Prognostic score model based on six m6A-related autophagy genes for predicting survival in esophageal squamous cell carcinoma.

BACKGROUND: Prognostic signatures based on autophagy genes have been proposed for esophageal squamous cell carcinoma (ESCC). Autophagy genes are closely associated with m6A genes. Our purpose is to identify m6A-related autophagy genes in ESCC and develop a survival prediction model. METHODS: Differential expression analyses for m6A genes and autophagy genes were performed based on TCGA and HADd databases followed by constructing a co-expression network. Uni-variable Cox regression analysis was performed for m6A-related autophagy genes. Using the optimal combination of feature genes by LASSO Cox regression model, a prognostic score (PS) model was developed and subsequently validated in an independent dataset. RESULTS: The differential expression of 13 m6A genes and 107 autophagy genes was observed between ESCC and normal samples. The co-expression network contained 13 m6A genes and 96 autophagy genes. Of the 12 m6A-related autophagy genes that were significantly related to survival, DAPK2, DIRAS3, EIF2AK3, ITPR1, MAP1LC3C, and TP53 were used to construct a PS model, which split the training set into two risk groups with significant different survival ratios (p = 0.015, 1-year, 3-year, and 5-year AUC = 0.873, 0.840, and 0.829). Consistent results of GSE53625 dataset confirmed predictive ability of the model (p = 0.024, 1-year, 3-year, and 5-year AUC = 0.793, 0.751, and 0.744). The six-gene PS score was an independent prognostic factor from clinical factors (HR, 2.362; 95% CI, 1.390-7.064; p-value = 0.012). CONCLUSION: Our study recommends 6 m6A-related autophagy genes as promising prognostic biomarkers and develops a PS model to predict survival in ESCC.

Prognostic Cell Death Index for Lung Adenocarcinoma: A Comprehensive Transcriptome-Based Analysis of Twelve Programmed Cell Death Pattern Genes.

OBJECTIVE: Lung adenocarcinoma (LUAD) is a prominent contributor to global cancer mortality, characterized by constrained prognosis. This study aimed to develop a novel prognostic indicator, the Cell Death Index (CDI), utilizing twelve programmed cell death (PCD) pattern genes, to predict the immune infiltration and prognosis in LUAD patients. METHODS: We collected PCD-related genes and identified prognostic PCD genes in the Cancer Genome Atlas (TCGA)-LUAD dataset, and made rigorous validation in the Clinical Proteomic Tumor Analysis Consortium (CPTAC)-LUAD cohorts. CDI was calculated using a multivariable Cox regression model. Functional enrichment and tumor microenvironment were evaluated. Drug sensitivity prediction and nomogram development were performed to assess CDI's potential value. RESULTS: The results revealed 10 PCD genes (ERO1A, CDK5R1, TRIM6, DNASE2B, ITPRIP, MRGPRX2, FGA, NDUFA13, NLRP2, and CD68) significantly associated with LUAD prognosis. The CDI was constructed and showed high accuracy in predicting patient survival with C-index values of 0.801 and 0.794 in the prognosis cohort and validation cohort, respectively. CDI is also indicative of variations in biological functions, tumor microenvironment, and immune cell infiltration including neutrophils, activated mast cells, activated dendritic cells, M0 macrophages, resting natural killer cells, γδT cells, and activated memory CD4+T cells. Furthermore, drug sensitivity analysis indicated potential targeted strategies. CONCLUSIONS: The CDI, based on PCD genes, serves as a robust prognostic tool for LUAD, offering profound insights into tumor biology, immune response, and personalized treatment strategies. This study underscores the pivotal role of PCD mechanisms in LUAD pathogenesis and identifies potential therapeutic targets.

Gender Differences in Prevalence and Clinical Correlates of Lipohypertrophy in Insulin-Exposed Patients with Diabetes Mellitus.

Purpose: The purpose of this systematic review was to assess potential gender differences in prevalence and clinical relevance of insulin-related lipohypertrophy (LH). Patients and Methods: Five electronic databases (PubMed, Embase, CNKI, Wanfang and VIP) were systematically searched for studies, from inception to 1st Sep 2022, on the prevalence of insulin-related LH. The eligibility of articles was independently screened, and the included studies were evaluated using standardized quality assessment tools. Results: A total of 22 studies mentioned the LH prevalence in different genders, of which two are about gestational diabetes; therefore, 20 studies were eventually included, providing data on 6238 patients. The prevalence of LH varied from 30.26% to 72.54%. Ten studies (4392 patients) were conducted with the adult diabetes patients of different genders over the age of 18, the total prevalence rate of LH was 51.73%, the LH prevalence in male gender was from 41.94% to 68.57% and the rate of the total population was 54.89% (2046 patients); The LH prevalence in female gender was from 33.18% to 70% and the rate of the total population was 48.98% (2346 patients), and the prevalence of LH was significantly different between male and female gender (P<0.001). Interestingly, only one study (n=1227) showed that there were dramatic differences between different genders (P<0.001), the subjects were T2DM patients, the LH prevalence rate of male vs female was 70.52% (299/424) VS 52.18% (419/803), while the other studies either only include T1DM or both T1DM and T2DM. Conclusion: The evidence shows that the results of gender differences in the LH prevalence are inconsistent with different types of DM. Probably, there is no gender differences in the LH prevalence in adult patients with T1DM, but it has a gender difference between male and female in T2DM. More strictly designed clinical studies are needed to further verify and reveal the underlying mechanisms.

Long non-coding RNA B4GALT1-Antisense RNA 1/microRNA-30e/SRY-box transcription factor 9 signaling axis contributes to non-small cell lung cancer cell growth.

Long non-coding (lnc) RNAs serve crucial functions in human cancers. However, the involvement of the lncRNA B4GALT1-antisense RNA 1 (AS1) in non-small cell lung cancer (NSCLC) has not been extensively studied. Reverse transcription-quantitative PCR was performed to detect B4GALT1-AS1 levels in NSCLC tissues and cell lines. Potential influences of B4GALT1-AS1 on biological functions of NSCLC were assessed through a series of in vitro experiments, and the molecular mechanism was determined via RNA immunoprecipitation (RIP) and bioinformatics analyses. The results of the present study demonstrated that knockdown of B4GALT1-AS1 significantly attenuated the proliferative ability and clonality of H1299 and A549 cells. In the present study, B4GALT1-AS1 competed as an endogenous RNA by sequestering microRNA-30e (miR-30e) leading to an enhanced expression of SRY-box transcription factor 9 (SOX9). The effects of silencing B4GALT1-AS1 on NSCLC cells proliferation could be ameliorated by inhibiting miR-30e or restoring SOX9. Hence, B4GALT1-AS1 acted as a lncRNA that drives tumor progression in NSCLC via the regulation of the miR-30e/SOX9 axis. The findings of the present study indicated that the B4GALT1-AS1/miR-30e/SOX9 axis maybe an effective target for NSCLC treatment and management.

miR-208b-5p inhibits invasion of non-small cell lung cancer through the STAT3 pathway by targeting interleukin-9.

Previous studies reported a dysregulation of micro (mi)R-208b-5p expression level in various types of human cancer; however, the role of miR-208-5p in non-small cell lung cancer (NSCLC) remains unclear. Therefore, the present study aimed to determine whether miR-208b-5p could regulate NSCLC progression. A total of 62 pairs of primary tumor and adjacent normal tissues were collected from patients with NSCLC. miR-208b-5p expression level was determined by reverse transcription-quantitative polymerase chain reaction. Furthermore, miR-208b-5p mimics was transfected into NSCLC A549 and H1299 cells in order to upregulate miR-208b-5p expression. Dual-luciferase reporter assay was utilized to investigate the associations between miR-208b-5p and IL9 mRNA. The results demonstrated that miR-208b-5p expression decreased in NSCLC tissues and cell lines. Furthermore, miR-208b-5p overexpression inhibited A549 and H1299 cell proliferation and invasiveness. miR-208b-5p was demonstrated to bind directly to the 3' untranslated region of interleukin-9 (IL-9) and therefore decreased its expression. In the NSCLC-derived cell lines, miR-208b-5p inactivated IL-9/signal transducer and activator of transcription 3 (STAT3) signaling pathway. Furthermore, enhanced IL-9 level decreased the miR-208b-5p-mediated suppression of epithelial-mesenchymal transition in NSCLC cells by inactivating the STAT3 signaling pathway. In conclusion, the findings from this study demonstrated that miR-208b-5p inhibited migration and invasion of NSCLC cells. The anti-tumor activity of miR-208b-5p may be mediated by IL-9 and STAT-3 pathway.

Fluorescence resonance energy transfer of CaF2: Eu2+, Tb3+ applied to dye-sensitized solar cells.

CaF2: Eu2+, Tb3+ introduced into dye-sensitized solar cells (DSSCs) were studied to examine the influence of luminescent materials on photoanodes using a simple method. The emission spectra of CaF2: Eu2+, Tb3+ included the blue light of Eu2+ (4f → 5d) at 430 nm and green emission of Tb3+ (5D4 → 7F5) at 542 nm under the monitoring wavelengths at 398 nm, which matched well the absorption range of the N719 dye in DSSCs. Energy transfer (ET) was verified between Eu2+ and Tb3+ ions and the efficiency of ET found to increase with Tb3+ concentration. Both the fluorescence resonance and luminescence-mediated ETs between phosphor and N719 dye were observed as the main contribution in improving photocurrent and power conversion efficiency (PCE) of these DSSCs. The PCE of DSSCs doped with phosphors was greatly increased by 5.16, to 43.3%, which was comparable to cells made of pure TiO2 photoanodes. Moreover, CaF2: Eu2+, Tb3+ enlarged the surface area of TiO2 photonaodes, which helped the adsorption performance of the TiO2 film.