A fibrous stromal component in hepatocellular carcinoma reveals a cholangiocarcinoma-like gene expression trait and epithelial-mesenchymal transition

Objective: To analyze the research hot spots and frontiers of molecular mechanisms of exercise on cancer via CiteSpace.Method: Related publications in the Web of Science Core Collection Science Citation Index Expanded were retrieved from inception to November 27th, 2021. Then we used CiteSpace to generate network maps and identify top authors, institutions, countries, keywords, co-cited authors, journals, references and research trends.Results: A total of 1,130 related publications were retrieved. The most productive author and journal were Lee W Jones and PLOS ONE. Hanahan D and Warburg O were the most cited authors. Fudan University and Shanghai Jiao Tong University were the leading institutions, while China was the leading country. Top-cited authors and references generally focused on the epidemiology and hallmarks of cancer. Top five keywords with both high frequency and high betweenness centrality were breast cancer, aerobic glycolysis, oxidative stress, gene expression, skeletal muscle. Keyword “warburg effect” ranked first with the highest citation burst, while “inflammation”, “hepatocellular carcinoma”, “epithelial mesenchymal transition”, and “adipose tissue” were emerging research foci.Conclusion: This study analyzed the research hot spots and frontiers of molecular mechanisms of exercise on cancer via CiteSpace. Based on the results, altered metabolism (aerobic glycolysis, insulin resistance, myokines), oxidative stress, gene expression and apoptosis were hot-research mechanisms of exercise on cancer. Emerging research foci of mechanisms were generally around inflammation, epithelial mesenchymal transition and adipokines. In addition, future studies could carry in-depth research of interactions between different mechanisms and try to elucidate the recommended doses and intensities of exercise for cancer, especially in breast, colorectal, prostate cancer and hepatocellular carcinoma.

Download Full-text

Faculty Opinions recommendation of A natural antisense transcript regulates Zeb2/Sip1 gene expression during Snail1-induced epithelial-mesenchymal transition.

Faculty Opinions – Post-Publication Peer Review of the Biomedical Literature ◽

10.3410/f.1103760.559879 ◽

2008 ◽

Author(s):

Avri Ben-Ze'ev

Keyword(s):

Gene Expression ◽

Antisense Transcript ◽

Epithelial Mesenchymal Transition ◽

Natural Antisense Transcript ◽

Mesenchymal Transition

Download Full-text

TNF-α induces epithelial-mesenchymal transition through NF-κB in hepatocellular carcinoma

Academic Journal of Second Military Medical University ◽

10.3724/sp.j.1008.2013.00271 ◽

2013 ◽

Vol 33 (3) ◽

pp. 271-276

Author(s):

Xing-rui KOU ◽

Ying-ying JING ◽

Guo-feng YU ◽

Meng-chao WU ◽

Li-xin WEI

Keyword(s):

Hepatocellular Carcinoma ◽

Epithelial Mesenchymal Transition ◽

Mesenchymal Transition ◽

Tnf Α

Download Full-text

Intergrated Analysis of ELMO1, Serves As a Link between Tumor Mutation Burden and Epithelial-Mesenchymal Transition in Hepatocellular Carcinoma

SSRN Electronic Journal ◽

10.2139/ssrn.3350534 ◽

2019 ◽

Author(s):

Hong Peng ◽

Yi Zhang ◽

Zhiwei Zhou ◽

Yu Guo ◽

Xiaohui Huang ◽

...

Keyword(s):

Hepatocellular Carcinoma ◽

Epithelial Mesenchymal Transition ◽

Tumor Mutation Burden ◽

Mesenchymal Transition ◽

Mutation Burden

Download Full-text

Correction to: Forkhead box (FOX) G1 promotes hepatocellular carcinoma epithelial-Mesenchymal transition by activating Wnt signal through forming T-cell factor-4/Betacatenin/FOXG1 complex

Journal of Experimental & Clinical Cancer Research ◽

10.1186/s13046-021-01900-2 ◽

2021 ◽

Vol 40 (1) ◽

Author(s):

Xingrong Zheng ◽

Jiaxin Lin ◽

Hewei Wu ◽

Zhishuo Mo ◽

Yunwen Lian ◽

...

Keyword(s):

Hepatocellular Carcinoma ◽

T Cell ◽

Epithelial Mesenchymal Transition ◽

Mesenchymal Transition ◽

T Cell Factor ◽

Forkhead Box ◽

Wnt Signal

An amendment to this paper has been published and can be accessed via the original article.

Download Full-text

A novel prognostic model based on epithelial-mesenchymal transition-related genes predicts patient survival in gastric cancer

World Journal of Surgical Oncology ◽

10.1186/s12957-021-02329-9 ◽

2021 ◽

Vol 19 (1) ◽

Author(s):

Wanting Song ◽

Yi Bai ◽

Jialin Zhu ◽

Fanxin Zeng ◽

Chunmeng Yang ◽

...

Keyword(s):

Gene Expression ◽

Gastric Cancer ◽

Risk Model ◽

Cox Regression ◽

Epithelial Mesenchymal Transition ◽

Risk Groups ◽

The Cancer Genome Atlas ◽

Critical Function ◽

Mesenchymal Transition ◽

Patient Prognosis

Abstract Background Gastric cancer (GC) represents a major malignancy and is the third deathliest cancer globally. Several lines of evidence indicate that the epithelial-mesenchymal transition (EMT) has a critical function in the development of gastric cancer. Although plentiful molecular biomarkers have been identified, a precise risk model is still necessary to help doctors determine patient prognosis in GC. Methods Gene expression data and clinical information for GC were acquired from The Cancer Genome Atlas (TCGA) database and 200 EMT-related genes (ERGs) from the Molecular Signatures Database (MSigDB). Then, ERGs correlated with patient prognosis in GC were assessed by univariable and multivariable Cox regression analyses. Next, a risk score formula was established for evaluating patient outcome in GC and validated by survival and ROC curves. In addition, Kaplan-Meier curves were generated to assess the associations of the clinicopathological data with prognosis. And a cohort from the Gene Expression Omnibus (GEO) database was used for validation. Results Six EMT-related genes, including CDH6, COL5A2, ITGAV, MATN3, PLOD2, and POSTN, were identified. Based on the risk model, GC patients were assigned to the high- and low-risk groups. The results revealed that the model had good performance in predicting patient prognosis in GC. Conclusions We constructed a prognosis risk model for GC. Then, we verified the performance of the model, which may help doctors predict patient prognosis.

Download Full-text

Pancreatic Cancers with High Grade Tumor Budding Exhibit Hallmarks of Diminished Anti-Tumor Immunity

Cancers ◽

10.3390/cancers13051090 ◽

2021 ◽

Vol 13 (5) ◽

pp. 1090

Author(s):

Hassan Sadozai ◽

Animesh Acharjee ◽

Thomas Gruber ◽

Beat Gloor ◽

Eva Karamitopoulou

Keyword(s):

Gene Expression ◽

Pancreatic Cancer ◽

Disease Progression ◽

Immune Escape ◽

Epithelial Mesenchymal Transition ◽

Tumor Budding ◽

Ductal Adenocarcinoma ◽

Low Grade ◽

High Grade ◽

Mesenchymal Transition

Tumor budding is associated with epithelial-mesenchymal transition and diminished survival in a number of cancer types including pancreatic ductal adenocarcinoma (PDAC). In this study, we dissect the immune landscapes of patients with high grade versus low grade tumor budding to determine the features associated with immune escape and disease progression in pancreatic cancer. We performed immunohistochemistry-based quantification of tumor-infiltrating leukocytes and tumor bud assessment in a cohort of n = 111 PDAC patients in a tissue microarray (TMA) format. Patients were divided based on the ITBCC categories of tumor budding as Low Grade (LG: categories 1 and 2) and High Grade (HG: category 3). Tumor budding numbers and tumor budding grade demonstrated a significant association with diminished overall survival (OS). HG cases exhibit notably reduced densities of stromal (S) and intratumoral (IT) T cells. HG cases also display lower M1 macrophages (S) and increased M2 macrophages (IT). These findings were validated using gene expression data from TCGA. A published tumor budding gene signature demonstrated a significant association with diminished survival in PDAC patients in TCGA. Immune-related gene expression revealed an immunosuppressive TME in PDAC cases with high expression of the budding signature. Our findings highlight a number of immune features that permit an improved understanding of disease progression and EMT in pancreatic cancer.

Download Full-text

MYC-targeted WDR4 promotes proliferation, metastasis, and sorafenib resistance by inducing CCNB1 translation in hepatocellular carcinoma

Cell Death and Disease ◽

10.1038/s41419-021-03973-5 ◽

2021 ◽

Vol 12 (7) ◽

Author(s):

Peng Xia ◽

Hao Zhang ◽

Kequan Xu ◽

Xiang Jiang ◽

Meng Gao ◽

...

Keyword(s):

Hepatocellular Carcinoma ◽

Epithelial Mesenchymal Transition ◽

P53 Protein ◽

Rna Modifications ◽

M Cell ◽

Mesenchymal Transition ◽

Akt Phosphorylation ◽

Repeat Domain ◽

Cell Cycle Transition

AbstractHepatocellular carcinoma (HCC) is one of the most common malignancies worldwide. However, there still remains a lack of effective diagnostic and therapeutic targets for this disease. Increasing evidence demonstrates that RNA modifications play an important role in the progression of HCC, but the role of the N7-methylguanosine (m7G) methylation modification in HCC has not been properly evaluated. Thus, the goal of the present study was to investigate the function and mechanism of the m7G methyltransferase WD repeat domain 4 (WDR4) in HCC as well as its clinical relevance and potential value. We first verified the high expression of WDR4 in HCC and observed that upregulated WDR4 expression increased the m7G methylation level in HCC. WDR4 promoted HCC cell proliferation by inducing the G2/M cell cycle transition and inhibiting apoptosis in addition to enhancing metastasis and sorafenib resistance through epithelial-mesenchymal transition (EMT). Furthermore, we observed that c-MYC (MYC) can activate WDR4 transcription and that WDR4 promotes CCNB1 mRNA stability and translation to enhance HCC progression. Mechanistically, we determined that WDR4 enhances CCNB1 translation by promoting the binding of EIF2A to CCNB1 mRNA. Furthermore, CCNB1 was observed to promote PI3K and AKT phosphorylation in HCC and reduce P53 protein expression by promoting P53 ubiquitination. In summary, we elucidated the MYC/WDR4/CCNB1 signalling pathway and its impact on PI3K/AKT and P53. Furthermore, the result showed that the m7G methyltransferase WDR4 is a tumour promoter in the development and progression of HCC and may act as a candidate therapeutic target in HCC treatment.

Download Full-text