Understanding Molecular Pathways and Targets of Brachyury in Epithelial-mesenchymal Transition (EMT) in Human Cancers

2016 ◽  
Vol 16 (7) ◽  
pp. 586-593 ◽  
Author(s):  
Wenzhe Song ◽  
Glenda C. Gobe
Keyword(s):  
Epithelial Mesenchymal Transition ◽  
Molecular Pathways ◽  
Mesenchymal Transition ◽  
Human Cancers

scholarly journals FOXQ1 Regulates Epithelial-Mesenchymal Transition in Human Cancers

2011 ◽  
Vol 71 (8) ◽  
pp. 3076-3086 ◽  
Author(s):  
Yuanyuan Qiao ◽  
Xia Jiang ◽  
Shuet Theng Lee ◽  
R.K. Murthy Karuturi ◽  
Shing Chuan Hooi ◽  
...  
Keyword(s):  
Epithelial Mesenchymal Transition ◽  
Mesenchymal Transition ◽  
Human Cancers

scholarly journals Circular RNA circ0005276 promotes the proliferation and migration of prostate cancer cells by interacting with FUS to transcriptionally activate XIAP

2019 ◽  
Vol 10 (11) ◽  
Author(s):  
Yang Feng ◽  
Yuxuan Yang ◽  
Xiaodan Zhao ◽  
Yameng Fan ◽  
Long Zhou ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Epithelial Mesenchymal Transition ◽  
Circular Rna ◽  
Host Gene ◽  
Circular Rnas ◽  
Mesenchymal Transition ◽  
Human Cancers ◽  
Apoptosis Protein ◽  
And Migration ◽  
And Function

Abstract Prostate cancer (PCa) is one of the major men’s malignancies with high mortality worldwide. Circular RNAs (circRNAs) have been shown to serve as essential regulators in human cancers. CircRNA can exert their functions by cooperating with their host genes. In the present study, microarray analysis revealed an upregulated mRNA in PCa samples. X-linked inhibitor of apoptosis protein (XIAP), a key regulator in the progression of human cancers. Through bioinformatics analysis, we determined that XIAP is a host gene for circRNA0005276. Therefore, this study focused on the interaction between circ0005276 and XIAP as well as their functions in PCa progression. The upregulation of XIAP and circ0005276 was determined in PCa tissues and cell lines. Moreover, we confirmed the positive regulation of circ0005276 on XIAP expression. Functionally, we validated that circ0005276 and XIAP promoted cell proliferation, migration and epithelial–mesenchymal transition. Mechanistically, we verified that circ0005276 interacted with FUS binding protein (FUS) so as to activate the transcription of XIAP. Rescue assays were conducted to determine the crucial role of XIAP in circ0005276 and FUS-mediated PCa cellular processes. Collectively, our study revealed the mechanism and function of circ0005276 and its host gene XIAP in PCa progression.

scholarly journals Overview of Evidence-Based Chemotherapy for Oral Cancer: Focus on Drug Resistance Related to the Epithelial-Mesenchymal Transition

Biomolecules ◽  
2021 ◽  
Vol 11 (6) ◽  
pp. 893
Author(s):  
Jingjing Sha ◽  
Yunpeng Bai ◽  
Huy Xuan Ngo ◽  
Tatsuo Okui ◽  
Takahiro Kanno
Keyword(s):  
Drug Resistance ◽  
Transcription Factors ◽  
Oral Cancer ◽  
High Throughput Screening ◽  
Epithelial Mesenchymal Transition ◽  
Chemotherapeutic Agents ◽  
Signal Pathways ◽  
Evidence Based ◽  
Molecular Pathways ◽  
Mesenchymal Transition

The increasing incidence of resistance to chemotherapeutic agents has become a major issue in the treatment of oral cancer (OC). Epithelial-mesenchymal transition (EMT) has attracted a great deal of attention in recent years with regard to its relation to the mechanism of chemotherapy drug resistance. EMT-activating transcription factors (EMT-ATFs), such as Snail, TWIST, and ZEB, can activate several different molecular pathways, e.g., PI3K/AKT, NF-κB, and TGF-β. In contrast, the activated oncological signal pathways provide reciprocal feedback that affects the expression of EMT-ATFs, resulting in a peritumoral extracellular environment conducive to cancer cell survival and evasion of the immune system, leading to resistance to multiple chemotherapeutic agents. We present an overview of evidence-based chemotherapy for OC treatment based on the National Comprehensive Cancer Network (NCCN) Chemotherapy Order Templates. We focus on the molecular pathways involved in drug resistance related to the EMT and highlight the signal pathways and transcription factors that may be important for EMT-regulated drug resistance. Rapid progress in antitumor regimens, together with the application of powerful techniques such as high-throughput screening and microRNA technology, will facilitate the development of therapeutic strategies to augment chemotherapy.

scholarly journals Association of the Epithelial–Mesenchymal Transition (EMT) with Cisplatin Resistance

2020 ◽  
Vol 21 (11) ◽  
pp. 4002 ◽  
Author(s):  
Milad Ashrafizadeh ◽  
Ali Zarrabi ◽  
Kiavash Hushmandi ◽  
Mahshad Kalantari ◽  
Reza Mohammadinejad ◽  
...  
Keyword(s):  
Drug Resistance ◽  
Cancer Cells ◽  
Tumor Cells ◽  
Epithelial Mesenchymal Transition ◽  
Therapy Resistance ◽  
Nuclear Factor Κb ◽  
Molecular Pathways ◽  
Cancer Resistance ◽  
Mesenchymal Transition ◽  
The Impact

Therapy resistance is a characteristic of cancer cells that significantly reduces the effectiveness of drugs. Despite the popularity of cisplatin (CP) as a chemotherapeutic agent, which is widely used in the treatment of various types of cancer, resistance of cancer cells to CP chemotherapy has been extensively observed. Among various reported mechanism(s), the epithelial–mesenchymal transition (EMT) process can significantly contribute to chemoresistance by converting the motionless epithelial cells into mobile mesenchymal cells and altering cell–cell adhesion as well as the cellular extracellular matrix, leading to invasion of tumor cells. By analyzing the impact of the different molecular pathways such as microRNAs, long non-coding RNAs, nuclear factor-κB (NF-ĸB), phosphoinositide 3-kinase-related protein kinase (PI3K)/Akt, mammalian target rapamycin (mTOR), and Wnt, which play an important role in resistance exhibited to CP therapy, we first give an introduction about the EMT mechanism and its role in drug resistance. We then focus specifically on the molecular pathways involved in drug resistance and the pharmacological strategies that can be used to mitigate this resistance. Overall, we highlight the various targeted signaling pathways that could be considered in future studies to pave the way for the inhibition of EMT-mediated resistance displayed by tumor cells in response to CP exposure.

scholarly journals RASSF10 Is a TGFβ-Target That Regulates ASPP2 and E-Cadherin Expression and Acts as Tumor Suppressor That Is Epigenetically Downregulated in Advanced Cancer

Cancers ◽  
2019 ◽  
Vol 11 (12) ◽  
pp. 1976 ◽  
Author(s):  
Antje M. Richter ◽  
Miriam M. Küster ◽  
Michelle L. Woods ◽  
Sara K. Walesch ◽  
Mira Y. Gökyildirim ◽  
...  
Keyword(s):  
Tumor Suppressor ◽  
Transforming Growth Factor Beta ◽  
Cell Cycle Progression ◽  
Transforming Growth Factor ◽  
Epithelial Mesenchymal Transition ◽  
Mesenchymal Transition ◽  
Protein Levels ◽  
Human Cancers ◽  
Tumor Suppressive Function ◽  
E Cadherin

The Ras Association Domain Family (RASSF) encodes members of tumor suppressor genes which are frequently inactivated in human cancers. Here, the function and the regulation of RASSF10, that contains a RA (Ras-association) and two coiled domains, was investigated. We utilized mass spectrometry and immuno-precipitation to identify interaction partners of RASSF10. Additionally, we analyzed the up- and downstream pathways of RASSF10 that are involved in its tumor suppressive function. We report that RASSF10 binds ASPP1 (Apoptosis-stimulating protein of p53) and ASPP2 through its coiled-coils. Induction of RASSF10 leads to increased protein levels of ASPP2 and acts negatively on cell cycle progression. Interestingly, we found that RASSF10 is a target of the EMT (epithelial mesenchymal transition) driver TGFβ (Transforming growth factor beta) and that negatively associated genes of RASSF10 are significantly over-represented in an EMT gene set collection. We observed a positive correlation of RASSF10 expression and E-cadherin that prevents EMT. Depletion of RASSF10 by CRISPR/Cas9 technology induces the ability of lung cancer cells to proliferate and to invade an extracellular matrix after TGFβ treatment. Additionally, knockdown of RASSF10 or ASPP2 induced constitutive phosphorylation of SMAD2 (Smad family member 2). Moreover, we found that epigenetic reduction of RASSF10 levels correlates with tumor progression and poor survival in human cancers. Our study indicates that RASSF10 acts a TGFβ target gene and negatively regulates cell growth and invasion through ASPP2. This data suggests that epigenetic loss of RASSF10 contributes to tumorigenesis by promoting EMT induced by TGFβ.

Sign in / Sign up

Export Citation Format

Share Document