The SUMO Family: Mechanisms and Implications in Thyroid Cancer Pathogenesis and Therapy.

(1) Background: Small ubiquitin-like modifiers (SUMOs) are pivotal in post-translational modifications, influencing various cellular processes, such as protein localization, stability, and genome integrity. (2) Methods: This review explores the SUMO family, including its isoforms and catalytic cycle, highlighting their significance in regulating key biological functions in thyroid cancer. We discuss the multifaceted roles of SUMOylation in DNA repair mechanisms, protein stability, and the modulation of receptor activities, particularly in the context of thyroid cancer.

A nomogram for enhanced risk stratification for predicting cervical lymph node metastasis in papillary thyroid carcinoma patients.

Background: Cervical lymph node metastasis (CLNM) significantly impacts the prognosis of papillary thyroid carcinoma (PTC) patients. Accurate CLNM prediction is crucial for surgical planning and patient outcomes. This study aimed to develop and validate a nomogram-based risk stratification system to predict CLNM in PTC patients.

Safety and effectiveness of carbon nanoparticles suspension-guided lymph node dissection during thyroidectomy in patients with thyroid papillary cancer: a prospective, multicenter, randomized, blank-controlled trial.

Objective: This study aimed to evaluate the effectiveness and safety of carbon nanoparticlesguided lymph node dissection during thyroidectomy in patients with papillary thyroid cancer(PTC).

Methods: Clinical trials consisted of two subgroups: unilateral lobectomy (UL; n=283) and total thyroidectomy (TT; n=286). From each subgroup, the patients were randomly assigned to two groups: the carbon nanoparticle group and control group.

Insight of novel biomarkers for papillary thyroid carcinoma through multiomics.

Introduction: The overdiagnosing of papillary thyroid carcinoma (PTC) in China necessitates the development of an evidence-based diagnosis and prognosis strategy in line with precision medicine. A landscape of PTC in Chinese cohorts is needed to provide comprehensiveness.

Methods: 6 paired PTC samples were employed for whole-exome sequencing, RNA sequencing, and data-dependent acquisition mass spectrum analysis.

Impaired thyroid hormone sensitivity increases the risk of papillary thyroid cancer and cervical lymph node metastasis.

Background: The association of thyroid hormone sensitivity with papillary thyroid carcinoma (PTC) is unclear. This study investigated the relationship between the thyroid hormone sensitivity indices and the risk of PTC and the influence of thyroid hormone sensitivity on the aggressive clinicopathologic features of PTC.

Methods: This retrospective study recruited 1225 PTC patients and 369 patients with benign nodules undergoing surgery in Zhongshan Hospital in 2020.

Siglec15 promotes the migration of thyroid carcinoma cells by enhancing the EGFR protein stability.

Purpose: Sialic acid-bound immunoglobulin-like lectin 15 (Siglec15) has emerged as a novel therapeutic target in tumor immunotherapy. This study is designed to investigate the function and mechanism of Siglec15 in thyroid carcinoma (THCA).

Materials And Methods: The information on patients with THCA from TGCA and GEO database were used to analyze the expression of Siglec15 in THCA.

A novel brick for bispecific antibody construction.

In recent years, the development of bispecific antibodies (bsAbs) has become a major trend in the biopharmaceutical industry. By simultaneously engaging two molecular targets, bsAbs have exhibited unique mechanisms of action that could lead to clinical benefits unattainable by conventional monoclonal antibodies. The type of structure used to construct a bsAb directly influences the distance, angle, degree of freedom, and affinity between the two antibody binding sites and the interaction between the two antigens or the cells where the antigens are located, which have been bound by the antibody.

Sialylation-dependent interaction between PD-L1 and CD169 promotes monocyte adhesion to endothelial cells.

The monocyte adhesion to endothelial cells is an early step in chronic inflammation. Interferon-γ (IFN-γ) is regarded as a master regulator of inflammation development. However, the significance and mechanisms of IFN-γ in the monocyte adhesion to endothelial cells remains largely unknown.

Exosomal ANXA1 derived from thyroid cancer cells is associated with malignant transformation of human thyroid follicular epithelial cells by promoting cell proliferation.

Exosomes are nano‑sized extracellular vesicles that can be released from cancer cells. It has been shown that cancer cell‑derived exosomes may be associated with carcinogenesis by transferring signaling proteins from malignant to neighboring non‑malignant cells. In addition, annexin A1 (ANXA1) is a well‑known oncogene, that can be released from extracellular vesicles by cancer cells.

miR-873-5p Inhibits Cell Migration and Invasion of Papillary Thyroid Cancer via Regulation of CXCL16.

Aim: Papillary thyroid cancer (PTC) is the most common type of thyroid cancer with an increasing morbidity. MicroRNAs (miRNAs) play the pivotal roles in PTC occurrence and development. The aim of this study was to investigate the biological functions of miR-873-5p and its underlying molecular mechanisms in PTC.

Acetylcholine promotes the self-renewal and immune escape of CD133+ thyroid cancer cells through activation of CD133-Akt pathway.

Nerves infiltrate the tumor microenvironment and stimulate the growth of cancer cells through the secretion of neurotransmitters. However, the contributions of nerves to the self-renewal capacity of cancer stem cells (CSCs) remain largely unknown. In this study, we found that CD133+ cancer cells were responsible for the initiation of thyroid cancer.

Upregulation of microRNA-143-3p induces apoptosis and suppresses proliferation, invasion, and migration of papillary thyroid carcinoma cells by targeting MSI2.

As a tumor-associated biological molecule, microRNA-143-3p (miR-143-3p) is implicated in the progression of papillary thyroid carcinoma (PTC). We conducted this study to elucidate the effects of miR-143-3p mediated by Musashi RNA binding protein 2 (MSI2) on the biological activities of PTC cells. The K1 cells with the lowest miR-143-3p expression were selected for the experiments.

Emerging roles of the long non-coding RNA 01296/microRNA-143-3p/MSI2 axis in development of thyroid cancer.

Thyroid cancer (TC) is an endocrine malignancy with rising incidence. Long non-coding RNAs (lncRNAs) can serve as diagnostic and prognostic biomarkers for TC. Thus, we studied roles of LINC01296 in TC progression.

IL-17A secreted from lymphatic endothelial cells promotes tumorigenesis by upregulation of PD-L1 in hepatoma stem cells.

Background & Aims: The microenvironment regulates hepatoma stem cell behavior. However, the contributions of lymphatic endothelial cells to the hepatoma stem cell niche remain largely unknown; we aimed to analyze this contribution and elucidate the mechanisms behind it.

Methods: Associations between lymphatic endothelial cells and CD133 hepatoma stem cells were analyzed by immunofluorescence and adhesion assays; with the effects of their association on IL-17A expression examined using western blot, quantitative reverse transcription PCR and luciferase reporter assay.

Long non-coding RNA MIAT promotes papillary thyroid cancer progression through upregulating LASP1.

Background: Accumulating evidences indicate that long non-coding RNAs (lncRNAs) play an important role in initiation and development of thyroid cancer. However, the underlying molecular mechanism remains elusive.

Methods: To explore potential oncogenic and tumor suppressive lncRNAs in papillary thyroid cancer (PTC), we performed RNA sequencing to discover differentially expression lncRNAs between PTC tissues and matched normal tissues.

CD133 promotes the self-renewal capacity of thyroid cancer stem cells through activation of glutamate aspartate transporter SLC1A3 expression.

CD133+ cancer stem cells are responsible for thyroid cancer initiation. The regulatory pathways essential for sustaining the self-renewal of thyroid cancer stem cells remain largely unknown. Glutamate signaling regulates the self-renewal ability of stem cells.

ROS-generating oxidase NOX1 promotes the self-renewal activity of CD133+ thyroid cancer cells through activation of the Akt signaling.

Thyroid cancer results from unregulated expansion of a self-renewing tumor-initiating cell population. The regulatory pathways essential for sustaining the self-renewal of tumor-initiating cells remain largely unknown. Reactive oxygen species (ROS) play a vital role in tumor initiation and progression.

Long Non-coding Antisense RNA TNRC6C-AS1 Is Activated in Papillary Thyroid Cancer and Promotes Cancer Progression by Suppressing TNRC6C Expression.

Evidences have shown the important role of long non-coding antisense RNAs in regulating its cognate sense gene in cancer biology. Investigate the regulatory role of a long non-coding antisense RNA TNRC6C-AS1 on its sense partner TNRC6C, and their effects on the aggressiveness and iodine-uptake ability of papillary thyroid cancer (PTC). TNRC6C-AS1 was identified as the target long non-coding RNA in PTC by using microarray analysis and computational analysis.

Monoubiquitination of Cancer Stem Cell Marker CD133 at Lysine 848 Regulates Its Secretion and Promotes Cell Migration.

CD133, a widely known marker of cancer stem cells, was recently found in extracellular vesicles. However, the mechanisms underlying CD133 translocation to the extracellular space remain largely unknown. Here we report that CD133 is monoubiquitinated.

Galectin-3 induced by hypoxia promotes cell migration in thyroid cancer cells.

Background: The aim of this study is to investigate the role of Galectin-3 in human thyroid cancer migration.

Methods: The expression of Galectin-3 in surgical specimens was investigated using immunohistochemistry and western blot. A papillary thyroid cancer cell line (B-cpap) and an anaplastic thyroid cancer cell line (8305c) were transfected with short-hairpin RNA against Galectin-3 (Gal-3-shRNA).

Stathmin decreases cholangiocarcinoma cell line sensitivity to staurosporine-triggered apoptosis via the induction of ERK and Akt signaling.

Cholangiocarcinoma is a rare, but highly fatal malignancy. However, the intrinsic mechanism involved in its tumorigenesis remains obscure. An urgent need remains for a promising target for cholangiocarcinoma biological therapies.

Long non-coding RNA CRNDE promotes gallbladder carcinoma carcinogenesis and as a scaffold of DMBT1 and C-IAP1 complexes to activating PI3K-AKT pathway.

Deleted in malignant brain tumors 1 (DMBT1) is deleted during cancer progression and as a potential tumor-suppressor gene in various types of cancer. However, its role in Gallbladder cancer remains poorly understood. DMBT1 has low-expression and deletion of copy number were detected in normal tissues and GBC cancer tissues by qRT-PCR.

The Interaction between Cancer Stem Cell Marker CD133 and Src Protein Promotes Focal Adhesion Kinase (FAK) Phosphorylation and Cell Migration.

CD133, a widely known cancer stem cell marker, has been proved to promote tumor metastasis. However, the mechanism by which CD133 regulates metastasis remains largely unknown. Here, we report that CD133 knockdown inhibits cancer cell migration, and CD133 overexpression promotes cell migration.

Quantitative assessment of preoperative serum thyrotropin level and thyroid cancer.

Thyroid stimulating hormone (TSH) is the major growth factor for thyrocytes, but the pathogenic role of serum TSH in thyroid cancer (TC) is unknown. The association between TSH level and the development of thyroid cancer has been widely evaluated recently. However, the results remain conflicting.