Papill ary thyroid carcinoma is the most common type ofthyroid malignancy. The tumor occur s largely in adults, usually those between the ages of 20 and 50 years; the female-to-male ratio is 4: I. Papill ary thyroid carcinoma is also the most common pediatr ic thyroid malignancy. There is a known etiologic link between this malignancy and exposure to radiation,either environmental or therapeutic. Most patients present e1inically with a mass, although incidental orunsuspected tumors are commonly identified. Because mos t papillary carcinomas are nonfunctional and findings on radiography are nonspecific, fine-needle aspiration plays an important role in the initial eva luation of any thyroid nodule and as aguide to subsequent therapy. Papillary carcinoma exhibits a wide variety of macroscopic pattem s and sizes. Tum ors can appear as encapsulated masses with irregular and selero tic borders, they can infiltrate into the surrounding parenchyma, and they frequently demonstrate multifocality.The masses are usually firm and gray-white, and dystrophic calcification is common. Direet extension beyond the thyroid capsule is uncommon. Figure 2. A: Intranuclear cytoplasmic inclusions are inva gina tions of eos inophilic cytoplasm into the nucleus . B: Psammoma bodies are concentrically laminated calcified papillary structures. C: Fine, delicate nuclear chromatin distribution shows nuclear grooves andfolds .A crys tallaid is seen in the centerofthe brightly eos inophilic col/oid.

https://journals.sagepub.com/doi/pdf/10.1177/014556130408301006

Papillary thyroid carcinoma.

PANoptosis is a new cell death proposed by Malireddi et al in 2019, which is characterized by pyroptosis, apoptosis and necroptosis, but cannot be explained by any of them alone. The interaction between pyroptosis, apoptosis and necroptosis is involved in PANoptosis. In this review, from the perspective of PANoptosis, we focus on the relationship between pyroptosis, apoptosis and necroptosis, the key molecules in the process of PANoptosis and the formation of PANoptosome, as well as the role of PANoptosis in diseases. We aim to understand the mechanism of PANoptosis and provide a basis for targeted intervention of PANoptosis-related molecules to treat human diseases. 

PANoptosis: A Cell Death Characterized by Pyroptosis, Apoptosis, and Necroptosis

The excessive apoptosis of human trophoblasts can cause pregnancy‑related diseases. It has been reported that fibronectin 1 (FN1) is closely associated with the invasion of human trophoblasts. The aim of the present study was to examine the effects of FN1 on the apoptosis of human trophoblasts and to investigate the underlying molecular mechanisms. It was found that FN1, a differentially expressed gene (DEG) in the GSE127170 dataset, was identified as the hub gene in a protein‑protein interaction (PPI) network generated using the cytoHubba plug‑in of Cytoscape software. The Metascape website was used to perform GO enrichment analysis, and the Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway database was used to perform KEGG pathway analysis. Experimental analyses revealed that FN1 expression was downregulated in the chorionic villus tissues of patients diagnosed with and mice subjected to spontaneous abortion (SA). CCK‑8 and flow cytometric assays revealed that the knockdown of FN1 decreased the viability and promoted the apoptosis of JEG‑3 and BeWo cells. In vivo experiments demonstrated that the knockdown of FN1 promoted the apoptosis of trophoblasts in the chorionic villus tissues obtained from mice subjected to SA, whereas FN1 overexpression increased cell viability and inhibited cell apoptosis. The protein levels of cleaved caspase‑3 and Bax were increased by the silencing of FN1 and decreased by FN1 overexpression. The protein expression levels of Bcl‑2, proliferating cell nuclear antigen (PCNA) and Ki67 were decreased by the silencing of FN1; however, the overexpression of FN1 increased these levels. The results of western blot analysis revealed that the knockdown of FN1 inhibited the PI3K/Akt signaling pathway, while the overexpression of FN1 activated the PI3K/Akt signaling pathway. Consistently, the apoptosis‑inhibiting effect of FN1 overexpression was reversed by a PI3K/Akt signaling pathway inhibitor, and the apoptosis‑promoting effect of FN1 silencing was reversed by a PI3K/Akt signaling pathway activator. On the whole, the findings of the present study demonstrate that the inhibition of FN1 induces the apoptosis of JEG‑3 and BeWo cells, and the overexpression of FN1 inhibits cell apoptosis by activating the PI3K/Akt signaling pathway.

/pdf/fibronectin-1-inhibits-the-apoptosis-of-human-trophoblasts-297x0plyms.pdf

Fibronectin 1 inhibits the apoptosis of human trophoblasts by activating the PI3K/Akt signaling pathway.

The aim of this study was to identify hub genes closely related to the pathogenesis and prognosis of thyroid carcinoma (THCA) by integrated bioinformatics analysis. In this study, through differential gene expression analysis, 1916 and 665 differentially expressed genes (DEGs) were obtained from The Cancer Genome Atlas (TCGA) and Gene Expression Omnibus (GEO) database, and 7 and 11 co-expressed modules were identified from the TCGA-THCA and GSE153659 datasets, respectively, by weighted gene co-expression network analysis. We identified 162 overlapping genes between the DEGs and co-expression module genes as candidate hub genes. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analyses of the 162 overlapping DEGs identified significant functions and pathways of THCA, such as thyroid hormone generation and metabolic process. A protein-protein interaction (PPI) analysis detected the top 10 hub genes (QSOX1, WFS1, EVA1A, FSTL3, CHRDL1, FABP4, PRDM16, PPARGC1A, PPARG, COL23A1). Finally, survival analysis, clinical correlation analysis, and protein abundance validation confirmed that 3 of the 10 hub genes were associated with survival prognosis of patients with THCA, and 8 of them were associated with the clinical stages of THCA. In summary, we identified hub genes and key modules that were closely related to THCA, and validated these genes by survival analysis, clinical correlation analysis, and Human Protein Atlas image analysis. Our results provide important information that will help to elucidate the pathogenesis of THCA and identify novel candidate prognostic biomarkers and potential therapeutic targets.

https://www.tandfonline.com/doi/pdf/10.1080/21655979.2021.1940615

Identification of hub genes in thyroid carcinoma to predict prognosis by integrated bioinformatics analysis.

Epithelial-to-mesenchymal transition (EMT) is a process that involves the transformation of polarized epithelial cells to attain a mesenchymal phenotype that presents an elevated migratory potential, invasiveness, and antiapoptotic properties. Many studies have demonstrated that EMT is a prominent event that is associated with embryogenesis, tumor progression, metastasis, and therapeutic resistance. The EMT process is driven by key transcription factors (such as Snail, Twist, ZEB, and TGF-β) and several long non-coding RNAs (lncRNAs) in many non-pathological as well as pathological conditions. In the present report, we have comprehensively discussed the oncogenic and tumor suppressor role of lncRNAs and their mechanism of action in the regulation of the EMT process in various cancers such as brain tumors, gastrointestinal tumors, and gynecological and urological tumors. We have also elaborated on the role of lncRNAs in the regulation of EMT-related transcription factors (such as Snail, Twist, ZEB, and TGF-β) and therapeutic response (chemoresistance and radioresistance). Lastly, we have emphasized the role of exosomal lncRNAs in the regulation of EMT, metastasis, and therapeutic response in the aforementioned cancers. Taken together, this review provides a detailed insight into the understanding of role of lncRNAs/exosomal lncRNAs in EMT, metastasis, and therapeutic response in human cancers. 

Long non-coding RNA/epithelial-mesenchymal transition axis in human cancers: Tumorigenesis, chemoresistance, and radioresistance.

PANoptosis is a newly-discovered cell death pathway that involves crosstalk and co-ordination between pyroptosis, apoptosis, and necroptosis processes. However, the roles of PANoptosis-related genes (PRGs) in prognosis and immune landscape of colon cancer remain widely unknown. Here, we performed a bioinformatics analysis of expression data of nineteen PRGs identified from previous studies and clinical data of colon cancer patients obtained from TCGA and GEO databases. Colon cancer cases were divided into two PRG clusters, and prognosis-related differentially expressed genes (PRDEGs) were identified. The patient data were then separated into two corresponding distinct gene clusters, and the relationship between the risk score, patient prognosis, and immune landscape was analyzed. The identified PRGs and gene clusters correlated with patient survival and immune system and cancer-related biological processes and pathways. A prognosis signature based on seven genes was identified, and patients were divided into high-risk and low-risk groups based on the calculated risk score. A nomogram model for prediction of patient survival was also developed based on the risk score and other clinical features. Accordingly, the high-risk group showed worse prognosis, and the risk score was related to immune cell abundance, cancer stem cell (CSC) index, checkpoint expression, and response to immunotherapy and chemotherapeutic drugs. Results of quantitative real-time polymerase chain reaction (qRT-PCR) showed that LGR5 and VSIG4 were differentially expressed between normal and colon cancer samples. In conclusion, we demonstrated the potential of PANoptosis-based molecular clustering and prognostic signatures for prediction of patient survival and tumor microenvironment (TME) in colon cancer. Our findings may improve our understanding of the role of PANoptosis in colon cancer, and enable the development of more effective treatment strategies.

/pdf/panoptosis-based-molecular-clustering-and-prognostic-2p3c0y8x.pdf

PANoptosis-based molecular clustering and prognostic signature predicts patient survival and immune landscape in colon cancer

Oxidative stress and ferroptosis exhibit crosstalk in many types of human diseases, including malignant tumors. We aimed to develop an oxidative stress- and ferroptosis-related gene (OFRG) prognostic signature to predict the prognosis and therapeutic response in patients with colorectal cancer (CRC). Thirty-four insertion genes between oxidative stress-related genes and ferroptosis-related genes were identified as OFRGs. We then performed bioinformatics analysis of the expression profiles of 34 OFRGs and clinical information of patients obtained from multiple datasets. Patients with CRC were divided into three OFRG clusters, and differentially expressed genes (DEGs) between clusters were identified. OFRG clusters correlated with patient survival and immune cell infiltration. Prognosis-related DEGs in three clusters were used to calculate the risk score, and a prognostic signature was constructed according to the risk score. In this study, patients in the low-risk group had better prognosis, higher immune cell infiltration levels, and better responses to fluorouracil-based chemotherapy and immune checkpoint blockade therapy than high-risk patients; these results were successfully validated with multiple independent datasets. Thus, low-risk CRC could be defined as hot tumors and high-risk CRC could be defined as cold tumors. To further identify potential biomarkers for CRC, the expression levels of five signature genes in CRC and adjacent normal tissues were further verified via an in vitro experiment. In conclusion, we identified 34 OFRGs and constructed an OFRG-related prognostic signature, which showed excellent performance in predicting survival and therapeutic responses for patients with CRC. This could help to distinguish cold and hot tumors in CRC, and the results might be helpful for precise treatment protocols in clinical practice.

/pdf/a-novel-oxidative-stress-and-ferroptosis-related-gene-mlqi391c.pdf

A novel oxidative stress- and ferroptosis-related gene prognostic signature for distinguishing cold and hot tumors in colorectal cancer

The molecular mechanism of the occurrence and development of papillary thyroid carcinoma (PTC) has been widely explored, but has not been completely elucidated. The present study aimed to identify and analyze genes associated with PTC by bioinformatics methods. Two independent datasets were downloaded from Gene Expression Omnibus (GEO) database. The differentially expressed genes (DEGs) between PTC tissues and matched non-cancerous tissues were identified using GEO2R tool. The common DEGs in the two datasets were screened out by VennDiagram package, and analyzed by the following tools: KOBAS, Database for Annotation, Visualization, and Integrated Discovery (DAVID), Search tool for the retrieval of interacting genes/proteins (STRING), UALCAN and Gene expression profiling interactive analysis (GEPIA). A total of 513 common DEGs, including 259 common up-regulated and 254 common down-regulated genes in PTC, were screened out. These common up-regulated and down-regulated DEGs were most significantly enriched in cytokine-cytokine receptor interaction and metabolic pathways, respectively. Protein-protein interactions (PPI) network analysis showed that the up-regulated genes: FN1, SDC4, NMU, LPAR5 and the down-regulated genes: BCL2 and CXCL12 were key genes. Survival analysis indicated that the high expression of FN1 and NMU genes significantly decreased disease-free survival of patients with thyroid carcinoma. In conclusion, the genes and pathways identified in the current study will not only contribute to elucidating the pathogenesis of PTC, but also provide prognostic markers and therapeutic targets for PTC.

Identification and analysis of genes associated with papillary thyroid carcinoma by bioinformatics methods.

BACKGROUND Besides environment and living habits, such as a sedentary lifestyle, smoking and drinking, genetic variation also plays an important role in the development of colorectal cancer (CRC). This study was aimed to investigate the role of miR-27a rs895819 polymorphism on CRC risk in Chinese population. METHODS In a case-control study including 208 CRC and 312 age- and gender-matched healthy control subjects, the rs895819 polymorphism was genotyped using the TaqMan allelic discrimination assay. Furthermore, a pooled analysis based on eligible studies was performed by using the STATA software. RESULTS Logistic regression analysis showed that the rs895819 polymorphism was not associated with CRC risk. However, a pooled analysis based on five studies from Chinese population showed a statistically significant association between the rs895819 polymorphism and CRC risk (GG vs AA: OR = 1.56, 95% CI = 1.27-1.92, Pz < .01; (AG + GG) vs AA: OR = 1.14, 95% CI = 1.01-1.30, Pz = .04; GG vs (AG + AA): OR = 1.54, 95% CI = 1.27-1.88, Pz < .01; G vs A: OR = 1.20, 95% CI = 1.09-1.33, Pz < .01). CONCLUSION Our study suggests that miR-27a rs895819 polymorphism plays an important role in CRC risk in Chinese population and may serve as a valuable biomarker for predicting an individual's susceptibility to CRC.

https://onlinelibrary.wiley.com/doi/pdf/10.1002/jcla.23497

The association of miR-27a rs895819 polymorphism with colorectal cancer risk in Chinese population.

LncRNA prostate cancer-associated transcript 1 (PCAT1) is a well-known oncogene, but the mechanisms of exosomes PCAT1 in colorectal cancer (CRC) remain largely unknown. Thus, the mechanisms of exosomes lncRNA PCAT1 were investigated. The expressions of exosomes lncRNA PCAT1 in tissues from stage 0-I and stage II-III CRC patients, and intestinal epithelial cell line FHC and two CRC cell lines, HT29 and HCT8 were measured by real-time quantitative PCR. The effects of lncRNA PCAT1 on adhesion and invasion of two CRC cell lines were investigated by cell-matrix adhesion and transwell assays. In addition, the target of PCAT1 (ZNF217) was validated using an RNA immune precipitation assay. Finally, the protein levels of MTA2, MTA3, SNAI1, and E-cadherin in normal participants, stage 0-I and stage II-III CRC patients, as well as two cell lines with stable ZNF217 knockdown were investigated by western blotting. The plasma exosomal lncRNA PCAT1 was found to be significantly increased in the CRC tissues and cell lines. In addition, lncRNA PCAT1 knockdown significantly inhibited the adhesion and invasion of HT29 and HCT8 cells. RIP assay results showed lncRNA PCAT1 could target ZNF217, and downregulation of lncRNA PCAT1 could decrease the protein expressions of ZNF217 in two CRC cells lines. Moreover, ZNF217 knockdown significantly decreased MTA2, MTA3, and SNAI1 expressions, but increased E-cadherin expressions in both CRC cells lines. Exosomal lncRNA PCAT1 can promote the adhesion and invasion of CRC cells, and PCAT1 overexpression may lead to ZNF217 upregulation that regulates EMT-related MTA2/MTA3/Snai1/E-cadherin signaling.

lncRNA PCAT1 might coordinate ZNF217 to promote CRC adhesion and invasion through regulating MTA2/MTA3/Snai1/E-cadherin signaling.

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