Analysis of the clonal origin and differences in the biological behavior of multifocal papillary thyroid carcinoma.

Papillary thyroid carcinoma (PTC) exhibits a trend of multifocal growth. However, the clonal origin of multiple cancer foci in the thyroid gland remains an issue of ongoing debate. In order to investigate the clonal origin and biological behavior differences of multifocal PTC (MPTC) from a unique perspective, a combination of dual gene and dual protein detection methods was used. The present study included 52 patients with MPTC. Immunohistochemical staining was used to assess the expression of v-raf murine sarcoma viral oncogene homolog B1 (BRAF) and telomerase reverse transcriptase (TERT) proteins, while quantitative PCR and Sanger sequencing were used to identify BRAF and TERT gene mutations. Based on the results, MPTC cases were classified into two clonal origins, namely intraglandular metastatic (71.2%) and independent multicentric origin (28.8%). BRAF protein expression and BRAF gene mutation were significantly higher in the intraglandular metastasis group than in the multicentric cancer group. However, no significant differences in TERT protein expression and TERT gene mutation were observed between the two groups. Sex, central lymph node metastasis rate, Hashimoto's thyroiditis and tumor distribution laterality were not found to differ significantly between the two groups. However, significant differences were detected in age at initial diagnosis, lateral cervical lymph node metastasis rate, tumor capsule invasion rate and maximum tumor diameter. The study found that MPTC predominantly occurs due to intraglandular metastasis, which is associated with stronger tumor invasiveness than cancer foci with multiple independent origins, as it is more likely to exhibit pathogenic gene mutations and abnormal protein expression, cervical lymph node metastasis and capsule invasion. Therefore, it is recommended that the surgical approaches and follow-up strategies for intraglandular metastatic MPTC should be aggressive and individualized.

Role of Epigenetic Factors in Determining the Biological Behavior and Prognosis of Hepatocellular Carcinoma.

BACKGROUND: The current study's objective is to evaluate the molecular genetic mechanisms influencing the biological behavior of hepatocellular carcinoma (HCC) by analyzing the transcriptomic and epigenetic signatures of the tumors. METHODS: Transcriptomic data were downloaded from the NCBI GEO database. We investigated the expression differences between the GSE46444 (48 cirrhotic tissues versus 88 HCC tissues) and GSE63898 (168 cirrhotic tissues versus 228 HCC tissues) data sets using GEO2R. Differentially expressed genes were evaluated using GO and KEGG metabolic pathway analysis websites. Whole genome bisulfite sequencing (WGBS) and Methylated DNA Immunoprecipitation Sequencing (MeDIP-Seq) data sets (26 HCC tissues versus 26 adjacent non-tumoral tissues) were also downloaded from the NCBI SRA database. These data sets were analyzed using Bismark and QSEA, respectively. The methylation differences between the groups were assessed using functional enrichment analysis. RESULTS: In the GSE46444 data set, 80 genes were upregulated, and 315 genes were downregulated in the tumor tissue (HCC tissue) compared to the non-tumor cirrhotic tissue. In the GSE63898 data set, 1261 genes were upregulated, and 458 genes were downregulated in the cirrhotic tissue compared to the tumor tissues. WGBS revealed that 20 protein-coding loci were hypermethylated. while the hypomethylated regions were non-protein-coding. The methylated residues of the tumor tissue, non-tumorous cirrhotic tissue, and healthy tissue were comparable. MeDIP-Seq, conducted on tumoral and non-tumoral tissues, identified hypermethylated or hypomethylated areas as protein-coding regions. The functional enrichment analysis indicated that these genes were related to pathways including peroxisome, focal adhesion, mTOR, RAP1, Phospholipase D, Ras, and PI3K/AKT signal transduction. CONCLUSIONS: The investigation of transcriptomic and epigenetic mechanisms identified several genes significant in the biological behavior of HCC. These genes present potential targets for the development of targeted therapy.

CT-based radiomic consensus clustering association with tumor biological behavior in clinical stage IA adenocarcinoma: a retrospective study.

Background: Research has demonstrated that radiomics models are capable of forecasting the characteristics of lung cancer. Nevertheless, due to radiomics' poor interpretability, its applicability in clinical settings remains restricted. This investigation sought to verify the correlation between radiomics features (RFs) and the biological behavior of clinical stage IA adenocarcinomas. Methods: A retrospective analysis was conducted on patients diagnosed with clinical stage IA lung adenocarcinoma who underwent resection between May 2005 and December 2018. Detailed radiomics examination of the primary tumor was carried out utilizing preoperative computed tomography (CT) images. Subsequently, patients were grouped based on their RFs using consensus clustering, enabling comparison of tumor biological characteristics among the clusters. Survival disparities among the clusters were evaluated through Kaplan-Meier and Cox analyses. Results: A consensus cluster analysis was performed on 669 patients [median age, 58 years; interquartile range (IQR), 50-64 years, 257 males, 412 females], and three distinct clusters were identified. Cluster 2 was associated with radiological solid adenocarcinoma [119 of 324 (36.7%), P<0.001], larger tumors with median tumor size of 2.1 cm with IQR of 1.7 to 2.5 cm (P<0.001), central tumor [91 of 324 (28.1%), P=0.002], pleural invasion [87 of 324 (26.9%), P<0.001], occult lymph node metastasis (ONM) [106 of 324 (32.7%), P<0.001], and a higher frequency of metastasis or recurrence [62 of 324 (19.1%), P<0.001]. The frequency of histological grade 3 was the highest in Cluster 3 [8 of 34 (23.5%), P<0.001]. Cluster 1 was associated with pure ground glass nodules (pGGNs) [184 of 310 (59.4%), P<0.001], smaller tumors with median tumor size of 1.1 cm with IQR of 0.8 to 1.4 cm (P<0.001), no pleural invasion [276 of 310 (89.0%), P<0.001], histological grade 1 [114 of 248 (46.0%), P<0.001], ONM negative [292 of 310 (94.2%), P<0.001], and a lower rate of metastasis or recurrence [298 of 310 (96.1%), P<0.001]. Conclusions: Differences in tumor biological behavior were detected among consensus clusters based on the RFs of clinical stage IA adenocarcinoma.

Effects of catechin on the malignant biological behavior of gastric cancer cells through the PI3K/Akt signaling pathway.

Catechin is a kind of flavonoids, mainly derived from the plant Camellia sinensis. It has a strong antioxidant effect, and it also has significant therapeutic effects on anti-cancer, anti-diabetes, and anti-infection. This study was intended to look at how catechin affected the malignant biological activity of gastric cancer cells. We used databases to predict the targets of catechin and the pathogenic targets of gastric cancer. Venn diagram was used to find the intersection genes, the Kyoto Encyclopedia of Genes and Genomes (KEGG) and Gene Ontology (GO) enrichment analyses were performed on intersection genes. Using the STRING database, the Protein-Protein Interaction (PPI) network was built. The top 8 genes were screened by Cytoscape 3.9.1, then their binding was verified by molecular docking. The proliferation ability, cell cycle, apoptosis and migration of gastric cancer cells were detected, as well as the protein expression levels of PI3K, p-AKT, and AKT and the mRNA expression levels of AKT1, VEGFA, EGFR, HRAS, and HSP90AA1 in gastric cancer cells. Our research revealed that different concentrations of catechin could effectively inhibit the proliferation and migration of gastric cancer cells, regulate the cell cycle, and promote the death of these cells, and it's possible that the PI3K/Akt pathway was crucial in mediating this impact. Moreover, adding the PI3K/Akt pathway agonist significantly reduced the promoting effect of catechin on the apoptosis of gastric cancer cells. This study suggested that catechin was a potential drug for the treatment of gastric cancer.

Role of ADP ribosylation factor guanylate kinase 1 in the malignant biological behavior of gastric cancer.

Aim: This study aims to investigate the influence of ASAP1 (ADP ribosylation factor guanylate kinase 1) on the malignant behavior of gastric cancer (GC) cells and to elucidate the potential molecular mechanisms involved in cancer development and progression. Methods: We assessed the impact of ASAP1 overexpression and knockdown on GC cell malignancy using CCK8, colony formation, flow cytometry (Annexin V/propidium iodide), Transwell migration, invasion, and scratch assays. Western blot analysis was used to assess the effects of ASAP1 on angiogenesis, matrix metalloproteinases (MMPs), apoptotic proteins, epithelial-mesenchymal transition (EMT)-related proteins, as well as AKT and p-AKT. The influence of ASAP1 knockdown was also evaluated in nude mice bearing BGC823 cell-derived tumors. Results: Our findings revealed that ASAP1 was significantly overexpressed in GC cells, enhancing their proliferation, invasion, and migration, while reducing apoptosis. Conversely, ASAP1 knockdown reversed these effects, markedly increasing the expression of cleaved-caspase 3 (Casp3), PARP, and the epithelial marker E-cadherin, and significantly decreasing MMP2, MMP9, VEGFA, and mesenchymal markers such as N-cadherin and vimentin. Additionally, it reduced AKT, and p-AKT levels (P < 0.01). Tumor growth in nude mice was suppressed following ASAP1 knockdown. Conclusion: The overexpression of ASAP1 significantly promotes malignant behaviors in GC cells, whereas its knockdown diminishes these effects. This modulation is potentially through the downregulation of VEGFA, leading to reduced angiogenesis, Cleaved-Casp3 and Cleaved-PARP overexpression, and a decrease in MMPs, EMT, AKT, and p-AKT activity.

Astragaloside â £ mediates the effect and mechanism of KPNB1 on biological behavior and tumor growth in prostate cancer.

Background: and purpose Prostate cancer is an comparatively prevalent clinical malignant tumor in men, impacting the lives of millions of men globally. This study measured the expression of Karyopherin Subunit Beta 1 (KPNB1) in prostate cancer cells, and made an effort to investigate how astragaloside IV affects the biological behavior, tumor growth, and mechanism of action of prostate cancer through KPNB1. Methods: Human prostate cancer and normal cells were obtained and KPNB1 expression levels in the two cells were determined using qPCR and WB. Prostate cancer cells were grouped according to the addition of astragaloside IV, KPNB1 inhibitor (importazole) alone and in combination. KPNB1, NF-κB, and cycle-related proteins were detected to be expressed at different levels in each group's cells by WB. MTT to assess the viability of the cells. To identify the cell cycle, use flow cytometry, and sphere formation experiment to observe sphere formation ability. Nude mice were purchased and subcutaneously inoculated with prostate cancer cells to establish a prostate cancer model, and grouped by tail vein injection of astragaloside IV and importazole. Tumor size was measured. KPNB1 and NF-κB expression in tumor tissues were detected by WB. The expression of proteins relevant to the cycle is observed by immunohistochemical methods. TUNEL was used to detect apoptosis of tissue cells. Results: KPNB1 expression was upregulated in prostate cancer cells (P < 0.05). KPNB1, NF-κB, and cycle-related protein levels were decreased by astragaloside IV and importazole both separately and together. Decreased viability of the cells and a higher percentage of cell cycle arrest in the G0 phase, apoptosis was increased, and sphere formation was decreased (P < 0.05). In vitro implantation experiments found that the application of astragaloside IV and importazole resulted in tumor growth inhibition, decreased KPNBI, NF-κB, and cyclin expression in tumor tissues, and promoted apoptosis in tumor tissues (P < 0.05). Conclusion: Prostate cancer cells' expression of KPNB1 is downregulated by astragaloside IV, which also prevents the cells from proliferating. It offers a conceptual framework for the use of astragaloside IV in the management of prostate cancer.

JARID2, a novel regulatory factor, promotes cell proliferation, migration, and invasion in oral squamous cell carcinoma.

BACKGROUND: Accurate regulation of gene expression is crucial for normal development and function of cells. The prognostic significance and potential carcinogenic mechanisms of the related gene JARID2 in OSCC are not yet clear, but existing research has indicated a significant association between the two. METHODS AND MATERIALS: The relationship between the expression of the JARID2 gene in tumor samples of OSCC patients and clinical pathological factors was analyzed using immunohistochemistry experiments and RT-qPCR analysis. Based on the clinical pathological data of patients, bioinformatics analysis was conducted using public databases to determine the function of JARID2 in OSCC. Knockdown OSCC cell lines were constructed, and the impact of JARID2 on the biological behavior of OSCC cell lines was assessed through CCK-8, wound healing assay, and transwell analysis. RESULTS: Immunohistochemistry experiments confirmed the correlation between JARID2 and the prognosis of OSCC patients, while RT-qPCR experiments demonstrated its expression levels in tissue and cells. CKK-8 experiments, wound healing assays, and Transwell experiments indicated that knocking down JARID2 had a negative impact on the proliferation, invasion, and migration of OSCC cells. Bioinformatics analysis results showed that the expression of JARID2 in OSCC is closely associated with patient gene co-expression, gene function enrichment, immune infiltration, and drug sensitivity. CONCLUSION: Our study indicates that JARID2 is a novel prognostic biomarker and potential therapeutic target for OSCC.

Earthworms alleviate microplastics stress on soil microbial and protist communities.

Microplastic (MP) pollution can exert significant pressure on soil ecosystems, however, the interactive effects of MPs on soil bacterial, fungal and protist communities remains poorly understood. Soil macrofauna, such as earthworms, can be directly affected by MPs, potentially leading to a range of feedbacks on the soil microbial community. To address this, we conducted a microcosm experiment to examine the effects of conventional (i.e., polyethylene, polystyrene) and biodegradable MPs (i.e. PBAT, polylactic acid) on the structure of the soil bacterial, fungal, and protist communities in the presence or absence of earthworms. We found that MP contamination negatively affected the diversity and composition of soil microbial and protist communities, with smaller-sized conventional MPs having the most pronounced effects. For example, compared with the unamended control, small-sized polyethylene MPs both significantly reduced the Shannon diversity of soil bacteria, fungi, and protist by 4.3 %, 37.0 %, and 9.1 %, respectively. Biodegradable MPs increased negative correlations among bacteria, fungi, and protists. However, earthworms mitigated these effects, enhancing the diversity and altering the composition of these communities. They also increased the niche width and stability of the soil microbial food web network. Our study indicated that earthworms help attenuate the response of soil microorganisms to MPs stress by influencing the diversity and composition of soil microorganisms and soil physicochemical properties and underscores the importance of considering macrofauna in MPs research.

Expression of circRNA-0036474 in esophageal cancer and its clinical significance.

Circular RNAs are considered to play important roles in the progression of different cancers such as esophageal squamous cell carcinoma. However, the functions of circular RNAs in esophageal squamous cell carcinoma are still not clear. This study aimed to investigate the role and mechanism of circRNA-0036474 in the progression of esophageal squamous cell carcinoma. The hsa_circ_0036474 expression levels were found to be elevated in both EC109 cells and esophageal squamous cell carcinoma tissue samples. Moreover, knockdown of circRNA-0036474 expression in the EC109 cells induced migration and invasion, characterized by the down-regulation of E-cadherin, and up-regulation of N-cadherin and vimentin. In addition, the over-expressed hsa_circ_0036474 significantly decreased the activity of EC109 cells, elevated E-cadherin expression but declined N-cadherin and vimentin expression. Moreover, over-expressed mir-223-3p levels and interfered RERG expression verified the role of hsa_circ_0036474 in inhibiting the invasion and migration of EC109 cells, reducing the expression of N-cadherin and vimentin, and promoting the expression of E-cadherin. In conclusion, circRNA-0036474 mitigated the progression of esophageal squamous cell carcinoma through regulating mir-223-3p/RERG axis, presenting a potential therapeutic target for the treatment.

MiR-34a-5p suppresses cutaneous squamous cell carcinoma progression by targeting SIRT6.

Cutaneous squamous cell carcinoma (cSCC) is a malignant tumor originating from epidermal or appendageal keratinocytes, with a rising incidence in recent years. Understanding the molecular mechanism driving its development is crucial. This study aims to investigate whether miR-34a-5p is involved in the pathogenesis of cSCC by targeting Sirtuin 6 (SIRT6).The expression levels of miR-34a-5p and SIRT6 were determined in 15 cSCC tissue specimens, 15 normal tissue specimens and cultured cells via real-time polymerase chain reaction (RT-qPCR). Pearson's correlation analysis was conducted to evaluate the relationship between miR-34a-5p and SIRT6 expression levels in cSCC tissues. A431 and SCL-1 cells were transfected with miR-34a-5p mimic, negative control or miR-34a-5p mimic together with recombinant plasmids containing SIRT6 gene. Cell counting kit-8, clone formation assay, wound healing assay, and flow cytometry were employed to assess the effects of these transfections on proliferation, migration, and apoptosis, respectively. The interaction between miR-34a-5p and SIRT6 was characterized using a dual-luciferase reporter assay.MiR-34a-5p expression was down-regulated in cSCC tissues significantly, while the SIRT6 expression was the opposite. A negative correlation was observed between the expression of miR-34a-5p and SIRT6 in cSCC tissues. Furthermore, overexpression of miR-34a-5p led to a significant reduction in the proliferation and migration abilities of A431 and SCL-1 cells, accompanied by an increase in apoptosis levels and a decrease in SIRT6 expression levels. MiR-34a-5p was identified as a direct target of SIRT6. Importantly, overexpression of SIRT6 effectively counteracted the inhibitory effect mediated by miR-34a-5p in cSCC cells.Our findings suggest that miR-34a-5p functions as a tumor suppressor in cSCC cells by targeting SIRT6.

Pepsinogen C Interacts with IQGAP1 to Inhibit the Metastasis of Gastric Cancer Cells by Suppressing Rho-GTPase Pathway.

AIM: This study systematically explored the biological effects and mechanisms of PGC on gastric cancer (GC) cells in vitro and in vivo. METHOD: The critical biological roles of PGC in GC were assessed via EdU staining, Hoechst staining, flow cytometry, mouse models, CCK-8, wound healing, transwell, and sphere-forming assays. The interaction study with IQ-domain GTPase-activating protein 1 (IQGAP1) was used by Liquid chromatography-mass spectrometry co-immunoprecipitation, immunofluorescence staining, CHX-chase assay, MG132 assay, and qRT-PCR. RESULTS: PGC inhibited the proliferation, viability, epithelial-mesenchymal transition, migration, invasion, and stemness of GC cells and promoted GC cell differentiation. PGC suppressed subcutaneous tumor growth and peritoneal dissemination in vivo. The interaction study found PGC inhibits GC cell migration and invasion by downregulating IQGAP1 protein and IQGAP1-mediated Rho-GTPase signaling suppression. In addition, PGC disrupts the stability of the IQGAP1 protein, promoting its degradation and significantly shortening its half-life. Moreover, the expression levels of PGC and IQGAP1 in GC tissues were significantly negatively correlated. CONCLUSION: PGC may act as a tumor suppressor in the development and metastasis of GC. PGC can downregulate its interacting protein IQGAP1 and inhibit the Rho-GTPase pathway, thereby participating in the inhibition of GC cell migration and invasion.

The biological behavior and clinical outcome of pituitary adenoma are affected by the microenvironment.

BACKGROUND: Pituitary adenoma is one of the most common brain tumors. Most pituitary adenomas are benign and can be cured by surgery and/or medication. However, some pituitary adenomas show aggressive growth with a fast growth rate and are resistant to conventional treatments such as surgery, drug therapy, and radiation therapy. These tumors, referred to as refractory pituitary adenomas, often relapse or regrow in the early postoperative period. The tumor microenvironment (TME) has recently been identified as an important factor affecting the biological manifestations of tumors and acts as the main battlefield between the tumor and the host immune system. MAIN BODY: In this review, we focus on describing TME in pituitary adenomas and refractory pituitary adenomas. Research on the immune microenvironment of pituitary adenomas is currently focused on immune cells such as macrophages and lymphocytes, and extensive research and experimental verifications are still required regarding other components of the TME. In particular, studies are needed to determine the role of the TME in the specific biological behaviors of refractory pituitary adenomas, such as high invasion, fast recurrence rate, and high tolerance to traditional treatments and to identify the mechanisms involved. CONCLUSION: Overall, we summarize the similarities and differences between the TME of pituitary adenomas and refractory pituitary adenomas as well as the changes in the biological behavior of pituitary adenomas that may be caused by the microenvironment. These changes greatly affect the outcome of patients.

Biological clock regulation by the PER gene family: a new perspective on tumor development.

The Period (PER) gene family is one of the core components of the circadian clock, with substantial correlations between the PER genes and cancers identified in extensive researches. Abnormal mutations in PER genes can influence cell function, metabolic activity, immunity, and therapy responses, thereby promoting the initiation and development of cancers. This ultimately results in unequal cancers progression and prognosis in patients. This leads to variable cancer progression and prognosis among patients. In-depth studies on the interactions between the PER genes and cancers can reveal novel strategies for cancer detection and treatment. In this review, we aim to provide a comprehensive overview of the latest research on the role of the PER gene family in cancer.

Canine Oral Melanoma: Questioning the Existing Information through a Series of Clinical Cases.

Twelve dogs with oral malignant melanomas (MM) were evaluated in this study, with demographic details indicating a balanced distribution of gender, age, and weight among various breeds. Tumor locations varied, with diverse surgical procedures being performed, including mandibulectomies and maxillectomies. Lymphadenectomies were conducted, revealing a 16.66% metastatic rate in regional lymph nodes. At the time of surgery, clinical staging identified stages I, II, and III, with most cases having non-infiltrated margins and a high mitotic index. Follow-up revealed local recurrences and metastases, prompting additional surgeries and affecting survival rates. This study reports varying outcomes, with some dogs completing one year without recurrence, while others experienced progressive disease, leading to six oral melanoma-related deaths. The characteristics of melanotic melanoma and amelanotic melanoma are observed in order to study differences between them, the degree of aggressiveness, the mortality rate and the possibility of future therapeutic targets. Although high pigmentation has been correlated with a better outcome, we could not find any significant correlation between survival and achromia. Oral benign melanomas might exist, and this could justify variabilities between stage and survival; however, carefulness is required due to their unpredictable behavior. The findings underscore the complexity of oral melanoma cases and highlight the need for further research on effective management strategies.

HSP90B1 regulates autophagy via PI3K/AKT/mTOR signaling, mediating HNSC biological behaviors.

Background: Autophagy, a crucial cellular mechanism, facilitates the degradation and removal of misfolded proteins and impaired organelles. Recent research has increasingly highlighted the intimate connection between autophagy and heat shock proteins (HSPs) in the context of tumor development. However, the specific role and underlying mechanisms of heat shock protein 90 beta family member 1 (HSP90B1) in modulating autophagy within head and neck squamous cell carcinoma (HNSCC) remain elusive. Methods: Quantitative real-time PCR (qRT-PCR), Western blot (WB), immunohistochemistry (IHC) were used to detect the expression in HNSC cell lines and tissues. The relationship between HSP90B1 and clinicopathologic features was explored based on TCGA (The Cancer Genome Atlas) data and IHC results. The biological functions of HSP90B1 were analyzed through in vitro and in vivo models to evaluate proliferation, migration, invasion, and autophagy. The mechanisms of HSP90B1 were studied using bioinformatics and WB. Results: HSP90B1 was upregulated in HNSC cells and tissues. High HSP90B1 levels were associated with T-stage, M-stage, clinical stage, and poor prognosis in HNSC patients. Functionally, HSP90B1 promotes HNSC cell proliferation, migration, invasion and inhibits apoptosis. We discovered that HSP90B1 obstructs autophagy and advances HNSC progression through the PI3K/Akt/mTOR pathway. Conclusion: Our study demonstrates that HSP90B1 is highly expressed in HNSC. Furthermore, HSP90B1 may regulate autophagy through the PI3K/Akt/mTOR pathway, mediating HNSC cell biological behaviors. These provide new insights into potential biomarkers and targets for HNSC therapy.

[Effect of CircCCND1 on the Malignant Biological Behaviors of H446 Lung Cancer Cells by Regulating the MiR-340-5p/TGIF1 Axis].

BACKGROUND: Lung cancer is a common malignant tumor of the lung. To explore the molecular mechanism of the occurrence and development of lung cancer is a hot topic in current research. Cyclic RNA D1 (CircCCND1) is highly expressed in lung cancer and may be a potential target for the treatment of lung cancer. The aim of this study was to investigate the effect of CircCCND1 on the malignant biological behaviors of lung cancer cells by regulating the miR-340-5p/transforming growth factor ß-induced factor homeobox 1 (TGIF1) axis. METHODS: The expression of CircCCND1, miR-340-5p, and TGIF1 mRNA in human normal lung epithelial cells BEAS-2B and human lung cancer H446 cells were detected. H446 cells cultured in vitro were randomly divided into control group, CircCCND1 siRNA group, miR-340-5p mimics group, negative control group, and CircCCND1 siRNA+miR-340-5p inhibitor group. Cell proliferation, mitochondrial membrane potential, apoptosis, migration, and invasion were detected, and the expressions of CircCCND1, miR-340-5p, TGIF1 mRNA, BCL2-associated X protein (Bax), cleaved Caspase-3, N-cadherin, E-cadherin, and TGIF1 proteins in each group were detected. The targeting relationship of miR-340-5p with CircCCND1 and TGIF1 was verified. RESULTS: Compared with BEAS-2B cells, CircCCND1 and TGIF1 mRNA were increased in H446 cells, and miR-340-5p expression was decreased (P<0.05). Knocking down CircCCND1 or up-regulating the expression of miR-340-5p inhibited the proliferation, migration and invasion of H446 cells, decreased the expression of TGIF1 mRNA and TGIF1 protein, and promoted cell apoptosis. Down-regulation of miR-340-5p could antagonize the inhibitory effect of CircCCND1 knockdown on the malignant biological behavior of H446 lung cancer cells. CircCCND1 may target the down-regulation of miR-340-5p, and miR-340-5p may target the down-regulation of TGIF1. CONCLUSIONS: Knocking down CircCCND1 can inhibit the malignant behaviors of lung cancer H446 cells, which may be achieved through the regulation of miR-340-5p/TGIF1 axis.

Studying the electrical, mechanical, and biological properties of BCZT-HA composites.

The piezoelectric properties of natural bone and their influence on bone growth have inspired researchers to study a range of bio-piezoelectric composite materials. By exploring these materials, researchers aim to understand better, how piezoelectricity can be controlled to promote bone growth and tissue regeneration. In this work, the prominent piezoelectric material, (Ba, Zr) TiO3 -x(Ba,Ca)TiO3 , abbreviated as BCZT, was selected as a possible bone growth enhancer in hydroxyapatite (HA) scaffolds. Initially, BCZT and hydroxyapatite (HA) powders were synthesized using the sol-gel method. Subsequently, various composite samples of BCZT-xHA were prepared using the conventional solid-state method. After sintering the samples at 1300°C, the phase structure, microstructure, density, and electrical properties were characterized. The samples' compressive strength was determined by analyzing the outcomes of basic compression tests. The biological behavior of the samples in terms of in vitro simulated body fluid immersion and MTT tests were evaluated. Our results revealed that among the BCZT-xHA samples, the BCZT-20HA sample had the best composition, considering its electrical, mechanical, and biological properties. A d33 value of 10 pC/N, dielectric permittivity of 110, and the g33 equal to 10.27 mV m/N resulted in the output voltage of 1.03 V. The results of the MTT assay test confirmed the noncytotoxic nature of the samples with the highest optical density in the BCZT-20HA sample.

Clinicopathological Characteristics and Prognosis Analysis of Lung Carcinoma With p40/TTF1 Coexpression and Lung Adenosquamous Carcinoma: Lung Carcinoma With p40/TTF1 Coexpression Is a Rare Tumor With High Metastatic Potential.

Background. Lung carcinoma with p40/TTF1 coexpression (LC-PTC) is a very rare tumor with poor prognosis, and few cases have been reported to date. Objectives. To better understand biological behavior and prognosis of LC-PTC. Methods. We collected 9 examples of LC-PTC and compared them with 36 lung adenosquamous carcinomas during the same period in clinicopathologic characteristics, biologic behaviour, and prognosis. Results. Lung carcinoma with p40/TTF1 coexpression mainly occurred in middle-aged and elderly men; 8 tumors belonged to the peripheral type, and 1 belonged to the central type. The rates of lymph node and distant metastasis were 88% (7/8) and 50% (4/8), respectively; 2 patients died during follow-up. Histologically, the LC-PTC showed nest-like growth pattern without glandular growth pattern; the surface of 2 tumors was covered with ciliated columnar epithelium and tumor cells grew under the columnar epithelium. In all patients, tumor cells diffusely coexpressed p40 and TTF1. Although there was no significant difference in the maximum diameter of tumor with lymph node metastasis or with distant metastasis between LC-PTC and lung adenosquamous carcinoma, LC-PTC had a higher rate of lymph node metastasis and distant metastasis. There was no significant difference in overall survival of patients between LC-PTC and lung adenosquamous carcinoma. Additional histologic evaluation of normal pulmonary structures revealed that p40/TTF1 coexpression cells existed in bronchial mucosa and the number of cells coexpressing p40/TTF1 increased gradually from proximal bronchus to distal bronchus. Conclusions. Lung carcinoma with p40/TTF1 coexpression is a rare tumor with high metastatic potential and may originate from p40/TTF1 coexpression cells in distal bronchial mucosa.

Exploring the biological behavior and underlying mechanism of KITLG in triple-negative breast cancer.

The tyrosine-kinase receptor that is specified by the KIT locus is demarcated by KITLG. This multifaceted factor is instrumental during in-utero germ and neural cell maturation and hematopoiesis, ostensibly reflecting its role in facilitating cell migration. Concurrently, KITLG is prone to a mutation in germ cell tumors, entailing a presumed connection to tumorigenesis. Despite this, the intricacies of its function in breast cancer and the relevant mechanisms remain elusive. Multiple independent databases depict a consistently low expression of KITLG within tissues affected by triple-negative breast cancers (TNBC), a trend strongly coupled with reduced survival rates. Interestingly, non-triple-negative breast cancers exhibit a markedly high expression of KITLG compared to the norm. An initial analysis of the GEO database speculates that KITLG may serve as an oncogene suppressor in TNBC, hinting at varied roles for KITLG isoforms within this disease context. In conclusion, our preliminary analysis offers valuable insights into the role and expression pattern of KITLG in TNBC. We provide evidence supporting its consideration as a promising new prognostic marker, thereby potentially enriching therapeutic strategies for TNBC. Indeed, given the limited advances in molecularly targeted therapy for TNBC, a significant need exists for a more precise therapeutic approach and a comprehensive understanding of its inherent mechanisms of action.

Growth rate per year of a soft tissue recurrent ameloblastoma.

Clinical Key Message: We present a case of recurring ameloblastoma in soft tissue, for which we have estimated the growth rate of the lesion. This information could help clinicians to establish follow-up protocols for the early diagnosis of recurrent ameloblastomas. Abstract: In the present paper, we present a case of recurring ameloblastoma in soft tissue, for which we have estimated the growth rate of the lesion. The area of the whole resected specimen was measured using the ImageJ guide for complex object area. After dividing the area of the recurrent tumor by the number of years during the follow-up, we found that the lesion growth rate was 5.3 cm2 per year. Although further studies are still necessary in the literature to assess the growth rate of ameloblastoma, the present report shows a different methodology to estimate it. This information could help clinicians to establish follow-up protocols for the early diagnosis of recurrent ameloblastomas.