Over-Expression and Prognostic Significance of FN1, Correlating With Immune Infiltrates in Thyroid Cancer

Geng, Qishun; Huang, Tao; Li, Lifeng; Shen, Zhibo; Xue, Wenhua; Zhao, Jie

doi:10.3389/fmed.2021.812278

Cited by 25 publications

(19 citation statements)

References 39 publications

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“…In thyroid cancer, overexpression of FN1 is found to be strongly correlated with the infiltration levels of M2 macrophages. 56 Similar results were also acquired from a study in Switzerland, showing that FN1 was linked to the M2 TAM phenotype in renal carcinoma, associated with poor survival and increased tumor stage. 57 Consistently, Yoshida et al 58 revealed that cellular FN1 promoted the secretion level of M2 marker (interleukin-10, IL-10) and reduced M1 marker (tumor necrosis factor-alpha, TNF-α) in macrophages in a concentration-dependent manner.…”

Section: Discussionsupporting

confidence: 72%

The Overexpression of Fibronectin 1 Promotes Cancer Progression and Associated with M2 Macrophages Polarization in Head and Neck Squamous Cell Carcinoma Patients

Zhou¹,

Du²,

Li³

et al. 2022

IJGM

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Purpose This study aimed to investigate the biological roles of fibronectin 1 (FN1) in head and neck squamous cell carcinoma (HNSCC) and its effects on macrophage M2 polarization. Methods We analyzed FN1 expression pattern and examined its clinical relevance in HNSCC progression by bioinformatic analysis. Small interfering RNA (siRNA) was utilized to silence FN1 in HNSCC cells. Cell counting kit-8 (CCK-8) assay, colony formation assay, Transwell assay and wound healing assay were performed to reveal the effect of FN1 on malignant behaviors of HNSCC cells. Moreover, a co-culture model of macrophages and HNSCC cells was established to investigate whether FN1 induce macrophage M2 polarization. Finally, we used bioinformatic methods to explore the possible FN1-related pathways in HNSCC. Results FN1 is significantly overexpressed in HNSCC patients and has been obviously correlated with higher pathological stage and poor prognosis. Downregulation of FN1 suppressed the proliferation, migration and invasion of HNSCC cells, and inhibited macrophage M2 polarization in vitro. In addition, “PI3K-Akt” and “MAPK” signaling pathways may be involved in the malignant process of FN1 in HNSCC. Conclusion The overexpression of FN1 promotes HNSCC progression and induces macrophages M2 polarization. FN1 may serve as a promising prognostic biomarker and therapeutic target in HNSCC.

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Section: Discussionsupporting

confidence: 72%

The Overexpression of Fibronectin 1 Promotes Cancer Progression and Associated with M2 Macrophages Polarization in Head and Neck Squamous Cell Carcinoma Patients

Zhou¹,

Du²,

Li³

et al. 2022

IJGM

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“…On the other hand, the disruptions of the structure or function of fibronectin can lead to remarkable changes in ECM organization and result in a number of disorders in organisms, including cancer [ 23 ]. The increased expression of FN1 gene has been reported in many types of cancer, including gastric [ 24 ], breast [ 25 ], thyroid [ 26 ], renal [ 27 ] and ovarian [ 28 ] cancers. Furthermore, in many cases, the up-regulation of FN1 indicates a poor prognosis for patients [ 24 , 26 , 28 ].…”

Section: Discussionmentioning

confidence: 99%

“…The increased expression of FN1 gene has been reported in many types of cancer, including gastric [ 24 ], breast [ 25 ], thyroid [ 26 ], renal [ 27 ] and ovarian [ 28 ] cancers. Furthermore, in many cases, the up-regulation of FN1 indicates a poor prognosis for patients [ 24 , 26 , 28 ]. The elevated expression level of fibronectin 1 is strongly related to modifications of extracellular space, and it contributes and promotes the spread, migration, proliferation and differentiation of cells [ 29 ].…”

Section: Discussionmentioning

confidence: 99%

Tracking the Molecular Scenarios for Tumorigenic Remodeling of Extracellular Matrix Based on Gene Expression Profiling in Equine Skin Neoplasia Models

Podstawski

Ropka‐Molik

Semik-Gurgul

et al. 2022

IJMS

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An important component of tissues is the extracellular matrix (ECM), which not only forms a tissue scaffold, but also provides the environment for numerous biochemical reactions. Its composition is strictly regulated, and any irregularities can result in the development of many diseases, including cancer. Sarcoid is the most common skin cancer in equids. Its formation results from the presence of the genetic material of the bovine papillomavirus (BPV). In addition, it is assumed that sarcoid-dependent oncogenic transformation arises from a disturbed wound healing process, which may be due to the incorrect functioning of the ECM. Moreover, sarcoid is characterized by a failure to metastasize. Therefore, in this study we decided to investigate the differences in the expression profiles of genes related not only to ECM remodeling, but also to the cell adhesion pathway, in order to estimate the influence of disturbances within the ECM on the sarcoid formation process. Furthermore, we conducted comparative research not only between equine sarcoid tissue bioptates and healthy skin-derived explants, but also between dermal fibroblast cell lines transfected and non-transfected with a construct encoding the E4 protein of the BP virus, in order to determine its effect on ECM disorders. The obtained results strongly support the hypothesis that ECM-related genes are correlated with sarcoid formation. The deregulated expression of selected genes was shown in both equine sarcoid tissue bioptates and adult cutaneous fibroblast cell (ACFC) lines neoplastically transformed by nucleofection with gene constructs encoding BPV1-E1^E4 protein. The identified genes (CD99, ITGB1, JAM3 and CADM1) were up- or down-regulated, which pinpointed the phenotypic differences from the backgrounds noticed for adequate expression pro-files in other cancerous or noncancerous tumors as reported in the available literature data. Unravelling the molecular pathways of ECM remodeling and cell adhesion in the in vivo and ex vivo models of epidermal/dermal sarcoid-related cancerogenesis might provide powerful tools for further investigations of genetic and epigenetic biomarkers for both silencing and re-initiating the processes of sarcoid-dependent neoplasia. Recognizing those biomarkers might insightfully explain the relatively high capacity of sarcoid-descended cancerous cell derivatives to epigenomically reprogram their nonmalignant neoplastic status in domestic horse cloned embryos produced by somatic cell nuclear transfer (SCNT).

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“…CD276, an immune checkpoint from the B7 superfamily, is highly expressed in TAMs and functionally suppressed DCs of TME. It can inhibit proliferation and activation of CTL, thus closely affecting tumor progression and metastasis (Geng, Huang et al 2022). Therefore, our study suggested that ALKBH1 might improve the prognosis of PAAD patients by downregulating CD276 expression.…”

Section: Discussionmentioning

confidence: 99%

m1A Regulator ALKBH1 and TRMT10B as Potential Prognostic Biomarkers and Related to Tumor Immune Microenvironment in Pancreatic Adenocarcinoma

Huang

et al. 2022

Preprint

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Background N1-methyladenosine (m1A) RNA methylation is crucial in the carcinogenesis and tumorous molecular pathogenesis. However, the detailed pathogenic mechanism of m1A regulators in pancreatic adenocarcinoma (PAAD) has not been comprehensively researched. Therefore, the purpose of this study was to investigate the role of m1A in PAAD prognosis and tumor microenvironment (TME).Methods The relationship between m1A regulators and the PAAD prognosis was analyzed with cBioportal database. RNA-seq transcriptome was obtained from The Cancer Genome Atlas (TCGA) and Genotype-Tissue Expression (GTEx) databases for differential expression analysis. The role of m1A regulators in the PAAD TME was analyzed with TISIDB database and R software. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analysis were performed by The Database for Annotation, Visualization, and Integrated Discovery (DAVID).Results In PAAD, we discovered 10 m1A regulators correlated to poor prognosis and were all upregulated. While up-regulated ALKBH1 and TRMT10B were associated with a better prognosis in PAAD patients. Further research found that ALKBH1 and TRMT10B significantly upregulated the infiltrating level of immune cells, especially CD4+ T cells. Additionally, they also affected the expression of immunomodulators, including CD276, TMEM173, TNFSF9, etc. Finally, GO and KEGG enrichment analysis proved that ALKBH1 and TRMT10B influenced the PAAD development by regulating the RNA polymerase II.Conclusion Promoted expression of ALKBH1 and TRMT10B was significantly related with a better prognosis in PAAD, the possible mechanism of which might associate with the alternation of the TME. ALKBH1 and TRMT10B were potential prognosis biomarkers and possible immunotherapeutic targets for PAAD.

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Over-Expression and Prognostic Significance of FN1, Correlating With Immune Infiltrates in Thyroid Cancer

Cited by 25 publications

References 39 publications

The Overexpression of Fibronectin 1 Promotes Cancer Progression and Associated with M2 Macrophages Polarization in Head and Neck Squamous Cell Carcinoma Patients

The Overexpression of Fibronectin 1 Promotes Cancer Progression and Associated with M2 Macrophages Polarization in Head and Neck Squamous Cell Carcinoma Patients

Tracking the Molecular Scenarios for Tumorigenic Remodeling of Extracellular Matrix Based on Gene Expression Profiling in Equine Skin Neoplasia Models

m1A Regulator ALKBH1 and TRMT10B as Potential Prognostic Biomarkers and Related to Tumor Immune Microenvironment in Pancreatic Adenocarcinoma

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