Secular trends in incidence and mortality of non-Hodgkin's lymphoma in China, 1990-2019, and predictions to 2030: Outlook for the future burden of disease.

BACKGROUND: The aim of this study was to analyze the trend of non-Hodgkin's lymphoma incidence and mortality in China from 1990 to 2019, along with assessing the effects of age, period, and cohort, as well as to predict future trends. MATERIAL AND METHODS: Using data from the Global Burden of Disease Study 2019 we calculated the estimated annual percentage changes in the incidence and mortality of non-Hodgkin's lymphoma. Age-period-cohort analysis was used to assess the independent effects of these elements. Incidence and mortality until 2030 were predicted using a Bayesian age-period-cohort approach. RESULTS: During 1990-2019, there was a significant increase in the age-standardized incidence and mortality rate in non-Hodgkin's lymphoma. Strong effects of birth cohort and period on non-Hodgkin's lymphoma incidence and mortality were observed. In terms of prediction, future non-Hodgkin's lymphoma incidence and mortality in China will continue to increase, while the mortality rate will decrease; for women, both the rates are projected to rise, but they will remain lower than men. CONCLUSIONS: Currently, the non-Hodgkin's lymphoma burden is high in China, and it is expected to continue increasing in the future. Policymakers need to prioritize addressing the factors contributing to sex differences in disease burden, including variations in environmental exposures and lifestyles among men and women.

New findings in prognostic factor assessment for adenocarcinoma of transverse colon: a comparison study between competing-risk and COX regression analysis.

Purpose: Competing-risk analysis was used to accurately assess prognostic factors for cancer-specific death in patients with adenocarcinoma of transverse colon (ATC), and the results were compared with those from a conventional Cox regression analysis. Materials and Methods: Patients diagnosed with ATC between 2000 and 2019 were selected from the Surveillance, Epidemiology, and End Results database. The crude mortality rates of patients with ATC were calculated and their differences were tested using the Gray's test, respectively. In performing multivariate analysis, the Cox regression model and the subdistribution hazard function (SD) in competing risk analysis were utilized, respectively. Results: This study included 21,477 eligible patients. The SD model indicated that age, etc. are actual independent prognostic factors. In contrast to previous recognition, the results of the Cox regression showed false-positives for sex and Carcinoembryonic antigen, and underestimated point-estimates in the stage and American Joint Committee on Cancer stage due to competing events. A detailed comparison of treatment revealed that the larger surgical scopes were prognostic risk factors compared with the smaller scope of local tumor excision, partial colectomy, or segmental resection. Patients treated with external proton beam radiotherapy had an increased risk compared with those with no radiotherapy and internal radiotherapy. Conclusions: After comparing the results of the two methods and mitigating the significant bias introduced by Cox regression, we found independent factors that really affect the prognosis of ATC. On the other hand, in terms of ATC, a larger surgical scope and external proton beam radiotherapy may not improve the long-term survival of patients. Therefore, when faced with ATC patients, these differences should be noted and treated differently from common colorectal cancer patients. Thus, clinicians are able to give more targeted treatment plans and prognostic assessments.

Spatiotemporal variation in sensitivity of urban vegetation growth and greenness to vegetation water content: Evidence from Chinese megacities.

Understanding the sensitivity of vegetation growth and greenness to vegetation water content change is crucial for elucidating the mechanism of terrestrial ecosystems response to water availability change caused by climate change. Nevertheless, we still have limited knowledge of such aspects in urban in different climatic contexts under the influence of human activities. In this study, we employed Google Earth Engine (GEE), remote sensing satellite imagery, meteorological data, and Vegetation Photosynthesis Model (VPM) to explore the spatiotemporal pattern of vegetation growth and greenness sensitivity to vegetation water content in three megacities (Beijing, Shanghai, and Guangzhou) located in eastern China from 2001 to 2020. We found a significant increase (slope > 0, p < 0.05) in the sensitivity of urban vegetation growth and greenness to vegetation water content (SLSWI). This indicates the increasing dependence of urban vegetation ecosystems on vegetation water resources. Moreover, evident spatial heterogeneity was observed in both SLSWI and the trends of SLSWI, and spatial heterogeneity in SLSWI and the trends of SLSWI was also present among identical vegetation types within the same city. Additionally, both SLSWI of vegetation growth and greenness and the trend of SLSWI showed obvious spatial distribution differences (e.g., standard deviations of trends in SLSWI of open evergreen needle-leaved forest of GPP is 14.36 × 10-2 and standard deviations of trends in SLSWI of open evergreen needle-leaved forest of EVI is 10.16 × 10-2), closely associated with factors such as vegetation type, climatic conditions, and anthropogenic influences.

Prediction of death probability in adenocarcinoma of the transverse colon: competing-risk nomograms based on 21,469 patients.

PURPOSE: Tumors in parts of the colon other than the transverse colon have been well studied, but little is known about adenocarcinoma of the transverse colon (ATC).The aim of this study was to construct nomograms using competing-risk model for accurately predicting the probability of cancer-specific and non-cancer-specific death in patients with ATC. METHODS: Data on eligible patients recorded during 2000-2019 in the Surveillance, Epidemiology, and End Results database were extracted and screened. Factors that influencing prognosis were screened for death from ATC (DATC) and death from other causes (DOC) using competing-risk analysis, including univariate and multivariate analyses based on Gray's test and the Fine-Gray model, respectively. Independent prognostic factors were identified and nomograms were constructed. For comparison, we also constructed a Cox model and an AJCC stage-only competing-risk model (AJCC model) for patients with DATC. Performance evaluations of the nomograms and comparison between the models were performed using calibration plots, Harrell's concordance index (C-index), receiver operating characteristic (ROC) curves, and the areas under the ROC curve (AUCs). The nomograms and models were validated using a validation cohort. The net reclassification index, integrated discrimination improvement, decision curves, and risk stratification were not assessed because no accepted methods were suited for competing-risk model. RESULTS: This study included 21,469 patients with ATC, and 17 and 9 independent influencing factors were identified for the construction of DATC nomograms (DATCN) and DOC nomograms (DOCN), respectively. In both the training and validation cohorts, the calibration curves indicated good agreement between the nomogram-based predictions and the actual observations in the two nomograms, respectively. The C-index of the DATCN was higher than 80% (80.3-83.3%) at 1, 3 and 5 years in both the training and validation cohorts, significantly outperforming the AJCC (76.7-78%) and Cox (75.4-79.5%) model. The C-index of the DOCN was also higher than 69% (69.0-73.6%). In terms of ROC curves at each time point, those of the DATCN were very close to the upper-left corner of the coordinate axis in both the training and validation cohorts, and their AUCs were larger than 84% (84.2-85.4%).The AUCs of the AJCC (78.4-81.1%) and Cox (79.4-81.5%) models were significantly lower (p < 0.05), and the curves were closer to the diagonal. The ROC curves of the DOCN was similar to those of the DATCN, and the AUCs were 68.5-74%. The DATCN and DOCN therefore had good consistency, accuracy, and stability, respectively. CONCLUSION: This study was the first to construct competing-risk nomograms for ATC. These nomograms have proved useful for accurately assessing patient prognoses and allowing more-individualized follow-up strategies, thereby reducing the mortality.

A Novel Successful Case of Nasal and Sinus Yolk Sac Tumor With SMARCB1 (INI-1) Deficiency: A Case Report.

Yolk sac tumors (YSTs) of the head and neck region account for only 1% of all malignant tumors of germ cell origin. YSTs with SMARCB1 deficiency are very aggressive. Only one nasal and sinus YST with SMARCB1-deficient carcinoma (SDC) was reported with follow-up information but the patient died 20 months after diagnosis. We report a successful case treated by surgery combined with radiotherapy and limited cycles of chemotherapy, achieving a good prognosis. A 55-year-old male was seen with a three-month history of right nasal congestion, right nasal hemorrhage and hyposmia. The tumor widely invaded multiple regions such as the sphenoid, ethmoid sinus, orbital medial wall, choana, right maxillary sinus, and right pterygopalatine fossa. After endoscopic surgery, he was diagnosed as SDC with pure YST differentiation. The patient underwent endoscopic surgery, combined with radiotherapy as well as three cycles of chemotherapy with etoposide and cisplatin (EP regimen) and finally achieved over one year of disease-free survival. YST with SDC in the nasal and sinus regions is very rare and hard to treat. We highlight the value of combined treatment options including surgery, radiotherapy and limited cycles of chemotherapy to achieve a good prognosis.

Breast Cancer Epidemiology and Survival Analysis of Shenyang in Northeast China: A Population-Based Study from 2008 to 2017.

Background: To investigate the status of breast cancer incidence, trends, and survival in women in urban Shenyang from 2008-2017 using large Cancer Registry data. Methods: Breast cancer incidence and mortality data were abstracted from the Shenyang Cancer Registry between 2008 and 2017. The crude and age-standardized incidence and mortality rates were calculated for each year. Average annual percentage changes (AAPC) were used to describe the change over time. Results: A total of 14,255 out of 18,782,956 women were diagnosed with breast cancer between 2008 and 2017 in urban Shenyang. The overall crude and age-standardized incidences were 75.89 and 43.42 per 100,000, respectively. The crude incidence increased from 61.93 per 100,000 in 2008 to 90.07 per 100,000 in 2017, with an AAPC of 5.10%. The crude mortality increased from 11.41 per 100,000 in 2008 to 17.29 per 100,000 in 2017, with an AAPC of 4.60. The highest age-specific incidence occurs in the 55-59 year age group at a rate of 140.67 per 100,000. During the study period, 2,710 women died from breast cancer. The overall crude and age-standardized mortality rates were 14.43 and 7.43 per 100,000, respectively. The highest age-specific mortality occurs at 80-84 years old at a rate of 57.57 per 100,000. The 3-year and 5-year survival rates for female breast cancer in urban Shenyang from 2008 to 2013 were 85.61% and 77.39%, respectively, and both declined with age. Conclusion: The incidence and mortality rates of breast cancer in Shenyang increased over time. Screening and control strategies should be enhanced, especially for perimenopausal females.

Upregulation of KLHL17 promotes the proliferation and migration of non-small cell lung cancer by activating the Ras/MAPK signaling pathway.

Analysis of the Gene Expression Profiling Interactive Analysis (GEPIA) database revealed that Kelch-like 17 (KLHL17) is overexpressed in non-small cell lung cancer (NSCLC) including adenocarcinoma (ADC) and squamous cell carcinoma (SCC). We therefore explored the role of KLHL17 in the development and progression of NSCLC. Immunohistochemistry and western blotting showed that KLHL17 expression was significantly higher in the tumor tissues from 173 patients with NSCLC, compared with the corresponding non-neoplastic tissue. In addition, upregulated KLHL17 expression was positively correlated with tumor size, lymph node metastasis and tumor node metastasis (TNM) stage, and affected the overall survival (OS) of patients with NSCLC. Consistent with clinical samples, in vitro studies demonstrated that KLHL17 expression was higher in various cell lines of NSCLC (A549, H1299, H460 and SK cells) as compared to normal human bronchial epithelial cells (HBE cells). Overexpression of KLHL17 in the cell lines of NSCLC with KLHL17-Flag plasmid promoted the proliferation and migration of tumor cells, which was associated with elevated activation of Rat sarcoma/Mitogen-activated protein kinases (Ras/MAPK) signaling and increased expression of cyclin D1, cyclin D-dependent kinases 4 (CDK4), matrix metalloproteinase 2 (MMP2) and Ras homolog gene family member A (RhoA). In contrast, knockdown of KLHL17 in the cell lines of NSCLC using KLHL17 small interfering RNA suppressed the proliferation and migration of tumor cells, in association with reduced activation of Ras/MAPK signaling and decreased expression of cyclin D1, CDK4, MMP2 and RhoA. Moreover, treatment of tumor cells with Ras inhibitor salirasib prevented KLHL17-induced Ras/MAPK activity as well as tumor proliferation and migration. These results suggest that upregulated KLHL17 in NSCLC promotes the proliferation and migration of tumor by activating Ras/MAPK signaling pathway. Therefore, KLHL17 may be a novel therapeutic target for the treatment of NSCLC.

LncRNA HOXC-AS3 promotes non-small-cell lung cancer growth and metastasis through upregulation of YBX1.

NSCLC is common and is the primary cause of cancer-related deaths due to a lack of early diagnosis and its propensity for metastasis. The pathogenesis of NSCLC is still unclear. Here, we explored the molecular mechanisms underlying NSCLC development, focusing on the HOXC-AS3/YBX1/HOXC8 axis. Human NSCLC specimens and cell lines were used. qRT-PCR and western blotting were utilised to examine the levels of HOXC-AS3/YBX1/HOXC8. CCK-8, colony formation, scratch wound healing and Transwell assays were performed to evaluate cancer cell proliferation, migration and invasion. A nude mouse xenograft model was used to examine tumour growth and metastasis in vivo. RNA pull-down, chromatin immunoprecipitation, coimmunoprecipitation and dual-luciferase assays were applied to validate the interactions of HOXC-AS3/YBX1, MDM2/YBX1 and the YBX1/HOXC8 promoter. The levels of HOXC-AS3 and HOXC8 were increased in human NSCLC specimens and cells. Knockdown of HOXC-AS3 suppressed NSCLC cell proliferation, migration and invasion, as well as tumour growth and metastasis in vivo. HOXC-AS3 directly bound to YBX1 to suppress its ubiquitination mediated by MDM2. YBX1 bound to the HOXC8 promoter and enhanced its transcription. Knockdown of HOXC8 inhibited the effects of HOXC-AS3 overexpression on NSCLC. HOXC-AS3 promotes NSCLC growth and metastasis by stabilising YBX1 and thus increasing HOXC8 transcription. Our study indicates that the HOXC-AS3/YBX1/HOXC8 axis could serve as a biomarker for NSCLC diagnosis or as a target for therapy development.

Driving forces of UHI changes in China's major cities from the perspective of land surface energy balance.

As remarkable human-induced temperature anomalies on the land surface, variations of urban heat island (UHI) and its driving factors have been investigated in numerous studies. However, few studies discussed the spatiotemporal heterogeneity of the driving forces exerted by land surface energy fluxes, i.e., net radiation, sensible heat, latent heat and heat storage, on UHI behaviors at large scale and long term. In this study, a comprehensive application of multisource datasets and statistical methods have been implemented based on land surface energy balance theory, the spatiotemporal variations of surface UHI intensity (urban-rural temperature difference) and changes of their driving forces have been quantified. The results demonstrate the dynamics of UHI intensity in 32 major cities of China from 2003 to 2017 are generally coherent with the common perception, the overall surface UHI intensity is 4.57 K higher in summer than in winter. The spatial variations of the fluxes that alter UHI intensity can be largely attributed to the varied energy interactions between vegetated/paved surface and atmosphere and the differences of background temperature and precipitation, the contribution of latent heat to UHI changes declines nearly 40% from semiarid/arid climate at the north to subtropical humid climate at the south, while the contributions of other fluxes are stable. The temporal changes of the effect of these fluxes, however, imply more complex mechanisms. The contributions of sensible heat and latent heat to UHI intensity variations are three times and eight times larger in the warm season than in the cold season respectively, indicating the influence of seasonality of background temperature, precipitation and vegetation. The low contributions of these fluxes in the cold season also suggest the significant effect of other driving forces such as anthropogenic heat, especially in semiarid/semihumid climate zones. This study highlights the temporal shifts of major driving forces of UHI intensity, the mitigation tactics for UHI in different cities and seasons should be customized for better validity.

Long Non-Coding RNA Signatures Associated with Ferroptosis Predict Prognosis in Colorectal Cancer.

BACKGROUND: Currently, colorectal cancer has become a common gastrointestinal malignancy that usually occurs in the colon and rectum, and ferroptosis plays a vital role in the pathology and progression of colorectal tumors. METHODS: A total of 627 patients (51 normal and 644 tumor samples) from The Cancer Genome Atlas (TCGA)-COAD and TCGA-READ were included in the study. Lasso and Cox's regression was employed to analyze the characteristic lncRNAs in colorectal cancer samples, and a distinctive prognostic model of ferroptosis-related lncRNAs was established. By analyzing the divergence between the high and low-risk groups of ferroptosis-related lncRNAs, 15 characteristic lncRNAs related to the prognosis of colorectal cancer were evaluated. Kaplan-Meier analysis, operation characteristic curve (ROC), nomogram, and gene set enrichment analyses (GSEA) further confirmed the validity of the characteristic prognostic model with ferroptosis-related lncRNAs. RESULTS: Kaplan-Meier analysis confirmed a high-risk group of ferroptosis-related lncRNA interrelated with a poor prognosis in colorectal cancer. AUC estimates of 1 -, 3 -, and 5-year survival rates for ferroptosis-related lncRNA characteristic models were 0.745, 0.767 and 0.789. GSEA analysis showed that immune and malignancy-related pathways were active in the high-risk score group. In addition, differential analyses of immune function, including Checkpoint, cytolytic, HLA, and T cell co-inhibition, differed significantly betwixt low - and high-risk groups.CD160, TNFRSF18, CD27, PDCD1, CD200R1, ADORA2A, TNFRSF14, LAIR1, CD244, CD40, TNFRSF4, CD70, TNFSF14, TNFRSF25, CD276, HHLA2, VTCN1, LAG3, TNFSF18, and other immune checkpoints had different expressions betwixt the high- and low-risk group. CONCLUSION: Fifteen kinds of lncRNAs with different expressions (AP003555.1, AC099850.3, AL031985.3, LINC01857, STPG3-AS1, AL137782.1, AC124067.4, AC012313.5, AC083900.1, AC010973.2, ALMS1-IT1, AC013652.1, AC133540.1, AP006621.2, AC018653.3) were closely associated with poor prognosis of colorectal cancer. These indicators were significantly correlated with the overall survival (OS) rate and could be used as prognostic evaluation criteria.

TBC1 domain family member 23 interacts with Ras-related protein Rab-11A to promote poor prognosis of non-small-cell lung cancer via ß1-integrin.

Non-small-cell lung cancer (NSCLC) accounts for approximately 80% of lung cancer cases. TBC1D23, a member of the TBC/RABGAP family, is widely expressed in human tissues; however, its role in NSCLC is currently unknown. Immunohistochemical analysis was conducted on 173 paraffin-embedded lung tissue sections from patients with NSCLC from 2014 to 2018 at the First Affiliated Hospital of China Medical University. MTT, colony formation assay, cell cycle assay, scratch assay, transwell assay, Western blotting and real-time PCR were employed on multiple NSCLC cell lines modified to knock down or overexpress TBC1D23/RAB11A. Immunoprecipitation, immunoprecipitation-mass spectrometry, immunofluorescence and flow cytometry were performed to explore the interaction between TBC1D23 and RAB11A and TBC1D23 involvement in the interaction between RAB11A and ß1 integrin in the para-nucleus. TBC1D23 was correlated with tumour size, differentiation degree, metastasis, TNM stage and poor prognosis. TBC1D23 was involved in the interaction between RAB11A and ß1 integrin in the para-nucleus, thus activating the ß1 integrin/FAK/ERK signalling pathway to promote NSCLC. Furthermore, TBC1D23 promoted NSCLC progression by inducing cell proliferation, migration and invasion. This study indicated the relationship between TBC1D23 expression and the adverse clinicopathological characteristics of patients with NSCLC, suggesting that TBC1D23 may be an important target for NSCLC treatment.

YBX1 regulated by Runx3-miR-148a-3p axis facilitates non-small-cell lung cancer progression.

BACKGROUND: Y-box binding protein 1 (YBX1) is a common oncogene in non-small-cell lung cancer (NSCLC), which is regulated by microRNAs (miRNAs) and transcription factors. This research aims to explore the function of YBX1, miR-148a-3p and Runt-related transcription factor 3 (Runx3) in NSCLC development, and analyze their interactions. METHODS: YBX1, miR-148a-3p and Runx3 levels were detected using quantitative reverse transcription polymerase chain reaction(RT-PCR), Western blotting or immunohistochemical staining. The functions of YBX1, miR-148a-3p and Runx3 were assessed by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT), colony formation, wound healing, transwell, flow cytometry, xenograft model and Western blotting analyses. The binding correlation was validated through dual-luciferase reporter analysis and chromatin immunoprecipitation (ChIP). RESULTS: YBX1 expression was upregulated, and miR-148a-3p and Runx3 levels were reduced in NSCLC samples and cell lines. YBX1 silence restrained NSCLC cell proliferation, migration, invasion and tumor growth, and enhanced apoptosis. YBX1 was targeted via miR-148a-3p. MiR-148a-3p knockdown promoted cell proliferation, migration, invasion and tumor growth, and repressed apoptosis, and these effects were abolished by YBX1 silence. Runx3 upregulation restrained cell proliferation, migration, invasion and tumor growth, and facilitated apoptosis. Runx3 bound with miR-148a-3p promotor to regulate miR-148a-3p expression. Runx3 silence modulated YBX1 expression though miR-148a-3p to promote NSCLC progression by increasing Cyclin D1, Cyclin B1, Slug-1, MMP-2 and MMP-9 levels. CONCLUSION: Runx3-miR-148a-3p axis targeted YBX1 to modulate NSCLC progression.

KLHL38 involvement in non-small cell lung cancer progression via activation of the Akt signaling pathway.

Lung cancer is the leading cause of cancer-related death worldwide. KLHL38 has been reported to be upregulated during diapause but downregulated after androgen treatment during the reversal of androgen-dependent skeletal muscle atrophy. This study aimed to clarify the role of KLHL38 in non-small cell lung cancer (NSCLC). KLHL38 expression was evaluated in tumor and adjacent normal tissues from 241 patients with NSCLC using immunohistochemistry and real-time PCR, and its association with clinicopathological parameters was analyzed. KLHL38 levels positively correlated with tumor size, lymph node metastasis, and pathological tumor-node-metastasis stage (all P < 0.001). In NSCLC cell lines, KLHL38 overexpression promoted PTEN ubiquitination, thereby activating Akt signaling. It also promoted cell proliferation, migration, and invasion by upregulating the expression of genes encoding cyclin D1, cyclin B, c-myc, RhoA, and MMP9, while downregulating the expression of p21 and E-cadherin. In vivo experiments in nude mice further confirmed that KLHL38 promotes NSCLC progression through Akt signaling pathway activation. Together, these results indicate that KLHL38 is a valuable candidate prognostic biomarker and potential therapeutic target for NSCLC.

MZT2A promotes NSCLC viability and invasion by increasing Akt phosphorylation via the MOZART2 domain.

Mitotic spindle organizing protein 2A (MZT2A) is localized at the centrosome and regulates microtubule nucleation activity in cells. This study assessed the role of MZT2A in non-small-cell lung cancer (NSCLC). Differential MZT2A expression was bioinformatically assessed using TCGA database, the GEPIA database, and Kaplan-Meier survival data to determine the association between MZT2A expression and NSCLC prognosis. Furthermore, NSCLC tissue specimens were evaluated by immunohistochemistry. MZT2A was overexpressed or knocked down in NSCLC cells using cDNA and siRNA, respectively. The cells were subjected to various assays and treated with the selective Akt inhibitor LY294002 or co-transfected with galectin-3-binding protein (LGALS3BP) siRNA. MZT2A mRNA and protein levels were upregulated in NSCLC lesions and MTZ2A expression was associated with poor NSCLC prognosis. MZT2A protein was also highly expressed in NSCLC cells compared with the expression in normal bronchial cells. MZT2A expression promoted NSCLC cell viability and invasion, whereas MTZ2A siRNA had the opposite effect on NSCLC cells in vitro. At the protein level, MZT2A induced Akt phosphorylation, promoting NSCLC proliferation and invasion (but the selective Akt inhibitor blocked these effects) through upregulation of LGALS3BP via the MTZ2A MOZART2 domain, whereas LGALS3BP siRNA suppressed MTZ2A activity in NSCLC cells. The limited in vivo experiments confirmed the in vitro data. In conclusion, MZT2A exhibits oncogenic activity by activating LGALS3BP and Akt in NSCLC. Future studies will assess MTZ2A as a biomarker to predict NSCLC prognosis or as a target in the control of NSCLC progression.

JMJD8 Promotes Malignant Progression of Lung Cancer by Maintaining EGFR Stability and EGFR/PI3K/AKT Pathway Activation.

JMJD8 is a JmjC domain-containing protein that has not been widely examined, despite its potential role in malignant tumor development. The underlying biological functions and molecular mechanisms of JMJD8 in non-small-cell lung cancer (NSCLC) remain unclear. Herein, we explored the relationship between JMJD8 and the activation of malignancy pathways in NSCLC. Immunohistochemical analyses revealed that high JMJD8 expression significantly correlated with cell differentiation and advanced TNM stages of NSCLC. The overexpression of JMJD8 promoted cell proliferation and invasion in vitro. Upon JMJD8 knockdown in lung cancer cell lines, cyclin B1, RhoA, RhoC, MMP9, and N-cadherin were down-regulated, and p21 and E-cadherin were conversely up-regulated. Key factors in the PI3K/AKT signaling pathway, such as p­AKT, showed clear decreases in expression; additionally, the expression of epidermal growth factor receptor (EGFR), which functions upstream of PI3K, was altered. Co-immunoprecipitation experiments indicated that JMJD8 interacts with EGFR, and JMJD8 knockdown accelerated EGFR degradation. Our results suggested that JMJD8 functions as an oncogenic regulator in NSCLC. We found that JMJD8 promotes carcinogenic activity in NSCLC cells by facilitating EGFR stability, thereby activating the downstream PI3K/AKT signaling pathway. JMJD8 shows potential as a prognostic marker for lung cancer patients, providing a new target for therapeutic strategies.

PCGF3 promotes the proliferation and migration of non-small cell lung cancer cells via the PI3K/AKT signaling pathway.

The Polycomb Group Ring Finger 3 (PCGF3) protein has been reported to be significantly upregulated in pancreatic islet tumors and related to signal transduction; however, its detailed mechanisms and biological roles in other tumors, including non-small cell lung cancer (NSCLC), remain unclear. This study investigated the function of PCGF3 in NSCLC and further elucidated its mechanism of action. The immunohistochemical analysis of 86 selected lung cancer tissues revealed that PCGF3 was highly expressed in NSCLC tissues and positively correlated with lymph node metastasis and p-TNM staging. Additionally, PCGF3 promoted cell proliferation in lung cancer by regulating CyclinB1, CyclinD1, and CDK4 expression, and also promoting their migration by regulating RhoA, RhoC, and CDC42. Furthermore, PCGF3 affected both the proliferation and migration of lung cancer cells by regulating the PI3K/AKT pathway, as verified by inhibiting this pathway using LY294002. The findings of this study suggested that PCGF3 is associated with poor prognosis in patients with NSCLC and could therefore be an important biomarker for treating and preventing NSCLC.

Silencing of CASC8 inhibits non-small cell lung cancer cells function and promotes sensitivity to osimertinib via FOXM1.

In a meta-analysis, the long noncoding RNA cancer susceptibility candidate 8 (CASC8) was found to be a cancer susceptibility gene closely related to lung cancer, but its functions in lung cancer are unknown. In the Cancer Genome Atlas database, the expression of CASC8 was significantly higher in non-small cell lung cancer than in adjacent normal tissues, and high expression of CASC8 was associated with poor prognosis in patients with lung adenocarcinoma. Silencing CASC8 inhibited proliferation, migration, and invasion in non-small cell lung cancer cell lines. Silencing CASC8 also promoted sensitivity to osimertinib through Forkhead box M1 (FOXM1). Therefore, this pathway can be exploited in patients with lung cancer resistant to targeted therapies. Our study revealed for the first time that silencing CASC8 inhibited the proliferation, migration, and invasion of non-small cell lung cancer cells and promoted their sensitivity to osimertinib, suggesting that CASC8 is closely related to the occurrence and development of non-small cell lung cancer. This may provide insight into mechanisms of treatment for non-small cell lung cancer.

Modeling and Mapping High Water Table for a Coastal Region in Florida using Lidar DEM Data.

Predicting and mapping high water table elevation in coastal landscapes is critical for both science application projects like inundation risk analysis and engineering projects like pond design and maintenance. Previous studies of water table mapping focused on the application of geostatistical methods, which cannot predict values beyond an observation spatial domain or generate an ideal pattern for regions with sparse measurements. In this study, we evaluated the multiple linear regression (MLR) and support vector machine (SVM) techniques for high water table prediction and mapping using fine spatial resolution lidar-derived Digital Elevation Model (DEM) data, and designed an application protocol of these two techniques for high water table mapping in a coastal landscape where groundwater, tide, and surface water are related. Testing results showed that SVM largely improved the high water table prediction with a mean absolute error (MAE) of 1.22 feet and root mean square error (RMSE) of 2.22 feet compared to the application of the ordinary Kriging method which could not generate a reasonable water table. MLR was also promising with a MAE of around 2 feet and RMSE of around 3 feet. The study suggests that both MLR and SVM are valuable alternatives to estimate high water table elevation in Florida. Fine resolution lidar DEMs are beneficial for high water table prediction and mapping.

KLHL18 inhibits the proliferation, migration, and invasion of non-small cell lung cancer by inhibiting PI3K/PD-L1 axis activity.

BACKGROUND: The expression of Kelch-like protein 18 (KLHL18) in non-small cell lung cancer (NSCLC) is lower than that in normal lung tissue according to the Gene Expression Profiling Interactive Analysis database. KLHL18 is a BTB domain protein and binds cullin 3 (CUL3). However, whether this complex participates in ubiquitination-mediated protein degradation in NSCLC is unclear. Therefore, we aimed to investigate the role of KLHL18 in human NSCLC cells. RESULTS: We found that KLHL18 is downregulated in cancer cells and is associated with poor prognosis. Further, its expression was significantly associated with tumor node metastasis (TNM) stage, lymph node metastasis, and tumor size. In vitro analysis of NSCLC cells showed that overexpressing KLHL18 inhibited cell proliferation, migration, and invasion. We found that the tumor-inhibitory effect of the KLHL18 protein was achieved by promoting the ubiquitination and degradation of phosphatidylinositol 3-kinase (PI3K) p85α and inhibiting the expression of PD-L1 protein, ultimately preventing tumor cell immune escape. CONCLUSIONS: Our results identified the tumor-suppressive mechanism of KLHL18 and suggested that it is closely related to NSCLC occurrence and development. Further investigation of the underlying mechanism may provide new targets for NSCLC treatment.

Mechanical Behavior of Single Patch Composite Repaired Al Alloy Plates: Experimental and Numerical Analysis.

In this paper, glass fiber reinforced polymer (GFRP) materials were used to repair cracked Al plates. In order to study the influences of resin properties and repair configurations, three resins and two patch configurations were selected to manufacture six groups of specimens. It turned out that only little differences (less than 3%) were found in tensile strength among the six groups. Compared with the parent plates, the strength recovery ratio was higher than 80% after the GFRP repair, representing excellent repair efficiency. Moreover, a finite element model (FEM) was established to analyze the failure process of the repaired structure under tensile loading. The FEM results show good agreement with the experimental results, indicating good precision. Both the experimental and numerical work found that the damage initiated in the plies adjacent to the crack surface and the failure modes was mainly delamination and fiber breakage. This work will be meaningful for the future application of GFRP in metallic structures.