identifying and constructing the regulatory networks of lncRNAs, miRNAs, and TPM4 in GC. Data from GSCALite, drug bank databases, and Connectivity Map (CMap) were used to analyze the sensitivity of drugs dependent on TPM4 expression. Gene Ontology (GO), enrichment analyses of the Kyoto Encyclopedia of Genes and Genomes (KEGG), wound healing assays, and (Matrigel) transwell experiments were used to investigate the biological functions of TPM4 in GC. Result: The findings of the comprehensive pan-cancer analysis revealed that TPM4 has a certain diagnostic and prognosis value in most cancers. Alterations in the expression of TPM4, including duplications and deep mutations, and epigenetic alterations revealed that TPM4 expression is related to the expression of DNA methylation inhibitors and RNA methylation regulators at high concentrations. Besides, TPM4 expression was found to correlate with immune cell infiltration, immune checkpoint (ICP) gene expression, the tumor mutational burden (TMB), and microsatellite instability (MSI). Neoantigens (NEO) were also found to influence its response to immunotherapy. A lncRNA-miRNA -TPM4 network was found to regulate GC development and progression. TPM4 expression was related to docetaxel,5-fluorouracil, and eight small molecular targeted drugs sensitivity. Gene function enrichment analyses revealed that genes that were co-expressed with TPM4 were enriched within the extracellular matrix (ECM)-related pathways. Wound-healing and (Matrigel) transwell assays revealed that TPM4 promotes cell migration and invasion. TPM4, as an oncogene, plays a biological role, perhaps via ECM remodeling in GC. Conclusions: TPM4 is a prospective marker for the diagnosis, treatment outcome, immunology, chemotherapy, and small molecular drugs targeted for pan-cancer treatment, including GC treatment. The lncRNA-miRNA-TPM4network regulates the mechanism underlying GC progression. TPM4 may facilitate the invasion and migration of GC cells, possibly through ECM remodeling.

Role of CD4+T, CD8+T Cells, and CD4+T/CD8+T Cell Ratio in Gastric Cancer and Its Clinical Significance.

Objective: To study the expression and clinical importance of CD4+T, CD8+T cells, and CD4+T/CD8+T cell percentage in gastric cancer (GC) patients. Methods: The blood count of CD4+T and CD8+T lymphocytes was ascertained via flow cytometry before surgery in 93 GC patients undergoing gastrectomy. The CD4+T, CD8+T, and Foxp3+T lymphocytes in cancerous and normal adjacent tissues and the presence of PD-L1 in cancerous tissues were detected via immunohistochemistry. The link between the permeation of CD4+T, CD8+T lymphocytes in venous blood, and cancer and normal adjacent tissues was analyzed. Results: Lauren histotype, TNM stage, lymphatic/nervous invasion, and NLR level were all considerably associated with peripheral CD4+T and CD8+T cell levels, whereas CD8+T lymphocytes were also associated with vascular invasion (p < 0.05). The CD4+T lymphocyte counts, CD4+T, and CD8+T cell percentage in GC tissues were found to have been decreased when compared to normal adjacent tissues, whereas the CD8+T and Foxp3+T lymphocyte count was higher in GC tissues (p < 0.05). According to a Spearman analysis, the CD4+T and CD8+T cell counts in tumor tissues were positively related to the Foxp3+T lymphocyte count (p < 0.05). Greater peripheral CD4+T lymphocyte counts and increased level of CD4+T/CD8+T percentage corresponded with greater CD4+T cell levels and increased CD4+T/CD8+T quantity in normal adjacent tissues. Higher levels of peripheral CD8+T cells corresponded with higher quantities of CD8+T cells in cancer tissues. A reduced CD4+T lymphocyte count, together with a reduced CD4+T/CD8+T percentage in venous blood, was consistent with a diminished CD4+T cell count along with a reduced CD4+T/CD8+T lymphocyte ratio in cancer and normal adjacent tissues. Conclusion: The peripheral quantity of CD4+T and CD8+T lymphocytes in GC patients can partly reflect the infiltrating state of these lymphocytes in cancer and normal adjacent tissues and can preliminarily predict immunotherapy response to a certain extent.

Expression and clinical prognostic value of CYB561 in breast cancer.

PURPOSE: The expression of cytochrome B561 (CYB561) and its role in breast cancer (BC) prognosis remain unclear. We analyzed the differential expression and prognostic value of CYB561 using online databases and a clinical cohort through bioinformatics and immunohistochemistry. METHODS: The differential expression of CYB561 and its association with BC were analyzed using the tumor immune estimation resource (TIMER), gene expression profiling interaction analysis2 (GEPIA2), Human Protein Atlas, Cancer Cell Line Encyclopedia, and Kaplan-Meier Plotter website. Important pathways of CYB561 enrichment were explored using gene set enrichment analysis. Immunohistochemistry detected CYB561 expression in normal breast, breast hyperplasia, ductal carcinoma in situ (DCIS), para-cancer, and invasive BC groups. Association between CYB561 expression and BC prognosis was analyzed using Kaplan-Meier and Cox regression analyses. RESULTS: CYB561 mRNA expression was higher in GEPIA and TIMER BC patients than in para-cancer tissues. CYB561 was expressed in the glandular epithelium and myoepithelium, with positive localization in the cytoplasm and cell membrane. CYB561 protein expression significantly differed among the groups. CYB561 expression was correlated with ERBB2/HER2 and infiltrating CD4+ T cells in GEPIA and TIMER BC patients and associated with HER2 status, histological grade, and molecular subtypes in the clinical cohort but not related to tumor-infiltrating lymphocytes. CYB561 mRNA overexpression predicted reduced recurrence-free survival and overall survival in BC. Patients with CYB561 expression had significantly reduced overall survival and increased risk of death. CONCLUSION: CYB561 can serve as an effective clinical prognostic biomarker for BC.

Ginsenoside Rh2 Suppresses Metastasis and Growth of Colon Cancer via miR-491.

Ginsenoside Rh2 is considered as a new direction for future cancer treatment because of its excellent anticancer effect. However, due to its low bioavailability, it cannot exert its significant anticancer effect when applied directly to the human body. Chitosan (CS), a nanomaterial, has been verified to be able to enhance drug efficacy via its coating for drugs. Thus, we designed this study to investigate the impact of CS-coated ginsenoside Rh2 on the metastasis and growth of colon cancer (CC). First, ginsenoside Rh2 chitosan tripolyphosphate (CS-Rh2-TPP) nanoparticles (NPs) were constructed, and MTT, transwell, scratch adhesion, and flow cytometry assays were carried out for determining the impact of CS-Rh2-TPP at various concentrations on growth, metastasis, and apoptosis of colon cancer cells (CCCs). qRT-PCR was used to detect the expression of mircoRNA-491 (miR-491) in CCCs. According to TEM-based image analysis, CS-Rh2-TPP NPs were spherical or spheroidal in even distribution, with a particle size of about 220 mm and a zeta potential of -44.58 ± 2.84 mV. Additionally, CCCs presented lower miR-491 than normal colon cells, and its relative expression in CCCs showed a stronger increase after intervention of CS-Rh2-TPP than that after intervention of ginsenoside Rh2. Moreover, CS-Rh2-TPP suppressed the activity, invasion, as well as migration of CCCs and accelerated their apoptosis more significantly than ginsenoside Rh2. According to these results, CS-Rh2-TPP is able to upregulate miR-491 in CCCs, thus suppressing the metastasis and growth of CC.

Efficacy and Safety of Apatinib for Elderly Patients with Advanced or Metastatic Gastric Cancer After Failure of at Least First-Line Chemotherapy: A Multi-Center, Single-Arm, Phase II Study.

BACKGROUND: Apatinib improves progression-free survival and overall survival with an acceptable safety profile in Chinese patients with chemotherapy-refractory advanced or metastatic gastric cancer. However, the efficacy and safety of apatinib are unclear for elderly patients. This study was undertaken to prospectively investigate the efficacy and safety of apatinib for elderly patients with unresectable advanced or metastatic gastric cancer, who experienced progression to at least one lines of chemotherapy. METHODS: This open-label, single-arm, phase II study enrolled patients aged ≥60 years with advanced gastric cancer, who experienced progression to one or more lines of chemotherapy at five centers in China. Patients received apatinib in an oral dose of 500mg or 250mg daily according to the research physicians' decision. The primary end point was progression-free survival, and the secondary end points were objective response rate, disease control rate, overall survival, and safety. RESULTS: Forty-eight patients were enrolled between June 2017 and September 2019. The median age was 65.5 years (range 60-80 years). Twenty-seven patients (56.3%) started treatment with an initial dose of 500 mg and 21 patients (43.7%) with 250 mg. The median progression-free survival and overall survival were 3.00 months (95% confidence interval, 2.17-3.84) and 8.10 months (95% confidence interval, 4.35-11.85), respectively. The objective response rate and disease control rate assessed by the investigators were 16.7% and 72.9%, respectively. The common side effects were fatigue (58.3%), hypertension (47.9%), abdominal pain (33.3%), proteinuria (29.2%), leukopenia (22.9%), and neutropenia (20.8%). Hypertension (22.9%) was the major grade 3/4 toxicity. CONCLUSION: These data suggest that apatinib is effective and relatively tolerable for elderly patients with unresectable advanced or metastatic gastric cancer who have received at least first-line chemotherapy.

Inhibitory Effect of Crocin Against Gastric Carcinoma via Regulating TPM4 Gene.

BACKGROUND: Gastric cancer (GC) is one of the most common malignant tumors and the second most frequent cause of cancer death worldwide. Crocin is a kind of bioactive constituent found in the stigmas of saffron, which has shown various pharmacological activities. METHODS: In this study, we investigated the inhibitory effect of crocin on gastric cancer AGS cells proliferation and explored the underlying mechanism. A series of methods were used including cell counting kit assay, gene microarray analysis, qRT-PCR, Celigo image cytometry, cell clone formation assay, Western blot, and cell xenograft growth in vivo. RESULTS: The results indicated that crocin inhibited AGS cells proliferation and promoted cell apoptosis. Further studies suggested that crocin decreased a series of genes expression, among which TPM4 gene downregulation inhibited the tumor cells proliferation and tumor growth in mice, and overexpression of TPM4 gene abolishes the inhibitory effect of crocin. Further study using microarray analysis suggested that knocking down of TPM4 altered genes related to the proliferation and apoptosis of cells. DISCUSSION: Crocin could inhibit the gastric cancer cells AGS cells proliferation by regulating TPM4 gene expression, and TPM4 may be a promising therapeutic target for GC treatment.

Pathogenesis and anti-proliferation mechanisms of Crocin in human gastric carcinoma cells.

Gastric cancer is the fourth most common cause of cancer death globally and the second most common in Asia. Many studies suggest that Crocin has the potential for gastric cancer antineoplastic combined chemotherapy protocols. Here we investigated genomic changes related to the inhibitory effect of Crocin, and elucidated the molecular mechanism of this inhibition in gastric carcinoma cells. We found that, compared with the control group, 216 significantly upregulated and 301 significantly downregulated genes were identified in Crocin-treated AGS cells. Many of these differentially expressed genes in AGS cells are involved in Nrf2-mediated oxidative stress response, p53 signaling, and integrin signaling, which suggested the mechanism of Crocin functions in therapy of gastric cancer. In summary, our study indicates that Crocin has the potential for gastric cancer adjuvant treatment through reducing cell oxidative stress levels.

Facile Preparation of Three-Dimensional MoS2 Aerogels for Highly Efficient Solar Desalination.

Aerogels, with porous channels for water supply and vapor escape, can provide many inherent advantages in solar desalination and wastewater treatment. For the first time, this work demonstrates the preparation of a novel three-dimensional (3D) MoS2-based aerogel with high porosity and mechanical stability by a facile strategy for solar desalination. This 3D MoS2 aerogel has an excellent light-absorbing efficiency of over 95% within the whole solar spectrum range, enabling a high evaporation efficiency of 88.0% under a low solar irradiation of 1.0 kW m-2 and superhigh evaporation efficiencies of over 90% under a slightly enhanced solar irradiation of 1.5-3.0 kW m-2 as well as a remarkable desalination performance. In addition, the excellent mechanical stability of this MoS2 aerogel renders it to be reused for at least 10 cycles with stable water productivity. Because of its 3D architectures with high porosity and easy separation, this MoS2-based aerogel also provides promising applications in solar-driven water purification, sterilization, and so forth.

Knockdown of SETDB1 inhibits breast cancer progression by miR-381-3p-related regulation.

BACKGROUND: SET domain bifurcated 1 (SETDB1) has been widely considered as an oncogene playing a critical role in many human cancers, including breast cancer. Nevertheless, the molecular mechanism by which SETDB1 regulates breast cancer tumorigenesis is still unknown. METHODS: qRT-PCR assay or western blot analysis was performed to assess the expression level of SETDB1 mRNA or protein, respectively. siSETDB1, pCMV6-XL5-SETDB1, miR-381-3p mimic, or miR-381-3p inhibitor was transfected into cells to regulate the expression of SETDB1 or miR-381-3p. MiRNA directly interacted with SETDB1 was verified by luciferase reporter assay and RNA immunoprecipitation. CCK-8 assay, colony formation assay, flow cytometric analysis, and transwell assay were used to detect the abilities of cell proliferation, cell cycle progression and migration, respectively. Animal model of xenograft tumor was used to observe the regulatory effect of SETDB1 on tumor growth in vivo. RESULTS: We verified that SETDB1 mRNA level was upregulated in breast cancer tissues and cell lines, and SETDB1 depletion led to a suppression of cell proliferation, cell cycle progression and migration in vitro, as well as tumor growth in vivo. SETDB1 was verified to be a target of miR-381-3p. Moreover, miR-381-3p overexpression suppressed cell proliferation, cell cycle progression and migration, whereas SETDB1 abated miR-381-3p-mediated regulatory function on breast cancer cells. CONCLUSIONS: This study revealed that SETDB1 knockdown might suppress breast cancer progression at least partly by miR-381-3p-related regulation, providing a novel prospect in breast cancer therapy.

miR-17-92 cluster is connected with disease progression and oxaliplatin/capecitabine chemotherapy efficacy in advanced gastric cancer patients: A preliminary study.

This study aimed to determine the role of plasma miR-17-92 cluster level in predicting chemoresistance in patients with gastric cancer (GC) undergoing oxaliplatin/capecitabine (XELOX) chemotherapy.Patients recently diagnosed with advanced GC were chosen as participants based on the inclusion criteria. The plasma levels of miR-17-5p, miR-18a, miR-19a/b, miR-20a, and miR-92-1 (miR-17-92 cluster) were determined through quantitative RT-PCR of blood samples from GC patients and healthy volunteers. All the patients received XELOX chemotherapy, and the effectiveness of the chemotherapy was evaluated.The miR-17-92 plasma level was increased in advanced GC patients and decreased after XELOX chemotherapy. Moreover, the miR-17-92 cluster level was associated with chemotherapy response but not with chemotherapy-related toxicity. The miR-17-92 cluster plasma level was decreased in chemosensitive patients, but not in chemoresistant patients, after chemotherapy. The sensitivity and specificity of the combined detection of the miR-17-92 cluster in patients with advanced GC were 100% each.The results suggest that the miR-17-92 plasma level is associated with the progression of advanced GC and effectiveness of XELOX chemotherapy.

Knockdown of SETDB1 inhibits breast cancer progression by miR-381-3p-related regulation

BACKGROUND: SET domain bifurcated 1 (SETDB1) has been widely considered as an oncogene playing a critical role in many human cancers, including breast cancer. Nevertheless, the molecular mechanism by which SETDB1 regulates breast cancer tumorigenesis is still unknown. METHODS: qRT-PCR assay or western blot analysis was performed to assess the expression level of SETDB1 mRNA or protein, respectively. siSETDB1, pCMV6-XL5-SETDB1, miR-381-3p mimic, or miR-381-3p inhibitor was transfected into cells to regulate the expression of SETDB1 or miR-381-3p. MiRNA directly interacted with SETDB1 was verified by luciferase reporter assay and RNA immunoprecipitation. CCK-8 assay, colony formation assay, flow cytometric analysis, and transwell assay were used to detect the abilities of cell proliferation, cell cycle progression and migration, respectively. Animal model of xenograft tumor was used to observe the regulatory effect of SETDB1 on tumor growth in vivo. RESULTS: We verified that SETDB1 mRNA level was upregulated in breast cancer tissues and cell lines, and SETDB1 depletion led to a suppression of cell proliferation, cell cycle progression and migration in vitro, as well as tumor growth in vivo. SETDB1 was verified to be a target of miR-381-3p. Moreover, miR-381-3p overexpression suppressed cell proliferation, cell cycle progression and migration, whereas SETDB1 abated miR-381-3p-mediated regulatory function on breast cancer cells. CONCLUSIONS: This study revealed that SETDB1 knockdown might suppress breast cancer progression at least partly by miR-381-3p-related regulation, providing a novel prospect in breast cancer therapy.