Long non-coding RNAs (lncRNAs) are involved in the numerous types of tumors. The aim of this study is to comprehend the pathological mechanism of lncRNA CASC19 in ovarian cancer. CASC19, miR-761 and CBX2 expression in the samples was quantitatively detected by real-time quantitative polymerase chain reaction (RT-qPCR) reaction. The proliferation and apoptosis levels of ovarian cancer cells were evaluated via cell counting kit-8 (CCK-8) and Flow cytometry assays. The targeting relationship and correlation of CASC19, miR-761 and CBX2 were investigated through luciferase reporter assay and Pearson assay. CASC19 and CBX2 were enriched in ovarian cancer, while miR-761 expression was decreased. Silencing CASC19 suppressed the cell growth and promoted cell apoptosis. CASC19 targeted the inhibition of miR-761 expression and regulated the level of CBX2. In addition, the miR-761 inhibitor reversed the inhibitory effect of si-CASC19 on the biological activity of ovarian cancer cells, while si-CBX2 restored the regulation of miR-761 inhibitor on the development of ovarian cancer. lncRNA CASC19 mediated the malignant progression of ovarian cancer through miR-761/CBX2 axis, which provided a potential therapeutic target for the cure of patients.

Gastric cancer (GC) is a widespread cancerous disease with an unfavorable prognosis, linc01105 appears to have a significant connection with the development of GC, but the precise regulatory mechanism remains obscure. Real-time quantitative polymerase chain reaction (RT-qPCR) was utilized to determine the expression of linc01105, miR-650, and TCEA3. Proliferative capacity of GC cells was measured by CCK8. Cell apoptosis rates were analyzed via flow cytometry assessment. The invasive capability was assessed through the Transwell experiment. The targeted regulation of linc01105, miR-650, and TCEA3 was validated through dual luciferase reporter gene assay. Low expression of linc01105, high expression of miR-650, and low expression of TCEA3 were observed in GC tumor tissues and cell lines. High expression of linc01105 was correlated with a positive prognosis in GC patients. linc01105 affected GC cell function by miR-650/TCEA3 axis. This study suggested that linc01105 may possess inhibitory functions towards GC. In addition, linc01105 may be a prognostic marker for GC.

The Hippo pathway and its transcription co-activator YAP play a critical role in the regulation of cell proliferation, apoptosis and the control of organ size. In the past several years, YAP has been found to be expressed in various human cancers, however, its expression in Nasopharyngeal Carcinoma (NPC) remains unstudied. In this report, we found that YAP was overexpressed in human NPC tissues, and its expression was also significantly higher in five NPC cell lines when compared with the nasopharyngeal epithelial cell line NP69 (P < 0.01). CNE1 and CNE1-GL cells treated with EOS had an enhanced expression level of phosphorylated YAP and downregulated expression of survivin, which inhibits the proliferation of CNE1 and CNE1-GL cells. These results highlight an important role of hippo pathway in the growth of nasopharyngeal carcinoma and implicate a potential mechanism of ethyl acetate extract of oratosquilla (EOS) preventing the proliferation of nasopharyngeal carcinoma.

Iron is an essential trace element for the human body, but having too much or too little of it can cause various biological issues. When ferrous ions react with hydrogen peroxide, they create highly reactive and soluble hydroxyl radicals that can damage cells through oxidation. This reaction, known as the Fenton reaction, can cause lipid peroxidation and ferroptosis. Understanding how Fenton reaction-mediated ferroptosis works is crucial in treating rheumatoid arthritis (RA). Whether supplementing iron to induce ferroptosis or suppressing Fenton reaction-mediated ferroptosis is the key to regulating the pathophysiology of RA and cancer. Therefore, targeting ferroptosis regulators could be a promising new direction in developing therapeutic drugs for RA and cancer, which warrants further research.

Growth hormone-releasing hormone (GH-RH) and its antagonists are believed to influence the progression of various tumor diseases. However, the specific effects of GH-RH-related genes on lung adenocarcinoma (LUAD) are yet to be deciphered. GH-RH-related gene set data, LUAD transcriptome data, and clinical data were available for download at the GeneCards, TCGA, and GEO databases. R software was used to conduct differential, regression, cluster, survival, gene expression, and tumor microenvironment analyses. Drugs associated with model genes were predicted using the CellMiner database. Expression of CYP17A1, IGF2BP1, IGFBP1 and VGF in LUAD cells was assayed via qRT-PCR. A total of 781 LUAD samples (TCGA-LUAD: 600; GSE50081: 181) and data on 1,555 GH-RH-related gene sets were obtained from public datasets. Two LUAD subtypes with different GH-RH gene expression were identified through cluster analysis. Significant differences were unveiled in prognosis between the two subtypes. A prognostic risk-scoring model was generated with genes screened from the PPI network, and afterward the model was validated. The model comprised 7 genes, specifically CLCA1, CYP17A1, DKK1, IGF2BP1, IGFBP1, RPE65, and VGF. CYP17A1 expression was low in LUAD, while IGF2BP1, IGFBP1, and VGF expression was high. Immune-related analysis revealed significant differences in immune cell infiltration levels between the high- and low-risk groups (P < 0.05), with mast cells and neutrophils showing significantly higher infiltration levels in the low-risk population. The 7-gene signature in the current study is of paramount importance for forecasting overall survival and the immune microenvironment of LUAD patients.

Numerous genes have been associated with colorectal cancer (CRC) treatment in prior studies, but the impact of radiotherapy-related autophagy genes (RRAGs) on CRC remains largely unexplored. The Cancer Genome Atlas (TCGA) and Gene Expression Omnibus (GEO) databases were implemented to screen out RRAGs significantly associated with survival, and a prognostic model was constructed. Samples were categorized into high- and low-risk groups with median riskscore. Immunomicroenvironment analysis, immunotherapy response prediction, enrichment analysis, tumor mutation analysis and drug prediction were performed in risk groups. Expression of signature genes in CRC cells was examined using quantitative reverse transcription polymerase chain reaction (qRT-PCR). There were 10 CRC-related RRAGs found. Prognostic models were built with RRAGs. Based on immune infiltration analysis, low-risk populations showed significantly greater levels of immune infiltration (P P ARHGEF17 mutation rate was 6%. Medications such as CGP-082996, Dasatinib, Erlotinib, and Salubrinal were more sensitive to high-risk group, whereas drugs such as FTI-277, DMOG, and Crizotinib were more sensitive to low-risk group. UGT1A6 and IRGM were significantly upregulated in tumor group as revealed by qRT-PCR. This study constructed a new prognostic model for CRC patients based on RRAGs, and a series of analysis results is conducive to providing more theoretical references and new insights into precision treatment of CRC patients.

Noncoding RNA regulatory networks play crucial roles in human breast cancer. The aim of this study was to establish a network containing multi-type RNAs and RBPs in triple-negative breast cancer (TNBC). Differential expression analyses of lncRNAs, miRNAs, and genes were performed using the GEO2R tool. Downstream RBPs and miRNAs were identified using respective databases. GO, KEGG, and protein-protein interaction were predicted. Expression of mRNAs, lncRNAs, and miRNAs were examined using TCGA and ENCORI. TMEM161B-AS1-miR-3646-SERPINB5 axis was validated with the expression level and cell function. TMEM161B-AS1-RBFOX1-SER-PINB5 axis was validated using RIP assays. A lncRNA-miRNA-mRNA network, a lncRNA-RBP-mRNA network, and a lncRNA-miRNA/RBP-mRNA network were constructed. Alterations in the expression levels of TMEM161B-AS1, miR-3646, and SERPINB5 were confirmed by real-time polymerase chain reaction as downregulation, upregulation, and downregulation, respectively. TMEM161B-AS1 inhibited TNBC cell proliferation, migration, and invasion. miR-3646 reversed the inhibitory effect of TMEM161B-AS1 on cell function, while SERPINB5 offset the miR-3646 effect. RB-FOX1 bound to SERPINB5 mRNAs, and TMEM161B-AS1 was involved in their interaction. This study revealed the ln-cRNA-miRNA/RBP-mRNA network in TNBC, providing more directions to study the molecular mechanism of TNBC.

Expression and functional dysregulation of ion channel genes are correlated with an unfavorable prognosis in lung adenocarcinoma (LUAD). Ion channel signature for predicting the prognosis of individuals with LUAD. 94 ion channel-related differentially expressed genes in LUAD were identified from TCGA-LUAD, and ion channel-based LUAD risk model was established and validated using the GEO cohort. Survival analysis outcomes demonstrated that low-risk LUAD patients were accompanied with higher survival rates. Cox analysis manifested that LUAD prognostic risk score was an independent prognosticactor. We plotted a nomogram with clinical utility based on LUAD risk score and clinical factors. Differentially expressed genes in LUAD patients of different risk groups were enriched in biological functions and signaling pathways related to ion channels, cancer transcription dysregulation, and immunity. Immune infiltration results suggested that LUAD patients with low risk scores exhibited better immune cell infiltration and function. Prediction results of immunotherapy response showed that LUAD patients with low risk scores had a higher chance of benefiting from immunotherapy. The drug prediction results showed that individuals with LUAD in the low-risk group were more sensitive to paclitaxel, BI 2536, pyrimethamine, and VX-680, while individuals with LUAD in the high-risk group to erlotinib, sorafenib, panitumumab, PHA-665752, and roscovitine. In summary, ion channel-related genes can provide valuable information for prognosis assessment and drug treatment of LUAD patients.

Circular RNAs (circRNAs) play a pivotal part in the advancement of multiple tumors. Nonetheless, the influence of Helicobacter pylori (H. pylori) infection on the expression of circRNA in gastric cancer remains less studied.

Breast cancer (BC) is one of the main causes of cancer-related death in women. The purpose of this study was to evaluate the expression of miR-605-5p in BC and its diagnostic and prognostic value. BC patients and healthy individuals who met the study criteria were included. Real-time fluorescence quantitative PCR (RT-qPCR) was used for the detection of miR-605-5p expression in BC patients and BC cell lines. The ROC curve was used for the assessment of the diagnostic value of miR-605-5p. The Kaplan-Meier survival curve was used to assess the prognostic value of miR-605-5p. CCK-8 and Transwell assays were performed to detect the effect of miR-605-5p on BC cell activity. The results of this study showed that miR-605-5p was markedly downregulated in BC and correlated with the clinicopathological features of the patients. The expression level of miR-605-5p has high diagnostic accuracy for distinguishing BC patients from healthy individuals. Low expression predicts an unfavorable prognosis for BC patients, while up-regulation of miR-605-5p inhibited the activity of BC cells. In summary, miR-605-5p has the potential to serve as an important molecular marker for prognostic analysis and prediction of BC patients.

Targeting PI3K/AKT/MTOR (PAM) signaling pathway may be a strategy at the fore for treating lung squamous cell carcinoma (LUSC). However, relationships of PAM pathway-related genes (PAGs) with LUSC prognosis are unknown. Therefore, identifying the prognostic significance of PAGs for LUSC is innovative and feasible. Transcriptomic data, clinical features, and PAGs of LUSC were obtained from public databases (TCGA, GEO). A PAGs-based prognostic model was built using regression analysis in TCGA-LUSC. Gene levels were assessed via qRT-PCR. Predictive performance was verified through multiple datasets. Differences in immune infiltration and anti-tumor immunity between risk groups were assessed by R packages. Sensitivity to common anti-cancer agents was tested using oncoPredict package. We identified a Riskscore model containing 11 PAGs. Patients were assigned into groups of high risk (HR) and low risk (LR) per median Riskscore. CAB39L, CDKN1A, and ITPR2 were significantly underexpressed in LUSC cells. TRAF2 and TRIB3 were significantly enhanced in LUSC cells. The LR group had a longer survival time. Prognostic values of one-, three-, and five-year ROC curves were good. Results were verified in GEO. Patients in LR group had higher immune infiltration levels of B cells and Tfh cells, and higher ssGSEA scores for APC_co_inhibition and T_cell_ co_stimulation. LR group had lower TIDE scores and lower IC50 values (Alpelisib, Ibrutinib, Sapitinib, and Savolitinib). We successfully built a reliable 11-gene Riskscore prognostic model. Patients in LR group had potential advantages in survival, immune response, and drug sensitivity. In summary, the results offered new insights into prognosis prediction, immunotherapy, and personalized treatment of LUSC.

Microplastics (MPs), pervasive environmental pollutants, have raised significant concerns regarding their potential impact on human health, particularly in relation to cancer. This review examines the current evidence linking MPs to various cancers, including ovarian, gastric, blood, brain, colorectal, lung, liver, breast, and cervical cancers. Recent studies indicate that MPs, including polystyrene nanoparticles (PS-NPs) and microplastics (PS-MPs), can exacerbate tumor progression through mechanisms such as oxidative stress, inflammation, and endocrine disruption. For instance, in ovarian cancer, PS-NP exposure has been shown to accelerate tumor growth, while in gastric cancer, PS-MPs alter gene expression to promote cancer progression. Blood cancer research highlights the presence of MPs in human blood, suggesting their potential systemic distribution and impact. MPs' ability to cross the blood-brain barrier raises concerns about brain cancer, where they may induce neurotoxicity. Similarly, MPs contribute to colorectal cancer by causing intestinal inflammation and gut microbiota alterations. Inhalation of MPs is linked to lung cancer due to chronic inflammation and oxidative stress. In liver cancer, MPs induce hepatic toxicity and promote carcinogenesis. Breast and cervical cancers are associated with MPs endocrine-disrupting properties, leading to increased cell proliferation and migration. This review underscores the urgent need for further research to elucidate the mechanisms through which MPs contribute to cancer and to inform public health strategies and regulatory policies aimed at mitigating the risks of microplastic exposure.

Lung adenocarcinoma (LUAD) is one of the most malignant tumors with significant implications for population health and life. Nicotinamide metabolism may play a pivotal part in influencing the prognosis of LUAD. This study aimed to figure out the potential value of nicotinamide metabolism-related genes (NMRGs) in LUAD prognosis.

This study was to screen for circRNAs associated with osimertinib resistance in lung adenocarcinoma (LUAD) and establish a circRNA-miRNA-mRNA ceRNA network.

Invasive ductal carcinoma (IDC) is a major type of breast cancer. The utilization of inhibitors targeting histone methyltransferases introduces novel therapeutic avenues for the treatment of cancer. Immunohistochemistry, Western blot, and reverse transcription quantitative polymerase chain reaction experiments were applied to assess the levels of EHMT2 in IDC and adjacent tissues. HCC70 cells were treated with EHMT2 inhibitors (UNC0646 and BIX-01294), and assessed using Cell Counting Kit-8 (CCK-8), terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) staining, and transwell assays to evaluate cell viability, apoptosis, and migratory capacity, respectively. The reactive oxygen species (ROS) levels were assessed using the 2',7'-dichlorodihydrofluorescein diacetate (DCFH-DA) fluorescent probe. The expressions of Hippo pathway were analyzed via Western blot assay. Immunofluorescence staining was employed to detect the subcellular localization changes in YAP expression. A xenograft tumor model of HCC70 cells was applied to validate the tumor-suppressive influences of EHMT2 inhibitors in vivo. We observed significant upregulation of EHMT2 in both IDC clinical samples and IDC cell lines, with high EHMT2 expression correlating with poor prognosis. After treatment with EHMT2 inhibitors UNC0646 or BIX-01294, HCC70 cells exhibited inhibition of proliferation and migratory capacity, alongside an increase in apoptosis rate and ROS production levels. UNC064 or BIX-01294 promoted the phosphorylation levels of MST1, LATS1, MOB1A, and YAP, indicating the activation of the Hippo pathway by EHMT2 inhibitors. Moreover, UNC0646 and BIX-01294 enhanced the cytoplasmic expression of YAP while inhibiting its nuclear localization, preventing its nuclear activation. EHMT2 was upregulated in IDC, and EHMT2 inhibitors suppressed IDC progression by modulating the Hippo signaling pathway.

Bladder cancer (BCa) is approximately the fourth most prevalent diagnosed cancer in men and is three times less common in women. Therefore, identifying biomarkers, developing more effective therapeutic strategies, and understanding the mechanisms underlying BCa tumor growth and progression are urgently required to improve survival rates. Therefore, we aim to investigate the expression of PTEN/Akt in tissue samples of both non-muscle invasive bladder cancer (NMIBC) and muscle-invasive bladder cancer (MIBC) patients (n = 70) and human BCa cell lines T24 and 5637, along with the potent role of ellagic acid (EA) in the modulation of the PTEN/Akt pathway and the resulting therapeutic potential. Results showed low-intensity nuclear or cytoplasmic PTEN staining or loss of PTEN expression in tumor cells and overexpression of p-Akt (Ser-473) with high intensity in the nucleus or cytoplasm. EA treatment of T24 and 5637 cells reduced cell viability, inflammation (NF-κB, COX-2), invasion (MMP-9), induced the caspase (cas-3 and cas-9) cascade signaling pathway, and induced cell apoptosis along with the suppression of the PI3K/PTEN/Akt signaling pathway after 48h in a dose-dependent manner. Thus, these data suggested that the EA showed a strong potential anti-cancer effect in T24 and 5637 cells. In conclusion, the expression of PTEN/p-Akt and the inverse relation indicated an alteration of the PTEN/Akt pathway, and such cases could benefit from treatment with EA in BCa.

Despite advancements in systemic therapy, the mortality rate for patients with metastatic melanoma remains around 70%, underscoring the imperative for alternative treatment strategies. Through the establishment of a chemoresistant melanoma model and a subsequent drug investigation, we have identified pacritinib, a medication designed for treating myelofibrosis and severe thrombocytopenia, as a potential candidate to overcome resistance to melanoma therapy. Our research reveals that pacritinib, administered at clinically achievable concentrations, effectively targets dacarbazine-resistant melanoma cells by suppressing IRAK1 rather than JAK2. Notably, melanoma-resistant cells exhibit elevated p-IRAK1 levels, while there is no discernible difference in p-JAK2 levels between sensitive and resistant cells. Additionally, analysis of melanoma patients indicates a higher expression of IRAK1, correlating with a significantly improved survival rate. Furthermore, the depletion of IRAK1 not only reduces cell viability in melanoma cells but also enhances the effectiveness of dacarbazine treatment. In a dacarbazine-resistant melanoma model, pacritinib demonstrates significant inhibition of tumor growth in mice, leading to enhanced overall survival. In the dacarbazine-sensitive melanoma model, the combination of pacritinib and dacarbazine is more effective than dacarbazine alone in reducing tumor growth and improving overall survival in mice. In summary, our findings highlight IRAK1 as a promising therapeutic target to overcome melanoma resistance, and pacritinib emerges as a valuable addition to the treatment armamentarium for melanoma.

Colorectal cancer (CRC) is a malignant tumor that affects patients worldwide, and its mortality rate is high. Although treatments that activate TNF-associated apoptosis-inducing ligand (TRAIL)-induced apoptosis have shown some efficacy, many CRC patients are resistant to TRAIL therapy. Our findings indicated that the lncRNA PTCSC1 is over-expressed in CRC. However, the mechanism underlying resistance to PTCSC1 in CRC is unclear. In this work, we determined the role of PTCSC1 in TRAIL-resistant CRC patients and explored possible molecular mechanisms. We found that TRAIL-sensitive HCT116 and SW480 cells expressed relatively lower levels of PTCSC1 than TRAIL-resistant HT-29 and caco-2 cells. Increased expression of PTCSC1 was here found to inhibited TRAIL-induced apoptosis in HCT116 and SW480 cells. Decreased expression of PTCSC1 increased TRAIL-induced apoptosis in HT-29 and caco-2 cells. The level of expression of PTCSC1 was related to their sensitivity to TRAIL-induced apoptosis. Furthermore, PTCSC1 decreased the expression of Death Receptor 4 (DR4) while increased the activation of serine/threonine kinase 1 (AKT) and Forkhead Box O3a (FOXO3a). Our findings therefore support the idea that targeting PTCSC1 function may represent a strategy to overcome TRAIL resistance in CRC through the DR4/AKT/FOXO3a pathway.

Prostate cancer and inflammation mechanism are closely related because chronic inflammation causes inflammatory cells to infiltrate into prostatic atrophy areas and proliferative inflammatory atrophy is accepted as the initiator of prostate cancer. The study included 90 patients (28 patients with benign prostatic hyperplasia (BPH), 35 patients with localized prostate cancer (LPCa), and 27 patients with metastatic prostate cancer (MPCa) and 90 healthy controls. Blood samples from 90 patients and 90 healthy people were used to isolate genomic DNA. Serum protein levels were detected using the ELISA technique, and genotyping was done using the PCR-RFLP method. It was found that genotype distributions of CCR3 gene rs4987053 and the COX-2 gene rs689466 variants showed a substantial difference between the groups (Control, BPH, LPCa, MPCa) (respectively P < 0.05, P < 0.001). In addition, a important difference was determined between the non-cancerous and the prostate cancer groups in the NOD1 gene rs5743336 variant genotype distributions (P < 0.05). However, no substantial relationship was determined between the rs16969415, rs1801157, rs2228014, rs2066847, rs4986791 variants, and a risk of prostate cancer. The serum IL-1β, LY96, and TLR4 protein levels differed significantly between the groups (Control, BPH, LPCa, MPCa) (P < 0.001). In addition, IL-1β was associated with rs689466, LY96 with rs2228014, rs5743336 genotypes (P < 0.05). As a conclusion, the CCR3 gene rs4987053, COX-2 gene rs689466, and NOD1 gene rs5743336 variations were determined to be closely associated with prostate cancer risk.

Cholangiocarcinoma (CCA) is a life-threatening malignancy, and there is an urgent need for new biomarkers to improve the prognosis of patients. The expression of ELF3 in CCA tumor and non-tumor tissues was examined in two cohorts. ELF3 expression and the methylation level of its promoter in CCA patients with various clinicopathological features were analyzed using the UALCAN website. Co-expressed genes significantly associated with ELF3 were screened using the LinkedOmics website. A protein-protein interaction (PPI) network for these co-expressed genes was constructed using the STRING website. Core co-expressed genes correlated with ELF3 were identified through random walk with restart (RWR) analysis. GeneMANIA was utilized to analyze the major biological functions within networks of kinases and TFs mediated by ELF3. Potential targeted drugs for CCA treatment were screened using the Connectivity Map (CMAP) database. ELF3 expression in CCA tissue was significantly increased compared with that in normal tissue. Among CCA patients with distinct clinicopathological features, ELF3 expression was notably elevated in tumor tissues compared to normal tissue, while ELF3 promoter's methylation levels in tumor tissue were significantly decreased. In total, 307 co-expressed genes, evidently relevant to ELF3, were identified through LinkedOmics analysis. RWR analysis revealed 61 co-expressed genes closely associated with ELF3. Enrichment analysis indicated that these genes control cell junctions and epithelial cell differentiation. GeneMANIA analysis uncovered that ELF3-involved regulatory networks of kinases and TFs were primarily linked to the regulation of immune cells and cell adhesion. CMAP analysis identified 10 potential small molecules for CCA treatment including 4 existing drugs used for other diseases. ELF3 shows promise as a diagnostic marker for CCA, and the drugs we have identified hold great potential for the treatment of this fatal disease.

Neuro-oncology is the study of brain and spinal cord neoplasms. Molecular targets and signaling pathways are pivotal in advancing modern healthcare, particularly in personalized medicine. Signaling pathways, which regulate cellular processes such as growth, division, and survival, are frequently dysregulated in cancer. Targeting these pathways has enabled the development of personalized therapies that improve efficacy while minimizing side effects. This approach has led to significant improvements in patient outcomes, reduced treatment toxicity, and a shift toward precision medicine, driving innovation in drug discovery. The integration of molecular targets and signaling pathways into clinical practice highlights their importance for enhancing patient care.