Invasive Behavior Research Articles

A hazard-based duration model for analyzing crossing risk exposure time of electric two-wheeler riders at signalized intersections

Electric two-wheeler riders' invasion behavior is a violation and a significant contributor to traffic safety concerns. Invasion duration, an essential parameter in invasion behavior, measures the travel time of an ETW rider in a motorized lane and represents the rider's risk exposure time. This paper endeavors to elucidate the characteristics of invasion behavior and model invasion duration. Using trajectory data, it addresses questions about the length, degree, duration, and two phases of invasion behavior. The hazard-based duration model is employed to fit the duration and analyze the factors influencing it. The results indicate that characteristics exhibit mean values of 3.23 s for duration, 8.313 m for length, and 0.629 m for degree. The log-logistic Accelerated Failure Time (AFT) model exhibits better performance for fitting invasion duration than the Weibull and the Log-normal AFT models. The findings of this paper can provide a reference for enhancing traffic safety and efficiency.

The Up-Regulated Expression of Mitochondrial Membrane Molecule RHOT1 in Gastric Cancer Predicts the Prognosis of Patients and Promotes the Malignant Biological Behavior of Cells.

Gastric cancer (GC) remains a major disease of high morbidity and mortality worldwide despite advances in diagnosis and treatment. Ras homolog family member T1 (RHOT1) plays an important role in several cancers. Our study aimed to analyze RHOT1 expression, to assess the relationship between its expression and the prognosis of patients, and know the impact of RHOT1 on GC cells. The Cancer Genome Atlas (TCGA) RNA-seq data was used for gene expression analysis, survival and prognostic analysis. Nomograms were created to analyze the pathological factors of GC patients. RHOT1 expression was up-regulated by analyzed TCGA-Stomach adenocarcinoma (STAD) data and verified by Polymerase Chain Reaction (PCR) assay in GC tissues and cell lines. Furthermore, RHOT1 up-regulation was significantly associated with shorter survival of GC patients. At last, after silencing the expression of RHOT1 in AGS cell lines, we found that the proliferative ability of the cells was significantly reduced, the cell invasion ability was significantly inhibited, the cell migration ability was also significantly weakened, the cell cycle was arrested in the G0/G1 phase, and apoptosis was significantly increased. So RHOT1 could impact the apoptosis, proliferation, invasion, and migration behavior of GC cells. We trust RHOT1 has the potential to become a new oncogene biomarker for diagnosis and prognosis as well as a new therapeutic target in GC.

Crocin inhibit the metastasis of MDA-MB-231 cell line by suppressing epithelial to mesenchymal transition through WNT/β-catenin signalling pathway.

Triple-negative breast cancer has the poorest prognosis and survival rates compared to other breast cancer subtypes due to its invasive behaviours. This type of cancer does not respond to biological therapies and exhibits resistance to available treatment options. Therefore, it is imperative to discover new therapeutics to address this challenge. In this study, a TNBC cell line was utilized to investigate the anti-metastatic effect of crocin on the Wnt/β-catenin pathway. Cell proliferation was assessed using the MTT assay, and the effects of crocin on migration were monitored through transwell and wound healing experiments. The expression of specific epithelial-mesenchymal transition marker genes was evaluated using real-time polymerase chain reaction, and β-catenin expression was also examined through real-time polymerase chain reaction. The findings revealed that crocin significantly inhibits cell proliferation and migration of tumour cells in a dose-dependent manner. Moreover, crocin decreased the expression of Vimentin, Snail, Zeb-1, and β-catenin. Additionally, crocin increased the expression of E-cadherin in the MDA-MB-231 cell line. The results demonstrated an association between crocin and the Wnt/β-catenin signalling pathway. In conclusion, this study establishes that crocin holds promise as a potential therapeutic option for triple-negative breast cancer.

Platelet count as a predictor of vascular invasion and extrahepatic metastasis in hepatocellular carcinoma: A systematic review and meta-analysis

BackgroundVascular invasion (VI) indicates highly invasive tumor biological behavior and is a major determining factor of poor survival and high risk of metastasis in hepatocellular carcinoma (HCC). Epidemiological evidence of the association between pretherapeutic platelet count (PLT) and the risk of VI and extrahepatic metastasis in HCC remains controversial. MethodsA systematic retrieval was executed in databases of PubMed, Embase, and Web of Science until Dec 2022. Effect size and 95% confidence interval (CI) were extracted or estimated to synthetically investigate the effects of pretherapeutic PLT on VI and extrahepatic metastasis. Meta-analyses were performed by using a random or a fixed effects model. ResultsFinally, the current meta-analysis included 15 studies with a total of 12,378 HCC patients. It was shown that, patients with a higher pretherapeutic level of PLT had a significantly increased risk of VI (11 studies,8,759 patients; OR = 1.44, 95%CI: 1.02–2.02) and extrahepatic metastasis (6 studies,8, 951 patients; OR = 2.51, 95% CI: 2.19–2.88) in comparison with patients with a lower PLT. Funnel plots and Begg's tests indicated that there were no significant publication biases. ConclusionThis meta-analysis shows that pretherapeutic elevated PLT is associated with an increased risk of VI and extrahepatic metastasis in HCC.

A modular microfluidic platform to study how fluid shear stress alters estrogen receptor phenotype in ER+ breast cancer cells

Metastatic breast cancer leads to poor prognoses and worse outcomes in patients due to its invasive behavior and poor response to therapy. It is still unclear what biophysical and biochemical factors drive this more aggressive phenotype in metastatic cancer; however recent studies have suggested that exposure to fluid shear stress in the vasculature could cause this. In this study a modular microfluidic platform capable of mimicking the magnitude of fluid shear stress (FSS) found in human vasculature was designed and fabricated. This device provides a platform to evaluate the effects of FSS on MCF-7 cell line, an estrogen receptor positive (ER+) breast cancer cell line, during circulation in the vessels. Elucidation of the effects of FSS on MCF-7 cells was carried out utilizing two approaches: single cell analysis and bulk analysis. For single cell analysis, cells were trapped in a microarray after exiting the serpentine channel and followed by immunostaining on the device (on-chip). Bulk analysis was performed after cells were collected in a microtube at the outlet of the microfluidic serpentine channel for western blotting (off-chip). It was found that cells exposed to an FSS magnitude of 10 dyn/cm2 with a residence time of 60 s enhanced expression of the proliferation marker Ki67 in the MCF-7 cell line at a single cell level. To understand possible mechanisms for enhanced Ki67 expression, on-chip and off-chip analyses were performed for pro-growth and survival pathways ERK, AKT, and JAK/STAT. Results demonstrated that after shearing the cells phosphorylation of p-AKT, p-mTOR, and p-STAT3 were observed. However, there was no change in p-ERK1/2. AKT is a mediator of ER rapid signaling, analysis of phosphorylated ERα was carried out and no significant differences between sheared and non-sheared populations were observed. Taken together these results demonstrate that FSS can increase phosphorylation of proteins associated with a more aggressive phenotype in circulating cancer cells. These findings provide additional information that may help inform why cancer cells located at metastatic sites are usually more aggressive than primary breast cancer cells.

Epithelial-Mesenchymal Transition: A Fundamental Cellular and Microenvironmental Process in Benign and Malignant Prostate Pathologies.

Epithelial-mesenchymal transition (EMT) is a crucial and fundamental mechanism in many cellular processes, beginning with embryogenesis via tissue remodulation and wound healing, and plays a vital role in tumorigenesis and metastasis formation. EMT is a complex process that involves many transcription factors and genes that enable the tumor cell to leave the primary location, invade the basement membrane, and send metastasis to other tissues. Moreover, it may help the tumor avoid the immune system and establish radioresistance and chemoresistance. It may also change the normal microenvironment, thus promoting other key factors for tumor survival, such as hypoxia-induced factor-1 (HIF-1) and promoting neoangiogenesis. In this review, we will focus mainly on the role of EMT in benign prostate disease and especially in the process of establishment of malignant prostate tumors, their invasiveness, and aggressive behavior. We will discuss relevant study methods for EMT evaluation and possible clinical implications. We will also introduce clinical trials conducted according to CONSORT 2010 that try to harness EMT properties in the form of circulating tumor cells to predict aggressive patterns of prostate cancer. This review will provide the most up-to-date information to establish a keen understanding of the cellular and microenvironmental processes for developing novel treatment lines by modifying or blocking the pathways.

Auraptene inhibits migration, invasion and metastatic behavior of human malignant glioblastoma cells: An in vitro and in silico study.

The present work examined the anti-metastatic effects of auraptene and their underlying mechanisms of action in U87 Glioblastoma multiforme (GBM) cells. To test the hypothesis, cell culture, Matrigel invasion assay, scratch wound healing assay, gelatin zymography assay, qRT-PCR, and western blot experiments were conducted. At sublethal concentrations of 12.5 and 25 µg/ml, auraptene exhibited a significant reduction in cell invasion and migration of U87 cells, as assessed using scratch wound healing and Transwell tests, respectively. The qRT-PCR and zymography experiments demonstrated a significant decrease in both mRNA expression and activities of MMP-2 and MMP-9 following auraptene treatment. Western blot analysis also showed that MMP-2 protein level and phosphorylation of metastasis-related proteins (p-JNK and p-mTOR) decreased in auraptene-treated cells. Molecular docking studies consistently demonstrated that auraptene exhibits a significant affinity towards MMP-2/-9, the ATP binding site of mTOR and JNK1/2/3. Auraptene inhibited the migration and invasion of GBM cells. This inhibitory effect was induced by modulating specific mechanisms, including suppressing MMPs, JNK, and mTOR activities.

Research on Water Invasion Law and Control Measures for Ultradeep, Fractured, and Low-Porosity Sandstone Gas Reservoirs: A Case Study of Kelasu Gas Reservoirs in Tarim Basin

The exploitation of ultradeep, fractured, and low-porosity gas reservoirs often encounters challenges from water invasion, exacerbated by the presence of faults and fractures. This is particularly evident in the Kelasu gas reservoir group, located in the Kuqa Depression of the Tarim Basin. The complexity of the water invasion patterns in these reservoirs demands a thorough investigation to devise effective water control measures. To elucidate the water invasion patterns, a combined approach of large-scale physical modeling and discrete fracture numerical simulations was adopted. These models allowed for the identification and categorization of water invasion behaviors in various gas reservoirs. Furthermore, production dynamic analysis was utilized to tailor water control strategies to specific invasion patterns. The large-scale physical simulation experiment revealed that water invasion in gas reservoirs is primarily influenced by high-permeability channels (faults + fractures), and that the gas production rate serves as the key factor governing gas reservoir development. The range of gas extraction rates spans from 3% to 5%. As the gas extraction rate increases, the extraction intensity diminishes and the stable production duration shortens. On the basis of the changes in the water breakthrough time and water production rate, a 2% gas extraction rate is determined as the optimal rate for the model. The embedded discrete fracture numerical simulation model further supports the findings of the physical simulation experiments and demonstrates that ① this type of gas reservoir exhibits typical nonuniform water invasion patterns, controlled by structural location, faults, and degree of crack development; ② the water invasion patterns of gas reservoirs can be categorized into three types, these being explosive water flooding and channeling along faults, uniform intrusion along fractures, and combined intrusion along faults and fractures; ③ drawing from the characteristics of water invasion in various gas reservoirs, combined with production well dynamics and structural location, a five-character water control strategy of “prevention, control, drainage, adjustment, and plugging” is formulated, with the implementation of differentiated, one-well, one-policy governance. The study concludes that a proactive approach, prioritizing prevention, is crucial for managing water-free gas reservoirs. For water-bearing reservoirs, a combination of three-dimensional water plugging and drainage strategies is recommended. These insights have significant implications for extending the productive lifespan of gas reservoirs, enhancing recovery rates, and contributing to the economic and efficient development of ultradeep, fractured, and low-porosity gas reservoirs.

Modelling the propagation of invasive tree species: A coupled differential equation approach

Invasive tree species pose a grave global threat to biodiversity, particularly impacting vulnerable grassland ecosystems. This paper presents a novel approach to simulate the invasion of ecosystems by these aggressive species. Our innovative coupled ODE‐PDE model offers explicit invasion simulations, a significant leap beyond traditional integro‐difference matrix models. With robust theoretical properties, including solution positivity, and drawing upon PDE theory, our model offers deeper insights into invasion behavior. Our model reveals that invasions undergo a prolonged quiescent phase before rapidly transitioning to a consistent rate of advancement after a critical point. This study not only sheds light on invasion dynamics but also charts a course for future exploration and potential model extensions.

Cyclin D1 in various cancers: Mechanisms and clinical implications

Gastrointestinal cancers, including esophageal, gastric, hepatic, pancreatic, and colorectal malignancies, present a significant global health challenge. Their distinct characteristics characterized by abnormal cell proliferation, invasive behavior, and tumor formation make them highly aggressive and detrimental to human health. These diseases often lead to malnutrition, organ failure, and obstruction. Cyclin D1 protein is a critical regulator of cell cycle progression and an essential marker for comprehending the complex landscape of cancer biology. This research provides an in-depth exploration of gastrointestinal cancers by shedding light on their adverse effects on the human body while emphasizing the critical role played by cyclin D1 within this challenging disease context. Extensively studied in colorectal cancer as well as esophageal squamous cell carcinoma (ESCC), gastric cancer, and pancreatic cancer contexts. Cyclin D1 emerges as a key player. Specifically, in cases of colorectal cancer, overexpression of cyclin D1 is frequently linked to aggressive tumor behavior brought on by APC gene mutations and abnormal Wnt signalling pathway activation. Esophageal cancer patients especially those with ESCC frequently exhibit elevated levels of Cyclin D1 indicating poor prognosis. A similar trend is observed in gastric cancer where increased expression of cyclin D1 is linked to disease severity.

Abstract A110: Clec4f is expressed in a subset of primary PDAC cells and confers invasive behavior

Abstract Pancreatic ductal adenocarcinoma (PDAC) is a particularly deadly disease with a 5-year survival rate of just 12%. Poor survival is due in part to late detection of aggressive disease coincident with distant metastases, most often in the liver. While multiple proteins have been implicated in driving PDAC metastasis, effective targeted therapeutics have yet to be developed. Therefore, understanding factors contributing to PDAC liver metastasis has significant implications for diagnosis and treatment of the disease. Evidence has emerged to suggest that a subpopulation of cells with a pre-disposition for successful seeding and outgrowth in the liver are cultivated at the primary site prior to dissemination. Investigating public datasets generated from mouse models of PDAC liver metastasis, we noted upregulation of C-type Lectin Domain Family 4 Member F (Clec4f), a galactose-binding receptor. Importantly, we also detected Clec4f expression in a subset of primary PDAC tumor epithelial cells, which established our hypothesis that Clec4f is a novel regulator of PDAC dissemination. Preliminary in vitro invasion assays demonstrate that PDAC cells engineered to overexpress Clec4f exhibit more invasive behavior compared to control cells, displaying a more mesenchymal phenotype upon confluence in 2D culture and increased invasive protrusion when grown as 3D spheroids compared to control cells. To better examine tumor-intrinsic Clec4f-expressing PDAC cells in isolation, we sorted Clec4f-expressing cells from a mouse PDAC tumor via FACS to culture in vitro. However, upon establishment in culture, the sorted cells lost Clec4f expression. Importantly, Clec4f expression in other cell types has been shown to be dependent on niche-derived TGFβ signaling, which has also been shown to regulate tumor cell invasiveness and dissemination in PDAC. This led us to probe for Clec4f-expressing tumor cells in a mouse model of PDAC lacking TGFβ receptor 2 (PKT model). In the PKT model, we observed no Clec4f-expressing tumor cells, which suggested that niche-derived TGFβ signaling is required for the upregulation of Clec4f in PDAC. Using a variety of established cellular markers, we also determined that Clec4f was co-expressed in a subset of Synaptophysin (Syp) positive enteroendocrine cells in PDAC tissue. We are currently working to determine which niche components in the tumor microenvironment provide the necessary signals to upregulate Clec4f expression in PDAC tumor cells. We expect the outcome of this study to shed light upon pro-dissemination niche dynamics in PDAC and how they contribute to the deadly process of liver metastasis. Citation Format: Bailey A. Bye, Richard M. Walsh, Austin E. Eades, Michael N. VanSaun. Clec4f is expressed in a subset of primary PDAC cells and confers invasive behavior [abstract]. In: Proceedings of the AACR Special Conference in Cancer Research: Pancreatic Cancer; 2023 Sep 27-30; Boston, Massachusetts. Philadelphia (PA): AACR; Cancer Res 2024;84(2 Suppl):Abstract nr A110.

Single cell sequencing revealed the mechanism of CRYAB in glioma and its diagnostic and prognostic value.

We explored the characteristics of single-cell differentiation data in glioblastoma and established prognostic markers based on CRYAB to predict the prognosis of glioblastoma patients. Aberrant expression of CRYAB is associated with invasive behavior in various tumors, including glioblastoma. However, the specific role and mechanisms of CRYAB in glioblastoma are still unclear. We assessed RNA-seq and microarray data from TCGA and GEO databases, combined with scRNA-seq data on glioma patients from GEO. Utilizing the Seurat R package, we identified distinct survival-related gene clusters in the scRNA-seq data. Prognostic pivotal genes were discovered through single-factor Cox analysis, and a prognostic model was established using LASSO and stepwise regression algorithms. Moreover, we investigated the predictive potential of these genes in the immune microenvironment and their applicability in immunotherapy. Finally, in vitro experiments confirmed the functional significance of the high-risk gene CRYAB. By analyzing the ScRNA-seq data, we identified 28 cell clusters representing seven cell types. After dimensionality reduction and clustering analysis, we obtained four subpopulations within the oligodendrocyte lineage based on their differentiation trajectory. Using CRYAB as a marker gene for the terminal-stage subpopulation, we found that its expression was associated with poor prognosis. In vitro experiments demonstrated that knocking out CRYAB in U87 and LN229 cells reduced cell viability, proliferation, and invasiveness. The risk model based on CRYAB holds promise in accurately predicting glioblastoma. A comprehensive study of the specific mechanisms of CRYAB in glioblastoma would contribute to understanding its response to immunotherapy. Targeting the CRYAB gene may be beneficial for glioblastoma patients.

Gαi2 Protein Inhibition Blocks Chemotherapy- and Anti-Androgen-Induced Prostate Cancer Cell Migration.

We have previously shown that heterotrimeric G-protein subunit alphai2 (Gαi2) is essential for cell migration and invasion in prostate, ovarian and breast cancer cells, and novel small molecule inhibitors targeting Gαi2 block its effects on migratory and invasive behavior. In this study, we have identified potent, metabolically stable, second generation Gαi2 inhibitors which inhibit cell migration in prostate cancer cells. Recent studies have shown that chemotherapy can induce the cancer cells to migrate to distant sites to form metastases. In the present study, we determined the effects of taxanes (docetaxel), anti-androgens (enzalutamide and bicalutamide) and histone deacetylase (HDAC) inhibitors (SAHA and SBI-I-19) on cell migration in prostate cancer cells. All treatments induced cell migration, and simultaneous treatments with new Gαi2 inhibitors blocked their effects on cell migration. We concluded that a combination treatment of Gαi2 inhibitors and chemotherapy could blunt the capability of cancer cells to migrate and form metastases.

Invasive behaviour of oak lace bug in forest ecosystems: a comparative analysis between thermophilous and mesophilous oak forests

Forest ecosystems provide invaluable ecological, economic, and social benefits, making them essential for global well-being. However, these ecosystems face various threats, including biological invasions by alien species. Among these, the oak lace bug (OLB), an invasive North American insect, has rapidly spread in Europe, impacting oak forests and raising concerns about its adaptation to new environments. OLB feeds on the undersides of oak leaves, extracting sap and causing chlorotic discoloration. Severe infestations lead to premature defoliation, increased susceptibility to diseases or pests and can also result in a substantial reduction in photosynthesis activity. This study aims to analyse OLB’s invasive behaviour in Romanian forest ecosystems, with a specific focus on the differences between thermophilous and mesophilous oak forests. The analysis covers 6 years of data and reveals critical insights. In the initial 4 years, OLB predominantly inhabited the extracarpathian regions of Romania, with concentrated presence in the southern, western, and northwestern areas. Forest ecosystems mainly affected between 2017 and 2020 were characterized by thermophilous oak forests in southern and western regions. However, in the last 2 years (2021–2022), OLB presence increased, particularly in lowland ecosystems, albeit with reduced damage intensity. The analysis also unveiled an adaptation and expansion of OLB in mesophilous forest ecosystems. Climatic factors, specifically temperature and precipitation, significantly influenced OLB’s behaviour, points with severe attacks exhibiting specific climatic conditions. In summary, this study provides crucial insights into OLB’s behaviour, emphasizing the role of climatic and environmental factors in its invasive tendencies.

Radiomic Analysis in Pituitary Tumors: Current Knowledge and Future Perspectives.

Radiomic analysis has emerged as a valuable tool for extracting quantitative features from medical imaging data, providing in-depth insights into various contexts and diseases. By employing methods derived from advanced computational techniques, radiomics quantifies textural information through the evaluation of the spatial distribution of signal intensities and inter-voxel relationships. In recent years, these techniques have gained considerable attention also in the field of pituitary tumors, with promising results. Indeed, the extraction of radiomic features from pituitary magnetic resonance imaging (MRI) images has been shown to provide useful information on various relevant aspects of these diseases. Some of the key topics that have been explored in the existing literature include the association of radiomic parameters with histopathological and clinical data and their correlation with tumor invasiveness and aggressive behavior. Their prognostic value has also been evaluated, assessing their role in the prediction of post-surgical recurrence, response to medical treatments, and long-term outcomes. This review provides a comprehensive overview of the current knowledge and application of radiomics in pituitary tumors. It also examines the current limitations and future directions of radiomic analysis, highlighting the major challenges that need to be addressed before a consistent integration of these techniques into routine clinical practice.

The importance of cancer-associated fibroblasts in targeted therapies and drug resistance in breast cancer.

Cancer-associated fibroblasts (CAFs) play a substantial role in the tumor microenvironment, exhibiting a strong association with the advancement of various types of cancer, including breast, pancreatic, and prostate cancer. CAFs represent the most abundant mesenchymal cell population in breast cancer. Through diverse mechanisms, including the release of cytokines and exosomes, CAFs contribute to the progression of breast cancer by influencing tumor energy metabolism, promoting angiogenesis, impairing immune cell function, and remodeling the extracellular matrix. Moreover, CAFs considerably impact the response to treatment in breast cancer. Consequently, the development of interventions targeting CAFs has emerged as a promising therapeutic approach in the management of breast cancer. This article provides an analysis of the role of CAFs in breast cancer, specifically in relation to diagnosis, treatment, drug resistance, and prognosis. The paper succinctly outlines the diverse mechanisms through which CAFs contribute to the malignant behavior of breast cancer cells, including proliferation, invasion, metastasis, and drug resistance. Furthermore, the article emphasizes the potential of CAFs as valuable tools for early diagnosis, targeted therapy, treatment resistance, and prognosis assessment in breast cancer, thereby offering novel approaches for targeted therapy and overcoming treatment resistance in this disease.

A CT-based diagnostic nomogram and survival analysis for differentiating grade 3 pancreatic neuroendocrine tumors from pancreatic ductal adenocarcinomas.

To construct a CT-based diagnostic nomogram for distinguishing grade 3 pancreatic neuroendocrine tumors (G3 PNETs) from pancreatic ductal adenocarcinomas (PDACs) and assess their respective survival outcomes. Patients diagnosed with G3 PNETs (n = 30) and PDACs (n = 78) through surgery or biopsy from two medical centers were retrospectively identified. Demographic and radiological information, including age, gender, tumor diameter, shape, margin, dilatation of pancreatic duct, and invasive behavior, were carefully collected. A nomogram was established after univariate and multivariate logistic regression analyses. The Kaplan-Meier survival was performed to analyze their survival outcomes. Factors with a p-value <0.05, including age, CA 19-9, pancreatic duct dilatation, irregular shape, ill-defined margin, pancreatic atrophy, combined pancreatitis, arterial/portal enhancement ratio, were included in the multivariate logistic analysis. The independent predictive factors, including age (OR, 0.91; 95% CI, 0.85-0.98), pancreatic duct dilatation (OR, 0.064; 95% CI, 0.01-0.32), and portal enhancement ratio (OR, 1,178.08; 95% CI, 5.96-232,681.2) were determined to develop a nomogram. The internal calibration curve and decision curve analysis demonstrate that the nomogram exhibits good consistency and discriminative capacity in distinguishing G3 PNETs from PDACs. Patients diagnosed with G3 PNETs exhibited considerably better overall survival outcomes compared to those diagnosed with PDACs (median survival months, 42 vs. 9 months, p < 0.001). The nomogram model based on age, pancreatic duct dilatation, and portal enhancement ratio demonstrates good accuracy and discriminative ability effectively predicting the probability of G3 PNETs from PDACs. Furthermore, patients with G3 PNETs exhibit better prognosis than PDACs.

Inhibitory effect of miR-377 on the proliferative and invasive behaviors of prostate cancer cells through the modulation of MYC mRNA via its interaction with BCL-2/Bax, PTEN, and CDK4.

The MYC gene is a regulatory and proto-oncogenic gene that is overexpressed in the majority of prostate cancers (PCa). Numerous studies have indicated that aberrant expression of microRNAs is involved in the initiation and progression of prostate cancer. In this investigation, we assessed the impact of miR-377 on MYC through luciferase assay. Real-time PCR was employed to determine whether miR-377 could reduce the levels of MYC mRNA in transfected PCa cell lines (PC-3 and DU145) and change in the mRNA levels of BCL-2/Bax, PTEN, and CDK4 as a consequence of MYC downregulation. Moreover, we analyzed the effects of miR-377 on apoptosis, proliferation, cell cycle, and wound healing. Our findings demonstrate that miR-377 effectively targets MYC mRNA, as confirmed by luciferase assay and Real-time PCR. We observed a significant reduction in BCL-2 and CDK4 expression, along with an increase in Bax and PTEN, in prostate cancer cell lines upon MYC suppression. Additionally, elevated levels of miR-377 in PCa cell lines induced apoptosis, inhibited proliferation and migration, and arrested the cell cycle. Taken together, these results unveil the inhibitory role of miR-377 in MYC function within PCa, thereby suggesting its potential as a therapeutic target for the treatment of this malignancy.

The migratory and invasive behaviour of malignant meningioma cells depends on glucose concentration and glycation

The migratory and invasive behaviour of malignant meningioma cells depends on glucose concentration and glycation

Downregulation of LPAR1 Promotes Invasive Behavior in Papillary Thyroid Carcinoma Cells.

Lysophosphatidic acid receptor 1 (LPAR1) has been identified as a biomarker in various cancer types. However, its biological function in papillary thyroid carcinoma (PTC) remains unknown. LPAR1 was identified as a key regulator of epithelial-mesenchymal transition (EMT) in PTC cells through bioinformatics analysis of TCGA and GEO datasets. PPI analysis and correlation with immune infiltrates were also conducted. LPAR1 expression was evaluated using Gepia2 and GTEx, and miRNA target gene prediction was done with multiMiR. To assess the expression of LPAR1, we extracted total RNA from both the BCPAP cell line and the normal human thyroid epithelial cell line Nthy-ori 3-1. The levels of LPAR1 expression were then measured using quantitative real-time polymerase chain reaction (qRT-PCR) in the BCPAP cell line, with a comparison to the Nthy-ori 3-1 cell line. 1081 genes were upregulated, and 544 were downregulated compared to normal tissue. LPAR1 was identified as a key candidate by analyzing the TCGA and GEO datasets. PPI data analysis showed interactions with metastasis-related proteins. Functional enrichment analysis indicated involvement in signaling pathways like phospholipase D and actin cytoskeleton regulation. LPAR1 expression correlated positively with immune infiltrates such as CD4+ T cells, macrophages, neutrophils, and myeloid dendritic cells but negatively with B cells. Additionally, miR-221-5p was predicted to target LPAR1 in PTC. Furthermore, our experimental data demonstrated that LPAR1 was under-expressed in the PTC cell line compared to the nonmalignant one (P < .01). LPAR1 suppresses metastasis and is linked to EMT, as evidenced by the decreased LPAR1 expression and increased miR-221-5p in PTC. This suggests its potential as a biomarker for diagnosis and prognosis and as a therapeutic target for EMT.