scholarly journals Corrigendum to “The Dual Role of TGFβ in Human Cancer: From Tumor Suppression to Cancer Metastasis”

2018 ◽  
Vol 2018 ◽  
pp. 1-1
Author(s):  
Jean-Charles Neel ◽  
Laure Humbert ◽  
Jean-Jacques Lebrun
Keyword(s):  
Tumor Suppression ◽  
Cancer Metastasis ◽  
Human Cancer ◽  
Dual Role

scholarly journals The Dual Role of TGFβ in Human Cancer: From Tumor Suppression to Cancer Metastasis

2012 ◽  
Vol 2012 ◽  
pp. 1-28 ◽  
Author(s):  
Jean-Charles Neel ◽  
Laure Humbert ◽  
Jean-Jacques Lebrun
Keyword(s):  
Cell Growth ◽  
Cancer Progression ◽  
Transforming Growth Factor Beta ◽  
Molecular Mechanisms ◽  
Cancer Metastasis ◽  
Transforming Growth Factor ◽  
Human Cancer ◽  
Adult Life ◽  
Dual Role

The transforming growth factor-beta (TGFβ) superfamily encompasses widespread and evolutionarily conserved polypeptide growth factors that regulate and orchestrate growth and differentiation in all cell types and tissues. While they regulate asymmetric cell division and cell fate determination during early development and embryogenesis, TGFβ family members play a major regulatory role in hormonal and immune responses, cell growth, cell death and cell immortalization, bone formation, tissue remodeling and repair, and erythropoiesis throughout adult life. The biological and physiological functions of TGFβ, the founding member of this family, and its receptors are of central importance to human diseases, particularly cancer. By regulating cell growth, death, and immortalization, TGFβ signaling pathways exert tumor suppressor effects in normal cells and early carcinomas. Thus, it is not surprising that a high number of human tumors arise due to mutations or deletions in the genes coding for the various TGFβ signaling components. As tumors develop and progress, these protective and cytostatic effects of TGFβ are often lost. TGFβ signaling then switches to promote cancer progression, invasion, and tumor metastasis. The molecular mechanisms underlying this dual role of TGFβ in human cancer will be discussed in depth in this paper, and it will highlight the challenge and importance of developing novel therapeutic strategies specifically aimed at blocking the prometastatic arm of the TGFβ signaling pathway without affecting its tumor suppressive effects.

scholarly journals Role of splice variants in the metastatic progression of prostate cancer

2012 ◽  
Vol 40 (4) ◽  
pp. 870-874 ◽  
Author(s):  
Rachel M. Hagen ◽  
Michael R. Ladomery
Keyword(s):  
Prostate Cancer ◽  
Cancer Metastasis ◽  
Splice Variants ◽  
Human Cancer ◽  
Metastatic Potential ◽  
Metastatic Progression ◽  
Cellular Phenotype ◽  
Prostate Cancer Metastasis ◽  
The Relationship

AS (alternative splicing) and its role in disease, especially cancer, has come to forefront in research over the last few years. Alterations in the ratio of splice variants have been widely observed in cancer. Splice variants of cancer-associated genes have functions that can alter cellular phenotype, ultimately altering metastatic potential. As metastases are the cause of approximately 90% of all human cancer deaths, it is crucial to understand how AS is dysregulated in metastatic disease. We highlight some recent studies into the relationship between altered AS of key genes and the initiation of prostate cancer metastasis.

Abstract P3-01-01: A dual role of natural killer cells in breast cancer metastasis

2020 ◽  
Author(s):  
Isaac S. Chan ◽  
Hildur Knútsdoóttir ◽  
Gayathri Ramakrishnan ◽  
Veena Padmanaban ◽  
Joel S. Bader ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Natural Killer Cells ◽  
Natural Killer ◽  
Cancer Metastasis ◽  
Breast Cancer Metastasis ◽  
Dual Role ◽  
Killer Cells

Role of miRNAs in human cancer metastasis: Implications for therapeutic intervention

2017 ◽  
Vol 44 ◽  
pp. 117-131 ◽  
Author(s):  
Mohammad Alam Jafri ◽  
Mohammed Hussein Al-Qahtani ◽  
Jerry William Shay
Keyword(s):  
Therapeutic Intervention ◽  
Cancer Metastasis ◽  
Human Cancer

scholarly journals Protrudin in protrudinG invadopodia: Membrane contact sites and cell invasion

2020 ◽  
Vol 219 (8) ◽  
Author(s):  
Amita Arora ◽  
Vesa M. Olkkonen
Keyword(s):  
Matrix Metalloproteinases ◽  
Cell Invasion ◽  
Cancer Metastasis ◽  
Dual Role ◽  
Pericellular Matrix ◽  
Matrix Degradation ◽  
Membrane Contact Sites ◽  
Contact Sites ◽  
Membrane Contact

Invadopodia are dynamic protrusions that harbor matrix metalloproteinases for pericellular matrix degradation. However, the mechanisms underlying their maturation are poorly understood. Pedersen et al. (2020. J. Cell Biol.https://doi.org/10.1083/jcb.202003063) demonstrate a dual role of Protrudin in invadopodia elongation and matrix degradation, central to cell invasion and cancer metastasis.

scholarly journals Identification of a Novel Metastasis-Related miRNAs-Based Signature for Predicting the Prognosis of Hepatocellular Carcinoma

2021 ◽  
Vol 2021 ◽  
pp. 1-14
Author(s):  
Yuan Chen ◽  
Guifu Wang ◽  
Hao Xu ◽  
Hao Wang ◽  
Dousheng Bai
Keyword(s):  
Hepatocellular Carcinoma ◽  
High Risk ◽  
Cancer Metastasis ◽  
Cox Regression ◽  
Human Cancer ◽  
Risk Groups ◽  
High Risk Group ◽  
Low Risk ◽  
Prognostic Signature

Hepatocellular carcinoma (HCC) is one of the most common internal malignancies worldwide and is associated with a poor prognosis. Abnormal expression of miRNAs is believed to play a role in the recurrent metastasis of HCC. However, limited studies on the role of miRNAs in HCC metastasis have been carried out. Therefore, this study is aimed at exploring the potential value of metastasis-related miRNAs (MRMs) in HCC. We retrieved MRMs were from the Human Cancer Metastasis Database. Differential miRNAs were identified for tumor samples of HCC patients and normal samples based on the TCGA database. Further, univariate and multivariate Cox regression analyses were used to screen MRMs known to be independent prognostic factors in HCC. These MRMs were then used to build a prognostic signature. All patients were classified into high-risk and low-risk groups based on the median of the signature scores. Moreover, GO and KEGG pathway enrichment analyses were performed to predict the function of these MRMs. Finally, a nomogram was constructed to predict the OS of patients at 1, 2, and 3 years. In our study, a total of seven prognostic MRMs (miR-140-3p, miR-9-5p, miR-942-5p, miR-324-3p, miR-29c-5p, miR-551a, and miR-149-5p) were identified and used for constructing the prognostic signature based on the training cohort. Patients in the low-risk HCC group showed better overall survival (OS) than those in the high-risk group. The results were validated using the validation cohort. In summary, the findings of this study provide evidence that MRMs-based prognostic signature is an independent biomarker in the prognosis of HCC patients.

Dual Role of microRNAs in Autophagy of Colorectal Cancer

2020 ◽  
Vol 20 ◽  
Author(s):  
Tanu Sharma ◽  
James A. Radosevich ◽  
Chandi C. Mandal
Keyword(s):  
Colorectal Cancer ◽  
Cancer Progression ◽  
Cancer Metastasis ◽  
Dual Role ◽  
Rna Molecules ◽  
Non Coding Rna ◽  
Evolutionarily Conserved ◽  
Attractive Therapeutic Target ◽  
Mirnas Expression

: Autophagy is an evolutionarily conserved pathway that eliminates unwanted proteins out of the cell and increases cell survival. But dysfunctional autophagy is associated with cancer progression, cellular adaptation, cancer metastasis and makes it an attractive therapeutic target. MicroRNAs (miRNAs) are small single-stranded non-coding RNA molecules that usually bind to 3’UTR of mRNAs. This interaction eventually inhibits protein synthesis by repressing translation and/or by degrading mRNAs. miRNAs play a crucial role in the regulation of autophagy and also behave as both tumor suppressors and promoters in colorectal cancer. This paper defines an overall molecular view of how miRNAs regulate the dual role of autophagy in colorectal cancer. It also highlights how long non-coding RNAs modulate miRNAs expression to regulate autophagy in colorectal cancer. Thus, targeting autophagy by miRNAs seems to be a potential therapeutic strategy for colorectal cancer.

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