The short and the long: non-coding RNAs and growth factors in cancer progression

2017 ◽  
Vol 45 (1) ◽  
pp. 51-64 ◽  
Author(s):  
Aldema Sas-Chen ◽  
Swati Srivastava ◽  
Yosef Yarden
Keyword(s):  
Growth Factors ◽  
Cancer Progression ◽  
Tumour Progression ◽  
Therapeutic Strategies ◽  
Signalling Pathways ◽  
Circulation System ◽  
Multistep Process ◽  
New Locations ◽  
Non Coding Rnas ◽  
Lines Of Evidence

A relatively well-understood multistep process enables mutation-bearing cells to form primary tumours, which later use the circulation system to colonize new locations and form metastases. However, in which way the emerging abundance of different non-coding RNAs supports tumour progression is poorly understood. Here, we review new lines of evidence linking long and short types of non-coding RNAs to signalling pathways activated in the course of cancer progression by growth factors and by the tumour micro-environment. Resolving the new dimension of non-coding RNAs in oncogenesis will probably translate to earlier detection of cancer and improved therapeutic strategies.

DLX6-AS1: a putative lncRNA candidate in multiple human cancers

2021 ◽  
Vol 23 ◽  
Author(s):  
Mohsen Sheykhhasan ◽  
Yaghoub Ahmadyousefi ◽  
Reihaneh Seyedebrahimi ◽  
Hamid Tanzadehpanah ◽  
Hamed Manoochehri ◽  
...  
Keyword(s):  
Cancer Progression ◽  
Critical Analysis ◽  
Molecular Mechanisms ◽  
Signalling Pathways ◽  
Biological Functions ◽  
Initial Development ◽  
Human Cancers ◽  
Expression Of Genes ◽  
Non Coding Rnas ◽  
Research Studies

Abstract Long non-coding RNAs (lncRNAs) have important roles in regulating the expression of genes and act as biomarkers in the initial development of different cancers. Increasing research studies have verified that dysregulation of lncRNAs occurs in various pathological processes including tumorigenesis and cancer progression. Among the different lncRNAs, DLX6-AS1 has been reported to act as an oncogene in the development and prognoses of different cancers, by affecting many different signalling pathways. This review summarises and analyses the recent research studies describing the biological functions of DLX6-AS1, its overall effect on signalling pathways and the molecular mechanisms underlying its action on the expression of genes in multiple human cancers. Our critical analysis suggests that different signalling pathways associated to this lncRNA may be used as a biomarker for diagnosis, or targets of treatment in cancers.

scholarly journals The Role of SATB1 in Tumour Progression and Metastasis

2019 ◽  
Vol 20 (17) ◽  
pp. 4156 ◽  
Author(s):  
Glatzel-Plucińska ◽  
Piotrowska ◽  
Dzięgiel ◽  
Podhorska-Okołów
Keyword(s):  
Cancer Progression ◽  
Poor Prognosis ◽  
Tumour Progression ◽  
Prognostic Significance ◽  
Distant Metastases ◽  
Mesenchymal Transition ◽  
Epithelial Cancers ◽  
Multistep Process ◽  
Satb1 Expression

Carcinogenesis is a long-drawn, multistep process, in which metastatic spread is an unequivocal hallmark of a poor prognosis. The progression and dissemination of epithelial cancers is commonly thought to rely on the epidermal-mesenchymal transition (EMT) process. During EMT, epithelial cells lose their junctions and apical-basal polarity, and they acquire a mesenchymal phenotype with its migratory and invasive capabilities. One of the proteins involved in cancer progression and EMT may be SATB1 (Special AT-Rich Binding Protein 1)—a chromatin organiser and a global transcriptional regulator. SATB1 organizes chromatin into spatial loops, providing a “docking site” necessary for the binding of further transcription factors and chromatin modifying enzymes. SATB1 has the ability to regulate whole sets of genes, even those located on distant chromosomes. SATB1 was found to be overexpressed in numerous malignancies, including lymphomas, breast, colorectal, prostate, liver, bladder and ovarian cancers. In the solid tumours, an elevated SATB1 level was observed to be associated with an aggressive phenotype, presence of lymph node, distant metastases, and a poor prognosis. In this review, we briefly describe the prognostic significance of SATB1 expression in most common human cancers, and analyse its impact on EMT and metastasis.

scholarly journals Non-Coding RNA m6A Modification in Cancer: Mechanisms and Therapeutic Targets

2021 ◽  
Vol 9 ◽  
Author(s):  
Da-Hong Chen ◽  
Ji-Gang Zhang ◽  
Chuan-Xing Wu ◽  
Qin Li
Keyword(s):  
Cancer Progression ◽  
Tumour Progression ◽  
Rna Modification ◽  
Circular Rnas ◽  
Considerable Research ◽  
Non Coding Rna ◽  
Non Coding Rnas ◽  
Higher Eukaryotes ◽  
Tumour Characteristics ◽  
The Relationship

Recently, N6-methyl-adenosine (m6A) ribonucleic acid (RNA) modification, a critical and common internal RNA modification in higher eukaryotes, has generated considerable research interests. Extensive studies have revealed that non-coding RNA m6A modifications (e.g. microRNAs, long non-coding RNAs, and circular RNAs) are associated with tumorigenesis, metastasis, and other tumour characteristics; in addition, they are crucial molecular regulators of cancer progression. In this review, we discuss the relationship between non-coding RNA m6A modification and cancer progression from the perspective of various cancers. In particular, we focus on important mechanisms in tumour progression such as proliferation, apoptosis, invasion and metastasis, tumour angiogenesis. In addition, we introduce clinical applications to illustrate more vividly that non-coding RNA m6A modification has broad research prospects. With this review, we aim to summarize the latest insights and ideas into non-coding RNA m6A modification in cancer progression and targeted therapy, facilitating further research.

scholarly journals The Use of Zebrafish Xenotransplant Assays to Analyze the Role of lncRNAs in Breast Cancer

2021 ◽  
Vol 11 ◽  
Author(s):  
Cecilia Zampedri ◽  
Williams Arony Martínez-Flores ◽  
Jorge Melendez-Zajgla
Keyword(s):  
Breast Cancer ◽  
Cancer Progression ◽  
High Throughput ◽  
Therapeutic Strategies ◽  
Cancer Markers ◽  
Non Coding Rnas ◽  
The Cost ◽  
Novel Model

Breast cancer represents a great challenge since it is the first cause of death by cancer in women worldwide. LncRNAs are a newly described class of non-coding RNAs that participate in cancer progression. Their use as cancer markers and possible therapeutic targets has recently gained strength. Animal xenotransplants allows for in vivo monitoring of disease development, molecular elucidation of pathogenesis and the design of new therapeutic strategies. Nevertheless, the cost and complexities of mice husbandry makes medium to high throughput assays difficult. Zebrafishes (Danio rerio) represent a novel model for these assays, given the ease with which xenotransplantation trials can be performed and the economic and experimental advantages it offers. In this review we propose the use of xenotransplants in zebrafish to study the role of breast cancer lncRNAs using low to medium high throughput assays.

scholarly journals Small intestinal neuroendocrine tumours and fibrosis: an entangled conundrum

2018 ◽  
Vol 25 (3) ◽  
pp. R115-R130 ◽  
Author(s):  
Anela Blažević ◽  
Johannes Hofland ◽  
Leo J Hofland ◽  
Richard A Feelders ◽  
Wouter W de Herder
Keyword(s):  
Growth Factors ◽  
Carcinoid Syndrome ◽  
Neuroendocrine Tumours ◽  
Tumour Progression ◽  
Clinical Pathology ◽  
Tumour Microenvironment ◽  
Signalling Pathways ◽  
Significant Morbidity ◽  
Complex Process ◽  
Small Intestinal

Small intestinal neuroendocrine tumours (SI-NETs) are neoplasms characterized by their ability to secrete biogenic amines and peptides. These cause distinct clinical pathology including carcinoid syndrome, marked by diarrhoea and flushing, as well as fibrosis, notably mesenteric fibrosis. Mesenteric fibrosis often results in significant morbidity by causing intestinal obstruction, oedema and ischaemia. Although advancements have been made to alleviate symptoms of carcinoid syndrome and prolong the survival of patients with SI-NETs, therapeutic options for patients with mesenteric fibrosis are still limited. As improved insight in the complex pathogenesis of mesenteric fibrosis is key to the development of new therapies, we evaluated the literature for known and putative mediators of fibrosis in SI-NETs. In this review, we discuss the tumour microenvironment, growth factors and signalling pathways involved in the complex process of fibrosis development and tumour progression in SI-NETs, in order to elucidate potential new avenues for scientific research and therapies to improve the management of patients suffering from the complications of mesenteric fibrosis.

A Review on AEG-1 oncogene regulating MicroRNA expression in Colon Cancer progression.

2020 ◽  
Vol 20 ◽  
Author(s):  
Sarubala Malayaperumal ◽  
Sushmitha Sriramulu ◽  
Ganesan Jothimani ◽  
Antara Banerjee ◽  
Surajit Pathak
Keyword(s):  
Cancer Progression ◽  
Therapeutic Strategies ◽  
Microrna Expression ◽  
Tumour Suppressor ◽  
Biological Functions ◽  
Posttranscriptional Gene Regulation ◽  
Proliferation And Apoptosis ◽  
Colon Cancer Progression ◽  
Non Coding Rnas ◽  
Very High

: MicroRNAs (miRS) are a class of small non-coding RNAs which perform a crucial function in posttranscriptional gene regulation. Dysregulation of this microRNAs are associated with many types of cancer progression. In tumorigenesis, downregulated microRNAs might function as tumour suppressor by repressing onco- genes, whereas overexpressed miRs might function as oncogenes by suppressing tumour suppressor. Similarly, Metadherin (also known AEG-1/ LYRIC), is an oncogene, whose levels are found to be very high in various cancers and plays a crucial role in proliferation of cells and invasion. Our review focuses on the study which shows alteration of microRNA expression profile and suppression of carcinogenesis when MTDH/AEG-1 is targeted. It summarises about the studies where downregulation and upregulation AEG-1 and microRNAs respectively, alter the biological functions of the cell, such as proliferation and apoptosis. Studies have reported that AEG-1 can be direct or indirect target of microRNA which could provide a new-insight to know the underlying molecular mechanism and might contribute to the progress of new therapeutic strategies for the disease.

scholarly journals METTL3 Depletion Contributes to HR+/HER2- Breast Cancer Progression and Drug Resistance via m6A Modification of Constituents of the CDKN1A/EMT and BAX/caspase-9/-3/-8 Signalling Pathways

2021 ◽  
Author(s):  
Dengjie Ouyang ◽  
Tao Hong ◽  
Mengdie Fu ◽  
Yitong Li ◽  
Liyun Zeng ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cancer Progression ◽  
Drug Sensitivity ◽  
Tumour Progression ◽  
Signalling Pathways ◽  
Caspase 9 ◽  
Her2 Breast Cancer ◽  
Potential Biomarker ◽  
Response To Chemotherapy ◽  
Mesenchymal Transformation

Abstract Background Chemotherapy is an important strategy for the treatment of hormone receptor positive / human epidermal growth factor receptor 2 negative (HR+/HER2-) breast cancer (BC), but this subtype has a low response to chemotherapy. Growing evidence indicates that N6-methyladenosine (m6A) is the most common RNA modification in eukaryotic cells and that methyltransferase-like 3 (METTL3) participates in tumour progression in several cancer types. Therefore, exploring the function of METTL3 in HR+HER2- BC initiation and development is still significant. Methods mRNA and protein expression levels were analysed by quantitative real-time polymerase chain reaction (qRT-PCR) and western blotting, respectively. Cell proliferation was detected by CCK-8 assays, cell migration was analysed by wound healing assays, and apoptosis was analysed by TUNEL assays. Finally, m6A modification was analysed by methylated RNA immunoprecipitation (MeRIP). Results Chemotherapy-induced downregulation of the m6A modification is regulated by METTL3 in HR+/HER2- BC. METTL3 knockdown in MCF-7/T47D cells weakened the drug sensitivity of HR+/HER2- BC cells by promoting tumour proliferation and metastasis and inhibiting apoptosis. Mechanistically, CDKN1A was subsequently recognized as a downstream target of METTL3 that activates the AKT pathway and promotes epithelial-mesenchymal transformation (EMT). Moreover, the RNA level of BAX was decreased due to a lower level of m6A modification mediated by METTL3, and apoptosis was inhibited by inactivation of caspase 3/9/8. Conclusion METTL3 regulates the proliferation, migration, and drug sensitivity of HR+/HER2- BC via activation of the CDKN1A/EMT and m6A-BAX/caspase 9/3/8 signalling pathways, which suggests its role as a potential biomarker for predicting the prognosis of patients with HR+/HER2- BC.

scholarly journals Intricate crosstalk between MYB and noncoding RNAs in cancer

2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Dingyu Hu ◽  
Wenjun Shao ◽  
Li Liu ◽  
Yanyan Wang ◽  
Shunling Yuan ◽  
...  
Keyword(s):  
Cancer Progression ◽  
Rna Processing ◽  
Malignant Tumors ◽  
Noncoding Rnas ◽  
Therapeutic Strategies ◽  
Circular Rnas ◽  
Biological Functions ◽  
Protein Coding ◽  
Non Coding Rnas ◽  
Myb Proteins

AbstractMYB is often overexpressed in malignant tumors and plays a carcinogenic role in the initiation and development of cancer. Deletion of the MYB regulatory C-terminal domain may be a driving mutation leading to tumorigenesis, therefore, different tumor mechanisms produce similar MYB proteins. As MYB is a transcription factor, priority has been given to identifying the genes that it regulates. All previous attention has been focused on protein-coding genes. However, an increasing number of studies have suggested that MYB can affect the complexity of cancer progression by regulating tumor-associated noncoding RNAs (ncRNAs), such as microRNAs, long-non-coding RNAs and circular RNAs. ncRNAs can regulate the expression of numerous downstream genes at the transcription, RNA processing and translation levels, thereby having various biological functions. Additionally, ncRNAs play important roles in regulating MYB expression. This review focuses on the intricate crosstalk between oncogenic MYB and ncRNAs, which play a pivotal role in tumorigenesis, including proliferation, apoptosis, angiogenesis, metastasis, senescence and drug resistance. In addition, we discuss therapeutic strategies for crosstalk between MYB and ncRNAs to prevent the occurrence and development of cancer.

Growth factors and associated signalling pathways in tumour progression and in cancer treatment

2019 ◽  
pp. 105-122
Author(s):  
Nadège Gaborit ◽  
Yosef Yarden
Keyword(s):  
Growth Factors ◽  
Tyrosine Kinases ◽  
Normal Tissue ◽  
Receptor Tyrosine Kinases ◽  
Tumour Progression ◽  
Signalling Pathways ◽  
Polypeptide Growth Factors ◽  
Growth Factor Signalling ◽  
Approved Drugs ◽  
Nuclear Alterations

To gain increased proliferation, blood supply, invasiveness, and resistance to cytotoxic treatments, cancer cells continuously secrete polypeptide growth factors, or they utilize factors produced by the associated normal tissue and the immunological microenvironment. The growth factors relay biochemical messages by binding with receptor tyrosine kinases (RTKs) located at the cell surface. In response to activation and receptor auto-phosphorylation, RTKs mobilize diverse signalling pathways, which culminate in cytoplasmic and nuclear alterations, including activation of gene expression programmes. This chapter describes several well-characterized growth factors, highlights the cognate receptors and downstream signalling pathways, and exemplifies involvement of specific growth factors in maintenance of the hallmarks of cancer. An account of clinically approved drugs able to intercept growth factor signalling closes this chapter.

Growth factors and associated signalling pathways in tumour progression and in cancer treatment

2019 ◽  
pp. 105-122
Author(s):  
Nadège Gaborit ◽  
Yosef Yarden
Keyword(s):  
Growth Factors ◽  
Tyrosine Kinases ◽  
Normal Tissue ◽  
Receptor Tyrosine Kinases ◽  
Tumour Progression ◽  
Signalling Pathways ◽  
Polypeptide Growth Factors ◽  
Growth Factor Signalling ◽  
Approved Drugs ◽  
Nuclear Alterations

To gain increased proliferation, blood supply, invasiveness, and resistance to cytotoxic treatments, cancer cells continuously secrete polypeptide growth factors, or they utilize factors produced by the associated normal tissue and the immunological microenvironment. The growth factors relay biochemical messages by binding with receptor tyrosine kinases (RTKs) located at the cell surface. In response to activation and receptor auto-phosphorylation, RTKs mobilize diverse signalling pathways, which culminate in cytoplasmic and nuclear alterations, including activation of gene expression programmes. This chapter describes several well-characterized growth factors, highlights the cognate receptors and downstream signalling pathways, and exemplifies involvement of specific growth factors in maintenance of the hallmarks of cancer. An account of clinically approved drugs able to intercept growth factor signalling closes this chapter.

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