Jian Liu

Objective This study aims to qualitatively and quantitatively assess the research landscape of palmitoylation in oncology using bibliometric analysis, thereby providing insights into research hotspots and emerging trends. Methods The data were sourced from the Web of Science Core Collection, retrieved using predefined search terms, and comprise review articles and original research papers published in English from 2004 to 2024. Bibliometric analysis and data visualization were performed using VOSviewer, CiteSpace, and Microsoft Excel. Results The United States and China are the leading contributors to research in this field, with Shanghai Jiao Tong University being the most prolific institution in terms of publication output. Current research hotspots in protein palmitoylation related to oncology primarily encompass the enzymatic mechanisms and dynamic regulation of palmitoylation, palmitoylation-mediated lipid metabolic reprogramming and tumorigenesis, palmitoylation-mediated tumor signaling pathways, and targeted cancer therapy strategies based on palmitoylation modification. Current research trends primarily focus on the modulation of critical enzymes and signaling pathways, which influence tumor biology and prognosis. Additionally, emphasis is placed on metabolic reprogramming mediated by protein palmitoylation within the tumor microenvironment, especially regarding its role in tumor responsiveness to chemotherapy and immunotherapy. Conclusion This study provides a comprehensive overview of recent advancements in research regarding protein palmitoylation modifications within oncology.

MiR-146b has been identified as being overexpressed in human bladder cancer (BCa) and implicated in promoting cancer cell invasion. However, its specific involvement in BCa cell growth remains unclear. In this study, we demonstrate that the downregulation of miR-146b significantly suppresses tumorigenic growth of human BCa cells both in vitro and in vivo by inducing G0/G1 cell cycle arrest. Specifically, miR-146b inhibition resulted in a significant reduction in colony formation (p < 0.05) and anchorage-independent growth in both UMUC3 and T24T cells, as measured by soft agar assays, with three independent replicates for each experiment. Notably, Cyclin D1 protein plays a crucial role in miR-146b-induced BCa cell proliferation, as confirmed by Western blotting (p < 0.05), with each experiment performed in triplicate. Mechanistic investigations reveal that miR-146b reduces mothers against decapentaplegic homolog 4 (SMAD4) mRNA stability by directly binding to its 3′ untranslated region (3′-UTR), leading to decreased SMAD4 expression. This reduction in SMAD4 levels promotes cellular myelocytomatosis (C-MYC) transcription, which in turn enhances Cyclin D1 transcription, ultimately facilitating BCa cell proliferation. The findings unveil a novel regulatory axis involving SMAD4/C-MYC/Cyclin D1 in mediating the oncogenic role of miR-146b in BCa cells. Statistical significance was determined using Student’s t-test, with p-values <0.05 considered significant. Together with its previously established function in BCa invasion, the results highlight the potential for developing miR-146b-based therapeutic strategies for treating human BCa patients.

Metastasis is responsible for at least 90% of colon cancer (CC)‐related deaths. Lipid metabolism is a critical factor in cancer metastasis, yet the underlying mechanism requires further investigation. Herein, through the utilisation of single‐cell sequencing and proteomics, we identified sulfotransferase SULT2B1 as a novel metastatic tumour marker of CC, which was associated with poor prognosis. CC orthotopic model and in vitro assays showed that SULT2B1 promoted lipid metabolism and metastasis. Moreover, SULT2B1 directly interacted with SCD1 to facilitate lipid metabolism and promoted metastasis of CC cells. And the combined application of SCD1 inhibitor CAY with SULT2B1‐ konockout (KO) demonstrated a more robust inhibitory effect on lipid metabolism and metastasis of CC cells in comparison to sole application of SULT2B1‐KO. Notably, we revealed that lovastatin can block the SULT2B1‐induced promotion of lipid metabolism and distant metastasis in vivo. Further evidence showed that SMC1A transcriptionally upregulated the expression of SULT2B1. Our findings unveiled the critical role of SULT2B1 in CC metastasis and provided a new perspective for the treatment of CC patients with distant metastasis.

(1) Background: This study aimed to establish a nomogram model for predicting the overall survival (OS) of medullary thyroid carcinoma (MTC) patients based on the Surveillance, Epidemiology, and End Results (SEER) database. (2) Methods: Patients with MTC in the SEER database from 2004 to 2015 were included and divided into a modeling group and an internal validation group. We also selected MTC patients from our center from 2007 to 2019 to establish an external validation group. Univariate and multivariate Cox regression analyses were used to screen for significant independent variables and to establish a nomogram model. Kaplan–Meier (K-M) curves were plotted to evaluate the influence of the predictors. The C-indexes, areas under the curves (AUCs), and calibration curves were plotted to validate the predictive effect of the model. (3) Results: A total of 1981 MTC patients from the SEER database and 85 MTC patients from our center were included. The univariate and multivariate Cox regression analyses showed that age, tumor size, N stage, and M stage were significant factors, and a nomogram model was established. The C-index of the modeling group was 0.792, and the AUCs were 0.811, 0.825, and 0.824. The C-index of the internal validation group was 0.793, and the AUCs were 0.847, 0.846, and 0.796. The C-index of the external validation group was 0.871, and the AUCs were 0.911 and 0.827. The calibration curves indicated that the prediction ability was reliable. (4) Conclusions: A nomogram model based on age, tumor size, N stage, and M stage was able to predict the OS of MTC patients.

Background: Circular RNAs (circRNAs) are a class of noncoding RNAs that are involved in the progression of many human cancers. The precise gene locus and the roles of circular RNA from Fibronectin type III domain containing 3B (FNDC3B) in OS and its mechanisms of action have not been fully explored. Materials and methods: qRT-qPCR assay was used to determine gene expressions. CCK8 Assay, EdU assay, wound-healing assay, transwell invasion assay and in vivo xenograft assay were used to perform functional investigations. RNA-FISH, immunofluorescence, RIP assay, RNA stability analysis were applied in mechanistic studies. Results: We found that circFNDC3B downregulated and FNDC3B mRNA upregulated in OS, and might be potential biomarkers for indicating disease progression and prognosis of OS patients. CircFNDC3B acted as a tumor suppressor gene to restrain OS progression and FNDC3B functioned as an oncogene to promote OS progression in vitro and in vivo. RNA binding protein RNA binding motif protein 47 (RBM47) could bind to the flanking introns of circFNDC3B to facilitate the generation of circFNDC3B, resulting in the reduction of FNDC3B mRNA and the circFNDC3B-FNDC3B mRNA imbalance. CircFNDC3B also inhibited FNDC3B mRNA expression by reducing its stability via competitively binding to Insulin-like growth-factor-2 mRNA binding protein (IGF2BP1). Conclusion: This study demonstrated that RBM47 and IGF2BP1 mediated circular FNDC3B/FNDC3B mRNA imbalance was involved in the malignant processes of OS.

Purpose To investigate the impact of lateral lymph node metastasis in papillary thyroid microcarcinoma (PTMC). Methods 5241 PTMC patients with follow-up information were enrolled in the current study. These patients underwent primary surgery in our situation from January 1997 to December 2016. Additionally, a validation cohort consisting of 274 PTMC patients who underwent primary surgery between January 2020 and December 2021 was also included. Univariable and multivariate logistic analyses were conducted to identify the association between clinicopathologic features and lateral lymph node metastasis (LLNM). Kaplan–Meier survival curve analysis was used to calculate the disease-free survival (DFS) rate. The fitting curve was generated to identify the quantitative relationship between central lymph node metastases (CLNM) and LLNM. Results Of 5241 PTMC patients, cervical lymph node metastasis was detected in 1494 (28.5%) cases, including 1364 (26.0%) with CLNM only and 130 (2.5%) with LLNM. With a median follow-up time of 60 months (interquartile range [IQR], 44–81), recurrence was detected in 114 patients (2.2%). Multivariate Cox regression analyses showed that LNM was the only independent risk factor for recurrence, with HR values of 3.03 in CLNM and 11.14 in LLNM, respectively. Tumor diameter >0.5 cm (hazard ratio [HR]:1.80), multifocality (HR:2.59), bilaterality (HR:2.13), extrathyroidal invasion (HR:2.13), and CLNM (HR:5.11) were independent risk factors for LLNM. The prevalence of LLNM escalated significantly with increasing number of lymph node involvement in CLNM when stratified by the number of metastatic lymph nodes and trend was observed similarly in the validation cohort. The fitting curve showed that the incidence of LLNM could be as high as 20.7% when the number of CLNM ≥ 5. Conclusions By analyzing a large database with follow-up information, our study provides evidence that LLNM is significantly correlated with tumor recurrence in patients with PTMC. Tumor size (>0.5 cm), multifocality, bilaterality, extrathyroidal extension (ETE) and CLNM are independent risk factors for LLNM.

Objective: To probe into the role of pyroptosis-related genes in gastric cancer. Methods: To establish pyroptosis-related genes, observe their expression in gastric cancer, and analyze the prognosis of pyroptosis-related genes in gastric cancer by single-factor COX, which showed that only GSDME had prognostic significance in gastric cancer. The mRNA expression profiles and lncRNA expression profiles of gastric cancer downloaded from the Cancer Genome Atlas were combined for weighted gene regulatory network analysis, after which the lncRNA nodes of the module to which GSDME belongs were extracted to obtain the lncRNAs−GSDME interactions, which were visualized with Cytoscape network plots. Finally, the effects of GSDME on the proliferation, migration, and apoptosis of gastric cancer cells were observed with CCK8, and flow cytometry. Results: Our results show that only GSDME has prognostic significance in gastric cancer, and show that it has an important role in a variety of tumors. In addition, our results show that 16 lncRNAs have a significant interaction with GSDME. Finally, the experimental analysis showed that knocking down the expression level of GSDME could affect the growth as well as apoptosis of gastric cancer cells. Conclusion: The significant prognostic significance of GSDME in gastric cancer and the fact that affecting GSDME expression inhibits gastric cancer cell growth suggest that GSDME can be used as a predictive biomarker.