Artificial intelligence assisted diagnosis of early tc markers and its application.

Thyroid cancer (TC) is a common endocrine malignancy with an increasing incidence worldwide. Early diagnosis is particularly important for TC patients, because it allows patients to receive treatment as early as possible. Artificial intelligence (AI) provides great advantages for complex healthcare systems by analyzing big data based on machine learning. Nowadays, AI is widely used in the early diagnosis of cancer such as TC. Ultrasound detection and fine needle aspiration biopsy are the main methods for early diagnosis of TC. AI has been widely used in the detection of malignancy in thyroid nodules by ultrasound images, cytopathology images and molecular markers. It shows great potential in auxiliary medical diagnosis. The latest clinical trial has shown that the performance of AI models matches with the diagnostic efficiency of experienced clinicians, and more efficient AI tools will be developed in the future. Therefore, in this review, we summarized the recent advances in the application of AI algorithms in assessing the risk of malignancy in thyroid nodules. The objective of this review was to provide a data base for the clinical use of AI-assisted diagnosis in TC, as well as to provide new ideas for the next generation of AI-assisted diagnosis in TC.

Application of thyroglobulin and anti-thyroglobulin antibody combined with emission computed tomography in the adjuvant diagnosis of differentiated thyroid carcinoma.

PURPOSE: Thyroid nodules are a kind of common endocrine system disease, with approximately 5% of them developing into malignant lesions, the most common of which belong to differentiated thyroid carcinoma (DTC). Accurate differential diagnosis using reliable methods and targeted treatment of benign and malignant thyroid nodules are of great significance to improve patient outcomes. This study mainly investigates the diagnostic value of thyroglobulin (Tg) and anti-thyroglobulin antibody (anti-TgAb) combined with emission computed tomography (ECT) in the adjuvant diagnosis DTC. METHODS: All the data of 387 histopathologically diagnosed DTC patients (observation group) and 151 patients with nodular goiter (control group) admitted between June 2019 and June 2021 were collected and retrospectively analyzed. Serum Tg and anti-TgAb levels were detected in all subjects. In addition, all patients in the observation group underwent thyroid ECT, and the results were compared with the pathological findings. The receiver operating characteristic (ROC) curve was drawn to analyze the diagnostic performance of Tg, TgAb and thyroid ECT, either alone or in combination, in patients with thyroid cancer (TC). RESULTS: The consistency test showed that Tg (Kappa-value = 0.370) and anti-TgAb (Kappa-value = 0.393) had generally consistent efficiency with pathological findings in the diagnosis of DTC; ECT (Kappa-value = 0.625) and the combined diagnosis of the three (Kappa-value = 0.757) showed higher consistency than the pathological diagnosis, of which the combined diagnosis contributed to an even higher consistency. The combined diagnosis of Tg, anti-TgAb, and thyroid ECT outperformed either of these alone in DTC diagnosis, with a sensitivity of 91.5%, a specificity of 86.1%, and an accuracy of 90%. CONCLUSIONS: The combination of Tg. anti-TgAb, and RNI can effectively improve the diagnostic accuracy of DTC and reduce the missed diagnosis rate, which has important reference significance for clinical diagnosis and treatment of TC.

Exosomal circular RNA hsa_circ_007293 promotes proliferation, migration, invasion, and epithelial-mesenchymal transition of papillary thyroid carcinoma cells through regulation of the microRNA-653-5p/paired box 6 axis.

Circular RNAs (circRNAs) or exosomes have been reported to exert key regulatory and/or communication functions in human cancer. Nevertheless, current literature on the effects of exosomal circRNAs on tumor invasion and metastasis in thyroid cancer is incomplete. The role of tumor-derived exosomes in driving in vitro papillary thyroid carcinoma (PTC) progression and metastasis requires further investigation. In our study, Exosomes were harvested from PTC patient serum and PTC cell culture medium. Gene expression analysis in PTC cell lines and exosomes was performed with quantitative reverse-transcription polymerase chain reaction. Transwell, wound healing, Western blot assays, and the cell counting kit-8 were applied for functional analysis. Dual-luciferase reporter assay was used to examine the interaction between hsa_circ_007293 (circ007293), microRNA (miR)-653-5p, and paired box 6 (PAX6). Results showed that circ007293 was enriched in exosomes derived from PTC patient serum and cell culture media. Moreover, circ007293 could enter PTC cells through exosomes, and exosomal circ007293 promoted PTC cell epithelial-mesenchymal transition, invasion, migration, and proliferation. circ007293 knockdown reversed the malignant phenotype of PTC cells in vitro. Additionally, circ007293 could competitively bind with miR-653-5p to regulate PAX6 expression. Notably, miR-653-5p overexpression or PAX6 inhibition suppressed the malignant effects of exosomal circ007293. These results evidenced that exosomal circ007293 induced EMT and augmented the invasive and migratory abilities of PTC cells via the miR-653-5p/PAX6 axis, suggesting that it may serve as a promising biomarker for cancer progression.

Activation of the TGF-ß1/Smad signaling by KIF2C contributes to the malignant phenotype of thyroid carcinoma cells.

Kinesin family member 2C (KIF2C) has been identified as a potential oncogene in various types of human cancers; however, the role of KIF2C in thyroid cancer has not yet been elucidated. Quantitative real-time polymerase chain reaction and western blotting were employed for gene expression analysis. Cell Counting Kit-8 and ethynyl-2'-deoxyuridine assays were performed to examine cell proliferation. Cell migration and invasion were assessed by wound-healing and transwell invasion assays. Results showed that KIF2C expression was upregulated in thyroid carcinoma cell lines. In addition, upregulation of KIF2C promoted the proliferation, migration, and invasion of thyroid carcinoma cells, while downregulation of KIF2C exerted the opposite effects. Overexpression of KIF2C induced the activation of transforming growth factor-ß1 (TGF-ß1)/Smad signaling in thyroid carcinoma cells. However, inhibition of TGF-ß1/Smad signaling through silencing TGF-ß1 attenuated the promoting effects of KIF2C overexpression on the malignant phenotype of thyroid carcinoma cells. Besides, overexpression of TGF-ß1 suppressed the inhibitory effect of KIF2C knockdown on the proliferation and metastasis of thyroid carcinoma cells. In conclusion, our findings demonstrated that KIF2C contributed to the malignant phenotype of thyroid carcinoma cells by inducing the activation of TGF-ß1/Smad signaling, thus uncovering a novel mechanism for thyroid carcinoma progression.

Silencing of AHNAK2 restricts thyroid carcinoma progression by inhibiting the Wnt/ß-catenin pathway.

AHNAK nucleoprotein 2 (AHNAK2) has been proposed to have an oncogenic role in various human cancers. However, the functional role of AHNAK2 in thyroid carcinoma (TC) progression has never been explored. In this study, quantitative real-time polymerase chain reaction and western blot were conducted to evaluate the expression of genes. The functional role of AHNAK2 was elucidated by cell count kit-8, colony-forming assay, wound-healing assay, and Transwell invasion assay. We found that AHNAK2 was highly expressed in thyroid carcinoma, and it was tightly correlated with the pathological stage in TC. The mRNA and protein levels of AHNAK2 were increased in TC cells. Silencing of AHNAK2 restricted the proliferation, metastasis, and epithelial-mesenchymal transition (EMT) of TC cells. AHNAK2 silencing inhibited the protein expression of ß-catenin and cyclin D1, and AHNAK2 overexpression had the opposite effects. Moreover, LiCl or ICG-001 exposure counteracted the effects of AHNAK2 silencing or upregulation on malignant phenotypes of TC cells. In conclusion, the knockdown of AHNAK2 restrained the proliferation, metastasis, and EMT of TC cells by inhibiting the Wnt/ß-catenin pathway, providing a new potential mechanism of AHNAK2 in understanding the oncogenesis and progression of TC.

Overexpression of serum lncRNA-ABHD11-AS1 as poor prognosis of patients with papillary thyroid carcinoma.

This paper was aimed at exploring the correlation of long non-coding RNA (lncRNA)-ABHD11 Antisense RNA1 (ABHD11-AS1) with the poor prognosis of patients with papillary thyroid carcinoma (PTC) and at investigating its effects on the survival of PTC cells. Serum was respectively collected from 64 PTC patients who were admitted to our hospital (PTC group) and from 50 healthy controls who underwent physical examinations (HC group) both from April 2011 to April 2015. The expression levels of ABHD11-AS1 in the serum were detected, and the values of it for diagnosis and prognosis (5-year follow-ups) were analyzed. The knockdown and overexpression models of ABHD11-AS1 in were constructed to explore the effects of the models on their proliferation, cycles and apoptosis. According to the data, the expression levels of serum ABHD11-AS1 in the PTC patients were remarkably higher than those in the healthy controls, and the area under the curve (AUC) for distinguishing the patients from the controls was 0.920. In the analysis of prognosis, the levels in patients with a poor prognosis were remarkably higher than those in patients with a good prognosis. According to the curves of overall survival rates (OSRs), the high levels of ABHD11-AS1 were remarkably correlated with the poor prognosis (a lower 5-year OSR). COX analysis showed that TNM staging, lymph node metastasis and ABHD11-AS1 were the independent prognostic factors of PTC patients. In the cell experiments, knocking down ABHD11-AS1 remarkably inhibited PTC cells from proliferation, arrested them in G0/G1 phase, and induced their apoptosis, negatively affecting their survival indices. Overexpressing this RNA had positive effects on the survival indices. Taken together, high levels of serum ABHD11-AS1 are related to the poor prognosis of PTC patients, and knocking down its expression can inhibit the survival of PTC cells.

Identification of HMMR as a prognostic biomarker for patients with lung adenocarcinoma via integrated bioinformatics analysis.

BACKGROUND: Lung adenocarcinoma (LUAD) is the most prevalent tumor in lung carcinoma cases and threatens human life seriously worldwide. Here we attempt to identify a prognostic biomarker and potential therapeutic target for LUAD patients. METHODS: Differentially expressed genes (DEGs) shared by GSE18842, GSE75037, GSE101929 and GSE19188 profiles were determined and used for protein-protein interaction analysis, enrichment analysis and clinical correlation analysis to search for the core gene, whose expression was further validated in multiple databases and LUAD cells (A549 and PC-9) by quantitative real-time PCR (qRT-PCR) and western blot analyses. Its prognostic value was estimated using the Kaplan-Meier method, meta-analysis and Cox regression analysis based on the Cancer Genome Atlas (TCGA) dataset and co-expression analysis was conducted using the Oncomine database. Gene Set Enrichment Analysis (GSEA) was performed to illuminate the potential functions of the core gene. RESULTS: A total of 115 shared DEGs were found, of which 24 DEGs were identified as candidate hub genes with potential functions associated with cell cycle and FOXM1 transcription factor network. Among these candidates, HMMR was identified as the core gene, which was highly expressed in LUAD as verified by multiple datasets and cell samples. Besides, high HMMR expression was found to independently predict poor survival in patients with LUAD. Co-expression analysis showed that HMMR was closely related to FOXM1 and was mainly involved in cell cycle as suggested by GSEA. CONCLUSION: HMMR might be served as an independent prognostic biomarker for LUAD patients, which needs further validation in subsequent studies.

LncRNA PVT1 Acts as a Tumor Promoter in Thyroid Cancer and Promotes Tumor Progression by Mediating miR-423-5p-PAK3.

INTRODUCTION: Thyroid cancer (TC) is an endocrine tumor whose risk of onset has been rising, so the deep understanding of its molecular mechanism helps formulate new treatment strategies. METHODS: This paper was aimed at exploring the regulatory mechanism of long non-coding RNA (LncRNA) plasmacytoma variant translocation 1 (PVT1) in TC. The expression of PVT1, miR-423-5p and p21-activated kinase 3 (PAK3) in TC tissues and cell lines was detected by real-time PCR. PAK3 levels were detected by Western blot. Regulatory relationships between target genes and the proliferation, invasion and apoptosis of cells and genes were analyzed. RESULTS: PVT1 and PAK3 upregulated while miR-423-5p downregulated in the tissues and cell lines. PVT1 downregulation inhibited TC cells from malignantly proliferating and invading, and promoted their apoptosis. PVT1 specifically regulated miR-423-5p, and its overexpression could weaken the anti-tumor effect of this miR on TC cells. In addition, miR-423-5p directly targeted PAK3, and knocking down its expression could weaken the inhibitory effect of PAK3 downregulation on TC progression. Besides, PVT1 acted as a competitive endogenous RNA to sponge this miR and thus regulate PAK3 expression. DISCUSSION: In conclusion, PVT1 can mediate the molecular mechanism of the miR-423-5p-PAK3 axis regulatory network on regulating TC, so it is a new direction of treating the disease.