Identification of a lipid homeostasis-related gene signature for predicting prognosis, immunity, and chemotherapeutic effect in patients with gastric cancer.

Gastric cancer (GC) is one of the most common and deadliest cancers worldwide. Lipid homeostasis is essential for tumour development because lipid metabolism is one of the most important metabolic reprogramming pathways within tumours. Elucidating the mechanism of lipid homeostasis in GC might significantly improve treatment strategies and patient prognosis. GSE62254 was applied to construct a lipid homeostasis-related gene signature score (HGSscore) by multiple bioinformatic algorithms including weighted gene coexpression network analysis (WGCNA) and LASSO-Cox regression. A nomogram based on HGSscore and relevant clinical characteristics was constructed to predict the survival of patients with GC. TIMER and xCell were used to evaluate immune and stromal cell infiltration in the tumour microenvironment. Correlations between lipid homeostasis-related genes and chemotherapeutic efficacy were analysed in GSCAlite. RT‒qPCR and cell viability assays were applied to verify the findings in this study. HGSscore was constructed based on eighteen lipid homeostasis-related genes that were selected by WGCNA and LASSO-Cox regression. HGSscore was strongly associated with advanced TNM stage and showed satisfactory value in predicting GC prognosis in three independent cohorts. Furthermore, we found that HGSscore was associated with the tumour mutation burden (TMB) and immune/stromal cell infiltration, which are related to GC prognosis, indicating that lipid homeostasis impacts the formation of the tumour microenvironment (TME). With respect to the GSCAlite platform, PLOD2 and TGFB2 were shown to be positively related to chemotherapeutic resistance, while SLC10A7 was a favourable factor for chemotherapy efficacy. Cell viability assays showed that disrupted lipid homeostasis could attenuate GC cell viability. Moreover, RT‒qPCR revealed that lipid homeostasis could influence expression of specific genes. We identified a lipid homeostasis-related gene signature that correlated with survival, clinical characteristics, the TME, and chemotherapeutic efficacy in GC patients. This research provides a new perspective for improving prognosis and guiding individualized chemotherapy for patients with GC.

Effects of dietary mulberry leaves on growth, production performance, gut microbiota, and immunological parameters in poultry and livestock: a systematic review and meta-analysis.

OBJECTIVE: This study aimed to assess the effects of dietary mulberry leaves on the growth, production performance, gut microbiota, and immunological parameters of poultry and livestock. METHODS: The PubMed, Embase, and Scopus databases were systematically analyzed to identify pertinent studies up to December 2022. The effects of mulberry leaf diet was assessed using the weighted mean difference, and the 95% confidence interval was calculated using a random-effects model. RESULTS: In total, 18 studies that sampled 2,335 poultry and livestock were selected for analysis. Mulberry leaves improved the average daily gain and reduced the feed/meat ratio in finishing pigs, and the average daily gain and average daily feed intake in chicken. In production performance, mulberry leaves lowered the half carcass weight, slaughter rate, and loin eye area in pigs, and the slaughter rate in chickens. Regarding meat quality in pigs, mulberry leaves reduced the cooked meat percentage, shear force, crude protein, and crude ash, and increased the 24 h pH and water content. In chickens, it increased the drip loss, shear force, 45 min and 24 h pH, crude protein, and crude ash. Mulberry leaves also affect the abundances of gut microbiota, including Bacteroides, Prevotella, Megamonas, Escherichia-Shigella, Butyricicoccus, unclassified Ruminococcaceae, Bifidobacterium, Lactobacillus, and Escherichia coli in poultry and livestock. Mulberry leaves at different doses were associated with changes in antioxidant capacity in chickens, and immune organ indexes in pigs. With respect to egg quality, mulberry leaves at different doses improved the shell strength, yolk color, eggshell thickness, and eggshell weight. However, moderate doses diminished the egg yolk ratio and the egg yolk moisture content. CONCLUSION: In general, dietary mulberry leaves improved the growth, production performance, and immunological parameters in poultry and livestock, although the effects varied at different doses.

DDX60 Promotes Migration and Invasion of Head and Neck Squamous Cell Carcinoma Cell through the NF-κB/IFI27 Signaling Pathway.

BACKGROUND: Despite its significance in multiple cancer types. the function and mechanism of DEXD/H box helicase 60 (DDX60) in head and neck squamous cell carcinoma (HNSCC) remain unreported. METHODS: Thirty paired HNSCC tissues and adjoining normal tissues and human normal oral epithelial keratinocytes (HOK) and four HNSCC cells (CAL27, SAS, CAL33, and SCC25) were analyzed for DDX60 expression by Semi-quantitative real-time PCR (SQ RT-PCR) and western blot. To investigate how DDX60 affects HNSCC cell migration and invasion, transwell experiments were performed. The western blot was implemented to understand the interaction among DDX60, Interferon Alpha Inducible Protein 27 (IFI27), and the NF-κB pathway. RESULTS: Results revealed the upregulation of DDX60 in HNSCC cell lines and tissues. Additionally, patients with upregulated DDX60 expression exhibited a dismal prognosis relative to those with downregulated expression. DDX60 enhanced the migration, invasion, and epithelial to mesenchymal transition (EMT) in HNSCC cells. The results from mechanistic studies revealed that DDX60 could promote the IFI27 expression following the activation of NF-κB pathway. CONCLUSION: DDX60 promoted the migratory and invasive capacities of HNSCC cells via the NF-κB/IFI27 axis.

Targeting eIF5A2 reduces invasion and reverses chemoresistance in SCC-9 cells in vitro.

BACKGROUND AND AIMS: Eukaryotic translation initiation factor 5A2 (EIF5A2) has been reported to be involved in metastasis and chemotherapy resistance in many human cancers. However, the effect and mechanism of EIF5A2 in oral cancer cells are unknown. Here, we investigated the effects of targeting EIF5A2 on chemotherapy resistance in oral cancer cells in vitro. METHODS: By using a lentiviral system, we investigated the effects of targeting EIF5A2 on the invasion, migration, growth, and chemosensitivity of SCC-9 cells to CDDP in vitro. Through the method of gene intervention, we explore the role of pro-apoptotic Bim and epithelial and mesenchymal marker E-cadherin protein in this process and the regulation of EIF5A2 on Bim and E-cadherin. RESULTS: Targeting EIF5A2 reduces invasion and migration in SCC-9 cells partly through upregulation of E-cadherin expression; Targeting EIF5A2 promotes cell apoptosis and inhibits cell survival as well as increasing chemosensitivity in SCC-9 cells through upregulation of Bim expression. CONCLUSION: EIF5A2 may be a novel potential therapeutic target for oral cancer by upregulation of Bim and E-cadherin.

Circ_0000140 Alters miR-527/SLC7A11-Mediated Ferroptosis to Influence Oral Squamous Cell Carcinoma Cell Resistance to DDP.

Background: While there is prior evidence for the ability of circular RNAs (circRNAs) to shape the cisplatin (DDP) resistance of cancers in human patients, there has been relatively little research to date focused on the interplay between circRNAs and DDP resistance in the context of OSCC progression to date. In the present analysis, the functional role that circ_0000140 plays as a mediator of chemoresistance to DDP was thus explored in greater detail. Methods: Both qPCR and Western immunoblotting were employed as appropriate to detect circ_0000140, miR-527, and SLC7A11 levels, while interactions among these factors were detected through RNA immunoprecipitation, RNA pull-down, and dual luciferase report assays. MTT assays were used to assess cellular viability as a means of gauging DDP sensitivity. Results: Both tissue samples from DDP-resistant OSCC patient tumors and OSCC cell lines resistant to DDP exhibited pronounced circ_0000140 upregulation. Knocking down this circRNA significantly increased the DDP sensitivity of both tested DDP-resistant OSCC cell lines and promoted ferroptosis, whereas knocking down miR-527 was sufficient to reverse these effects, which were recapitulated by miR-527 overexpression. Conversely, the effects of overexpressing miR-527 were reversed by the restoration of SLC7A11 expression. Consistently, this circRNA was able to increase DDP IC50 values and to suppress ferroptosis in both tested cell lines through this miR-527/SLC7A11 signaling axis. Conclusion: These results revealed that circ_0000140/miR-527/SLC7A11-mediated ferroptosis may provide novel insights into the development of this cancer type and the emergence of chemoresistance in the future.

Identification of Aging and Young Subtypes for Predicting Colorectal Cancer Prognosis and Immunotherapy Responses.

Colorectal cancer (CRC) is critically related to aging and severely threatens human lives. To better explore the effects of aging on CRC progression and therapy outcome, a reliable aging subtypes identification of CRC is urgently desired. Here, 28 aging-related genes associated with the CRC prognosis were selected by univariate Cox analyses. Based on these 28 genes, CRC patients were divided into the aging subtype and young subtype by non-negative matrix factorization clustering. Aging subtype and young subtype of CRC were identified with distinct molecular features and clinical prognosis. The aging subtype was characterized by upregulation of senescence-associated secretory phenotype, higher frequencies of TP53 and immune checkpoint molecules, and high sensitivity to protein kinase and angiogenesis inhibitors. Furthermore, 14 genes were selected by LASSO penalized Cox regression analyses for aging-related risk signature construction. The constructed aging risk signature exhibited good prediction and the nomogram showed robust discrimination power over the traditional CRC staging system. In conclusion, this study successfully established aging subtype and young subtype of CRC, which is helpful to identify patients with aging characteristics to evaluate prognosis and treatment outcomes. Introducing aging-based subtypes into clinical concern and patient prognostication provides new opportunities for personalized CRC treatment.

MYBL2 regulates de novo purine synthesis by transcriptionally activating IMPDH1 in hepatocellular carcinoma cells.

BACKGROUND: Metabolic reprogramming is a hallmark of cancer, alteration of nucleotide metabolism of hepatocellular carcinoma (HCC) is not well-understood. MYBL2 regulates cell cycle progression and hepatocarcinogenesis, its role in metabolic regulation remains elusive. PATIENTS AND METHODS: Copy number, mRNA and protein level of MYBL2 and IMPDH1 were analyzed in HCC, and correlated with patient survival. Chromatin Immunoprecipitation sequencing (Chip-seq) and Chromatin Immunoprecipitation quantitative polymerase chain reaction (ChIP-qPCR) were used to explore the relationship between MYBL2 and IMPDH1. Metabolomics were used to analyze how MYBL2 affected purine metabolism. The regulating effect of MYBL2 in HCC was further validated in vivo using xenograft models. RESULTS: The Results showed that copy-number alterations of MYBL2 occur in about 10% of human HCC. Expression of MYBL2, IMPDH1, or combination of both were significantly upregulated and associated with poor prognosis in HCC. Correlation, ChIP-seq and ChIP-qPCR analysis revealed that MYBL2 activates transcription of IMPDH1, while knock-out of MYBL2 retarded IMPDH1 expression and inhibited proliferation of HCC cells. Metabolomic analysis post knocking-out of MYBL2 demonstrated that it was essential in de novo purine synthesis, especially guanine nucleotides. In vivo analysis using xenograft tumors also revealed MYBL2 regulated purine synthesis by regulating IMPDH1, and thus, influencing tumor progression. CONCLUSION: MYBL2 is a key regulator of purine synthesis and promotes HCC progression by transcriptionally activating IMPDH1, it could be a potential candidate for targeted therapy for HCC.

Necrosulfonamide ameliorates intestinal inflammation via inhibiting GSDMD-medicated pyroptosis and MLKL-mediated necroptosis.

Inflammatory bowel disease (IBD) is a chronic relapsing disorder of the gastrointestinal tract, while the present therapeutic efficacy is insufficient. In recent years, numerous studies have shown that necrosulfonamide (NSA) played a protective role in many inflammatory diseases by blocking mixed lineage kinase domain-like protein (MLKL) polymerization. However, the protective effect of NSA in dextran sodium sulfate (DSS)-induced colitis has not been reported. In the present study, we used DSS to establish mouse models of acute colitis to explore the proactive effect of NSA. Our study showed that NSA alleviated symptoms of DSS-induced colitis through reducing weight loss and disease activity index (DAI) score. Furthermore, NSA inhibited macrophages and CD4+/CD8 + T-cell accumulation in colon tissue caused by DSS. In addition, we found that NSA had the therapeutic effects on DSS-induced colitis. Mechanistically, we detected the expression level of phosphorylated MLKL, the release of LDH, cytokines, and N-gasdermin D (N-GSDMD) to examine necroptosis and pyroptosis pathways. We found NSA alleviated the severity of DSS-induced colitis by inhibiting the expressions of phosphorylated MLKL and N-GSDMD in vivo. In vitro experiments, we found NSA inhibited the release of inflammatory factors and LDH and the expressions of N-GSDMD in bone marrow-derived macrophages. Furthermore, we found NSA inhibited the expression of phosphorylated MLKL and necroptosis of NCM460 cell through western blot and flow cytometer. In general, this study reveals that NSA inhibits pyroptosis and necroptosis pathways to eventually alleviate intestinal inflammation, which may serve as a potential candidate for IBD therapy.

Litter-derived nitrogen reduces methane uptake in tropical rainforest soils.

Litter comprises a major nutrient source when decomposed via soil microbes and functions as subtract that limits gas exchange between soil and atmosphere, thereby restricting methane (CH4) uptake in soils. However, the impact and inherent mechanism of litter and its decomposition on CH4 uptake in soils remains unknown in forest. Therefore, to declare the mechanisms of litter input and decomposition effect on the soil CH4 flux in forest, this study performed a litter-removal experiment in a tropical rainforest, and investigated the effects of litter input and decomposition on the CH4 flux among forest ecosystems through a literature review. Cumulative annual CH4 flux was -3.30 kg CH4-C ha-1 y-1. The litter layer decreased annual accumulated CH4 uptake by 8% which greater in the rainy season than the dry season in the tropical rainforest. Litter decomposition and the input of carbon and nitrogen in litter biomass reduced CH4 uptake significantly and the difference in CH4 flux between treatment with litter and without litter was negatively associated with N derived from litter input. Based on the literature review about litter effect on soil CH4 around world forests, the effect of litter dynamics on CH4 uptake was regulated by litter-derived nitrogen input and the amount soil inorganic nitrogen content. Our results suggest that nitrogen input via litter decomposition, which increased with temperature, caused a decline in CH4 uptake by forest soils, which could weaken the contribution of the forest in mitigating global warming.

Long noncoding RNA SNHG8 promotes chemoresistance in gastric cancer via binding with hnRNPA1 and stabilizing TROY expression.

AIMS: To determine SNHG8's function and potential mechanisms in gastric cancer (GC) chemoresistance. METHODS: We assessed SNHG8 expression in GC cell lines, GC/CDDP cell lines (cell lines treated with cisplatin), and 42 GC tissues and SNHG8 levels in the lncRNA microarray analysis of AGS/CDDP and AGS cell lines. We also examined GC cell viability in vivo and in vitro and its apoptosis level with Flow cytometry assays. SNHG8 was localized in subcells using fluorescence in situ hybridization (FISH) and cell fraction assays, hnRNPA1's link to SNHG8 was determined utilizing RNA immunoprecipitation (RIP) and FISH assays, gene expression profiles were assessed employing RNA transcriptome sequencing, and hnRNPA1's relationship with TROY was ascertained with the RIP assay. RESULTS: SNHG8 increased significantly in GC cell lines and GC tissues. However, a decrease in its expression promoted sensitivity to chemotherapy and inhibited DNA damage repair in vitro and in vivo. SNHG8 appeared to regulate TROY expression via linking with hnRNPA1. Reducing TROY levels considerably stimulated GC cell chemosensitivity, whereas heightening them partially rescued the rate of chemoresistance caused by downregulating SNHG8. CONCLUSION: In summary, the "SNHG8/hnRNPA1-TROY" axis is crucial to GC chemoresistance.

miR-23a-3p Regulates Runx2 to Inhibit the Proliferation and Metastasis of Oral Squamous Cell Carcinoma.

Objective: To investigate the effects of microRNA-23a (miR-23a-3p) and Runx2 on malignant progression of oral cancer cells and their possible molecular mechanisms. Methods: Fluorescence quantitative PCR (qPCR) was used to detect the expression of miR-23a-3p and Runx2 in human oral squamous cell carcinoma tissues and paracancerous tissues. The dual luciferase reporter assay was used to evaluate the targeted regulation of miR-23a-3p on Runx2. A subcutaneous xenograft model was established to investigate the tumor-suppressive effect of miR-23a-3p. Cells were transfected with miR-23a-3p mimics and negative control NC. CCK-8 assay, EDU assay, Transwell assay, and clone formation assay were used to detect malignant evolution of cells. Western blotting was used to detect the expression of Runx2, PTEN, and PI3K/Akt. The cells were simultaneously transfected with miR-23a-3p mimics and Runx2 to detect the malignant evolution of cells. Results: The expression of miR-23a-3p was downregulated in oral squamous cell carcinoma tissues, while the expression of Runx2 was upregulated. Overexpression of miR-23a-3p or inhibition of Runx2 inhibited the malignant progression of oral squamous cell carcinoma CAL-27 and TSCCA. Overexpression of miR-23a-3p inhibits the growth of oral cancer tumors. miR-23a-3p inhibits the PTEN/PI3K/Akt signaling pathway through Runx2. Overexpression of Runx2 reverses the tumor-suppressive effect of miR-23a-3p. Conclusion: miR-23a-3p can inhibit the PI3K/Akt signaling pathway by targeting Runx2 and inhibit the malignant evolution of oral cancer.

Optical properties and application potential of a hybrid cavity compound grating structure.

In this paper, we propose a new type of metal-insulator-metal (MIM) hybrid cavity compound grating micro-structure array, which can achieve dual narrowband super-absorption in the near-infrared window. The thin plasmonic microstructure effectively modulates coupling and hybridization effects between surface plasmon polaritons of different transmission resonance cavities to form designable dual narrowband resonance states to achieve near-infrared operation proving manipulation of the optical characteristics in the near-infrared light field. Furthermore, we conduct an in-depth theoretical exploration of the structure's unique properties, such as its high-quality factor, low noise, super-absorption, precise control, and the physical mechanism of its excellent performance in ambient refractive index sensing and detection. This study provides developmental insights for the miniaturization, easy modulation, and multi-function development of surface plasmon superabsorbers while broadening their application in near-infrared environment refractive index detection. The proposed microstructure is also suitable for integration with optical elements.

MXRA8 is an immune-relative prognostic biomarker associated with metastasis and CD8+ T cell infiltration in colorectal cancer.

Background: Colorectal cancer (CRC) is the second most common cause of cancer-related deaths worldwide. Tumor metastasis and CD8+ T cell infiltration play a crucial role in CRC patient survival. It is important to determine the etiology and mechanism of the malignant progression of CRC to develop more effective treatment strategies. Methods: We conducted weighted gene co-expression network analysis (WGCNA) to explore vital modules of tumor metastasis and CD8+ T cell infiltration, then with hub gene selection and survival analysis. Multi-omics analysis is used to explore the expression pattern, immunity, and prognostic effect of MXRA8. The molecular and immune characteristics of MXRA8 are analyzed in independent cohorts, clinical specimens, and in vitro. Results: MXRA8 expression was strongly correlated with tumor malignancy, metastasis, recurrence, and immunosuppressive microenvironment. Furthermore, MXRA8 expression predicts poor prognosis and is an independent prognostic factor for OS in CRC. Conclusion: MXRA8 may be a potential immunotherapeutic and prognostic biomarker for CRC.

Auxiliary diagnosis of Lung Cancer on the basis of a Serum Protein Biomarker Panel.

Objectives: In this study, we established a serum protein biomarker panel (consisting of Pro-SFTPB, CA125, Cyfra21-1, and CEA) and evaluated the feasibility and performance for the auxiliary diagnosis of lung cancer in the Chinese population. Materials and Methods: The current study was a single-center study based on the Chinese population and performed in two cohorts (training cohort and validation cohort). Serum concentrations of Pro-SFTPB, CA125, Cyfra21-1, and CEA were measured by a bead-based flow fluorescence immunoassay. The discrimination performance of the model was assessed using sensitivity, specificity, and the area under the receiver operating characteristic (ROC) curve (AUC). Results: For the biomarker panel model, the AUC was 0.88 (95% CI, 0.85-0.91) in the training cohort and 0.90 (95% CI, 0.86-0.92) in the validation data cohort, which was significantly greater than the AUC of each biomarker alone. For the nodule risk model, the AUC was improved to 0.96 (95% CI, 0.94-0.98) in the training cohort and 0.95 (95% CI, 0.93-0.97) in the validation cohort. In addition, the biomarker panel model yielded an AUC of 0.78 (95% CI, 0.74-0.81) for stage I & II lung cancer, better than the performance of individual biomarker alone. Conclusions: It was demonstrated that 4-protein biomarker panel had a significant performance in identifying lung cancer patients from healthy controls, especially combining with the nodule size. Specifically, it yielded excellent discrimination for identifying early-stage lung cancer patients than individual biomarker alone. A future large-scale study is underway to further define the clinical application of this method for the early diagnosis of lung cancer among Chinese populations.

Duodenal gastrointestinal stromal tumors: A retrospective study based on a 13 years experience of a single center in China.

AIM: Duodenal gastrointestinal stromal tumors (GISTs) constitute a small rare subset. This study aims to analyze the prognostic differences between duodenal and jejunoileal GISTs and evaluate the clinical treatment and prognostic characteristics of patients with duodenal GISTs. METHODS: Data of patients with primary duodenal or jejunoileal GISTs were collected. Patients were matched through propensity score matching (PSM). Perioperative and long-term outcomes of patients with duodenal GISTs were compared based on surgical approach. RESULTS: Altogether, 101 duodenal and 219 jejunoileal GISTs were identified. In patients with duodenal GISTs, 79 (78%) underwent local resection (LR) and 22 (22%) underwent pancreaticoduodenectomy (PD). Patients undergoing PD had a longer postoperation stay (18.5 vs 13 days, P = 0.001) and more complications (Clavien-Dindo I-II complications for PD vs LR, 31.8 vs 15.2%; Clavien-Dindo III-V complications for PD vs LR, 22.7 vs. 2.5%; P < 0.001). There was no difference in recurrence-free survival (RFS) (P = 0.8) or overall survival (OS) (P = 0.9) when comparing patients who underwent LR versus PD. Multivariable analysis showed that tumor size >5 cm was the only independent predictor of shorter RFS (P = 0.004) and OS (P = 0.012). After matching, there was no significant difference in RFS and OS between patients with duodenal versus jejunoileal GISTs (both P > 0.05). CONCLUSION: The prognosis of duodenal and jejunoileal GISTs are similar. Recurrence and OS of duodenal GISTs primarily depend on tumor size. For duodenal GISTs, LR is associated with comparable long-term survival when compared to PD, but with superior short-term outcomes.

Genome-wide association study of body size traits in Wenshang Barred chickens based on the specific-locus amplified fragment sequencing technology.

Chicken body size (BS) is an economically important trait, which has been assessed in many studies for genetic selection. However, previous reports detected functional chromosome mutations or regions using gene chips. The present study used the specific-locus amplified fragment sequencing (SLAF-seq) technology to perform a genome-wide association study (GWAS) of purebred Wenshang Barred chickens. A total of 250 one-day-old male chickens were assessed in this study. Body size in individual birds was measured at 56 days. SLAF-seq was used to genotype and GWAS analysis was carried out using the general linear model (GLM) of the TASSEL program. A total of 1,286,715 single-nucleotide polymorphisms (SNPs) were detected, of which 175,211 were tested as candidate SNPs for genome-wide association analysis using the TASSEL general linear model. Three SNPs markers reached genome-wide significance. Of these, chrZ:81729634, chrZ:81841715, and chrZ:81954149 at 81,729,634, 81,841,715, and 81,954,149 bp of GGA Z were significantly associated with body diagonal length at 56 days (BDL56); and tibia length at 56 days (TL56). These SNPs were close to three genes, including ZCCHC7, PAX5, and MELK. These results open new horizons for studies on BS and should promote the use of Chinese chickens, especially Wenshang Barred chickens.

The aggressive surgical treatment and outcome of a colon cancer patient with COVID-19 in Wuhan, China.

BACKGROUND: Cancer patients are at increased risk of novel coronavirus disease 2019 (COVID-19). Currently, surgeries for cancer patients with COVID-19 are generally suggested to be properly delayed. CASE PRESENTATION: We presented a 69-year-old Chinese female colon cancer patient with COVID-19, the first case accepted the surgical treatment during the pandemic in China. The patient developed a fever on January 28, 2020. After treatments with Ceftriaxone and Abidol, her fever was not moderated yet. A repeat chest computed tomography (CT) scan showed significantly exacerbated infectious lesions with a positive result for severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) nucleic acid. An abdomen CT scan indicated the tumor of ascending colon with local wrapped changes. She was diagnosed with 'Severe novel coronavirus pneumonia' and 'Incomplete bowel obstruction: Colon cancer?'. After actively anti-inflammatory and anti-viral therapies, a right colectomy with lymph node dissection was performed on March 11, followed by a pathological examination. The patient successfully recovered from COVID-19 pneumonia and incomplete bowel obstruction after surgery without any postoperative related complications and was discharged on the 9th day after operation. Significant degeneration, necrosis and slough of focal intestinal and colonic mucosal epithelial cells were observed under microscope. No surgeons, nurses or anesthetists in our team were infected with SARS-CoV-2. CONCLUSIONS: It is meaningful and imperative to share our experience of protecting health care personnels from SARS-CoV-2 infection and providing references for optimizing treatment of cancer patients, at least for the operative intervention with absolute necessity or surgical emergency, during the outbreak of COVID-19.

Interferon regulatory factor-1 suppresses DNA damage response and reverses chemotherapy resistance by downregulating the expression of RAD51 in gastric cancer.

Recent studies have shown that IRF-1 plays a significant role in various tumour-induced chemoresistance, but its role and mechanism in gastric cancer-associated chemoresistance are not clear. Our study showed that IRF-1 expression could reverse gastric cancer-related chemoresistance. Dysregulated DNA repair is an important cause of chemoresistance. We established a chemoresistant gastric cancer cell line and found that drug-resistant gastric cancer cells had increased DNA repair ability and that IRF-1 regulated DNA damage repair. Further studies showed that IRF-1 inhibited the expression of RAD51 directly by binding to the RAD51 promoter to affect DNA damage repair; this binding reversed resistance. However, restoring the expression of RAD51 halted the inhibitory effect of IRF-1 partially. Also, we revealed that the overexpression of IRF-1 in a mouse model synergized with chemotherapeutic drugs to inhibit tumour growth. Finally, IRF-1 expression correlated with RAD51 expression in gastric cancer specimens. The expression of IRF-1 and RAD51 are both related to the survival duration of patients with gastric cancer. These results suggest that targeting IRF-1-RAD51 could be an effective approach to reversing multidrug resistance in gastric cancer.

Linewidth reduction effect of a cavity-coupled dual-passband plasmonic filter.

We propose a novel cavity-coupled MIM nano-hole array structure that exhibits a tunable dual passband in the near-infrared regime. When compared with the traditional single metal film, the designed structure provides a coupling effect between Gspp and SPP to significantly reduce the linewidths of the two transmission peaks. We also reveal the physical origin of the positive and negative influence of the cavity effect on the transmission of high-frequency and low-frequency peaks. This work supplies a new modulation theory for plasmonic devices based on the EOT phenomenon and has a wide application prospect in the fields of infrared sensor, plasmonic filter, and hyperspectral imaging.

Long noncoding RNA metastasis-associated lung adenocarcinoma transcript 1 cooperates with enhancer of zeste homolog 2 to promote hepatocellular carcinoma development by modulating the microRNA-22/Snail family transcriptional repressor 1 axis.

Metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) is an oncogenic long noncoding RNA that has been found to promote carcinogenesis and metastasis in many tumors. However, the underlying role of MALAT1 in the progression and metastasis of hepatocellular carcinoma (HCC) remains unclear. In this study, aberrantly elevated levels of MALAT1 were detected in both HCC specimens and cell lines. We found that knockdown of MALAT1 caused retardation in proliferation, migration, and invasion both in vivo and in vitro. Mechanistic investigations showed that Snail family transcriptional repressor 1 (SNAI1) is a direct target of microRNA (miR)-22 and that MALAT1 modulates SNAI1 expression by acting as a competing endogenous RNA for miR-22. Inhibition of miR-22 restored SNAI1 expression suppressed by MALAT1 knockdown. Furthermore, MALAT1 facilitated the enrichment of enhancer of zeste homolog 2 (EZH2) at the promoter region of miR-22 and E-cadherin, which was repressed by MALAT1 knockdown. Cooperating with EZH2, MALAT1 positively regulated SNAI1 by repressing miR-22 and inhibiting E-cadherin expression, playing a vital role in epithelial to mesenchymal transition. In conclusion, our results reveal a mechanism by which MALAT1 promotes HCC progression and provides a potential target for HCC therapy.