scholarly journals miRNAs Involved in Esophageal Carcinogenesis and miRNA-Related Therapeutic Perspectives in Esophageal Carcinoma

2021 ◽  
Vol 22 (7) ◽  
pp. 3640
Author(s):  
Giovanni Zarrilli ◽  
Francesca Galuppini ◽  
Valentina Angerilli ◽  
Giada Munari ◽  
Marianna Sabbadin ◽  
...  
Keyword(s):  
Cell Biology ◽  
Predictive Biomarker ◽  
Premalignant Lesions ◽  
Cancer Development ◽  
Cancer Therapies ◽  
Regulatory Pathways ◽  
Therapeutic Implications ◽  
Anti Cancer ◽  
Non Coding Rnas ◽  
Esophageal Carcinogenesis

MicroRNAs (miRNAs) are small non-coding RNAs that play a pivotal role in many aspects of cell biology, including cancer development. Within esophageal cancer, miRNAs have been proved to be involved in all phases of carcinogenesis, from initiation to metastatic spread. Several miRNAs have been found to be dysregulated in esophageal premalignant lesions, namely Barrett’s esophagus, Barrett’s dysplasia, and squamous dysplasia. Furthermore, numerous studies have investigated the alteration in the expression levels of many oncomiRNAs and tumor suppressor miRNAs in esophageal squamous cell carcinoma and esophageal adenocarcinoma, thus proving how miRNAs are able modulate crucial regulatory pathways of cancer development. Considering these findings, miRNAs may have a role not only as a diagnostic and prognostic tool, but also as predictive biomarker of response to anti-cancer therapies and as potential therapeutic targets. This review aims to summarize several studies on the matter, focusing on the possible diagnostic–therapeutic implications.

scholarly journals The Challenging Riddle about the Janus-Type Role of Hsp60 and Related Extracellular Vesicles and miRNAs in Carcinogenesis and the Promises of Its Solution

2021 ◽  
Vol 11 (3) ◽  
pp. 1175
Author(s):  
Sabrina David ◽  
Alessandra Maria Vitale ◽  
Alberto Fucarino ◽  
Federica Scalia ◽  
Giuseppe Vergilio ◽  
...  
Keyword(s):  
Cell Membrane ◽  
Extracellular Vesicles ◽  
Cancer Development ◽  
Cancer Therapies ◽  
Ongoing Research ◽  
Pathological Conditions ◽  
Anti Cancer ◽  
Evolutionarily Conserved ◽  
The Impact

Hsp60 is one of the most ancient and evolutionarily conserved members of the chaperoning system. It typically resides within mitochondria, in which it contributes to maintaining the organelle’s proteome integrity and homeostasis. In the last few years, it has been shown that Hsp60 also occurs in other locations, intracellularly and extracellularly, including cytosol, plasma-cell membrane, and extracellular vesicles (EVs). Consequently, non-canonical functions and interacting partners of Hsp60 have been identified and it has been realized that it is a hub molecule in diverse networks and pathways and that it is implicated, directly or indirectly, in the development of various pathological conditions, the Hsp60 chaperonopathies. In this review, we will focus on the multi-faceted role of this chaperonin in human cancers, showing the contribution of intra- and extracellular Hsp60 in cancer development and progression, as well as the impact of miRNA-mediated regulation of Hsp60 in carcinogenesis. There are still various aspects of this intricate biological scenario that are poorly understood but ongoing research is steadily providing new insights and we will direct attention to them. For instance, we will highlight the possible applications of the Hsp60 involvement in carcinogenesis not only in diagnosis, but also in the development of specific anti-cancer therapies centered on the use of the chaperonin as therapeutic target or agent and depending on its role, pro- or anti-tumor.

scholarly journals Targeting HIF-1α Function in Cancer through the Chaperone Action of NQO1

2020 ◽  
Author(s):  
Eduardo Salido ◽  
David J. Timson ◽  
Isabel Betancor-Fernández ◽  
Rogelio Palomino-Morales ◽  
Angel L. Pey
Keyword(s):  
Associated Factors ◽  
Current Knowledge ◽  
Cancer Development ◽  
Cancer Therapies ◽  
Pharmacological Modulation ◽  
Oxygen Homeostasis ◽  
Anti Cancer ◽  
Molecular Determinants ◽  
The Stability ◽  
Alpha Function

HIF-1α is a master regulator of oxygen homeostasis involved in different stages of cancer development. Thus, HIF-1α inhibition represents an interesting target for anti-cancer therapy. It was recently shown that HIF-1α interaction with NQO1 inhibits its proteasomal degradation, thus suggesting that targeting the stability of NQO1 could led to destabilization of HIF-1α as a therapeutic approach. Since the molecular interactions of NQO1 with HIF-1α are beginning to be unraveled, we review here our current knowledge on the intracellular functions and stability of NQO1, its pharmacological modulation by small ligands, and the molecular determinants of its roles as a chaperone of many different proteins including cancer-associated factors such as p53 and p73α. This knowledge is then discussed in the context of potentially targeting the intracellular stability of HIF-1α by acting on its chaperone, NQO1. This could result in novel anti-cancer therapies.

scholarly journals Correlation of MET and PD-L1 expression in malignant melanoma

2020 ◽  
Author(s):  
Kyu Young Song ◽  
Sabina Desar ◽  
Thomas Pengo ◽  
Ryan Shanley ◽  
Alessio Giubellino
Keyword(s):  
Predictive Biomarker ◽  
Human Melanoma ◽  
Cancer Therapies ◽  
Metastatic Lesions ◽  
Melanocytic Lesions ◽  
Color Deconvolution ◽  
Anti Cancer ◽  
Hepatocyte Growth ◽  
Melanoma Tissue ◽  
Benign Melanocytic Nevi

Abstract Background: The proto-oncogene MET, the hepatocyte growth factor (HGF) receptor, is a transmembrane receptor tyrosine kinase (RTK) with a prominent role in tumor metastasis and resistance to anti-cancer therapies. Melanoma demonstrates relatively frequent MET aberrations, including MET gene amplification. Concurrently, PD-L1, with its ability to evade anti-tumor immune responses, has emerged as a prominent therapeutic target in melanoma and other malignancies and its expression is used as a predictive biomarker of response to immunotherapy. Methods: We performed immunohistochemistry analysis of MET and PD-L1 in 18 human melanoma cell lines derived from both primary and metastatic lesions; we then performed the same analysis in a human melanoma tissue microarray (TMA) containing 100 melanocytic lesions, including 42 cutaneous malignant melanomas, 20 mucosal melanoma, 21 metastatic melanomas and 17 benign melanocytic nevi as controls. After color deconvolution, TMA cores were identified and segmented to isolate staining and calculate the percentage of positive cells in each core. Results: Overall, MET expression was higher in metastatic lesions and it was higher in tumors with increased PD-L1 expression. Moreover, a positive correlation between MET and PD-L1 expression was found in metastatic melanoma. Conclusions: These data suggest that testing for expression of these markers should be conducted in patients with melanoma with metastatic disease and selective therapies targeting these proteins should be considered for advanced disease.

Long Non-Coding RNAs in Melanoma Development and Biology

2020 ◽  
Vol 14 (02) ◽  
pp. 145-166
Author(s):  
Olga Vera ◽  
Neel Jasani ◽  
Florian A. Karreth
Keyword(s):  
Cancer Therapies ◽  
Cellular Processes ◽  
Melanoma Diagnosis ◽  
Cell Metastasis ◽  
Regulation Of Metabolism ◽  
Wide Range ◽  
Anti Cancer ◽  
Non Coding Rnas ◽  
Identification And Characterization

Melanoma is the most aggressive and deadly type of skin cancer and presents a major clinical challenge due to its ability to rapidly metastasize and become resistant to immune and targeted therapies. The identification and characterization of new molecular targets and pathways involved in the initiation, progression, and maintenance of melanoma will be critical for the development of superior treatments. Long non-coding RNAs (lncRNAs), a class of non-coding RNAs involved in regulating numerous cellular processes including tumor progression, cancer cell metastasis, and resistance to anti-cancer therapies, may be viable therapeutic targets in melanoma. In this review, we describe lncRNAs that contribute to melanoma development through microRNA (miRNA) sponging, regulation of metabolism, modification of the epigenome, or modulation of pro-tumorigenic signaling pathways. While more work remains to be done to characterize lncRNAs in melanoma, gaining a better understanding of their functions promises to yield a wide range of possibilities to improve melanoma diagnosis, prognosis, and treatment.

scholarly journals Adaptation and learning of molecular networks as a description of cancer development at the systems-level: Potential use in anti-cancer therapies

2013 ◽  
Vol 23 (4) ◽  
pp. 262-269 ◽  
Author(s):  
Dávid M. Gyurkó ◽  
Dániel V. Veres ◽  
Dezső Módos ◽  
Katalin Lenti ◽  
Tamás Korcsmáros ◽  
...  
Keyword(s):  
Molecular Networks ◽  
Cancer Development ◽  
Cancer Therapies ◽  
Anti Cancer ◽  
Adaptation And Learning ◽  
Potential Use

scholarly journals Correlation of MET and PD-L1 Expression in Malignant Melanoma

Cancers ◽  
2020 ◽  
Vol 12 (7) ◽  
pp. 1847
Author(s):  
Kyu Young Song ◽  
Sabina Desar ◽  
Thomas Pengo ◽  
Ryan Shanley ◽  
Alessio Giubellino
Keyword(s):  
Predictive Biomarker ◽  
Human Melanoma ◽  
Cancer Therapies ◽  
Metastatic Lesions ◽  
Melanocytic Lesions ◽  
Programmed Death ◽  
Color Deconvolution ◽  
Anti Cancer ◽  
Hepatocyte Growth ◽  
Benign Melanocytic Nevi

The proto-oncogene MET, the hepatocyte growth factor (HGF) receptor, is a transmembrane receptor tyrosine kinase (RTK) with a prominent role in tumor metastasis and resistance to anti-cancer therapies. Melanoma demonstrates relatively frequent MET aberrations, including MET gene amplification. Concurrently, programmed death-ligand 1 (PD-L1), with its ability to evade anti-tumor immune responses, has emerged as a prominent therapeutic target in melanoma and other malignancies and its expression is used as a predictive biomarker of response to immunotherapy. We performed immunohistochemistry analysis of MET and PD-L1 in 18 human melanoma cell lines derived from both primary and metastatic lesions, and in a human melanoma tissue microarray containing one hundreds melanocytic lesions, including primary cutaneous melanomas, primary mucosal melanomas, metastatic melanomas and benign melanocytic nevi as controls. After color deconvolution, each core was segmented to isolate staining and calculate the percentage of positive cells. Overall, MET expression was higher in tumors with increased PD-L1 expression. Moreover, a robust correlation between MET and PD-L1 expression was found in samples from metastatic melanoma and not in primary cutaneous or mucosal melanoma. These data suggest that relative expression levels of these proteins in combination is a marker of advanced disease and testing for expression of these markers should be considered in patients with melanoma.

Tumour–host interactions: implications for developing anti-cancer therapies

2006 ◽  
Vol 8 (30) ◽  
pp. 1-32 ◽  
Author(s):  
Bedrick B. Gadea ◽  
Johanna A. Joyce
Keyword(s):  
Cancer Progression ◽  
Molecular Mechanisms ◽  
Model Systems ◽  
Cancer Development ◽  
Tumour Suppressor Genes ◽  
Cancer Therapies ◽  
Host Interactions ◽  
Normal Functions ◽  
Anti Cancer ◽  
Local Host

Cancers are a complex set of proliferative diseases that arise in most cases through multi-step pathways involving an accumulation of genetic and epigenetic changes. These steps include inactivation of tumour suppressor genes and activation of oncogenes. However, in addition to genetic mutations in the tumour cells themselves, the local host environment can act as a critical modulator of cancer progression, having either tumour-suppressive or tumour-promoting effects depending on the stage and site of cancer development. Because stromal cells can have these opposing functions during cancer development and progression, a recurring theme throughout this review will be that of balance: maintaining the normal functions of these co-opted cells, yet selectively inhibiting their pro-tumourigenic functions. To achieve this equilibrium, we need to understand the molecular mechanisms by which normal cells become modified by cancer cells before we can hope to target these functions selectively. Here, we will discuss recent efforts to address these key challenges and offer perspectives on the translation of discoveries made in model systems to the clinic.

scholarly journals The Urokinase Receptor: A Multifunctional Receptor in Cancer Cell Biology. Therapeutic Implications

2021 ◽  
Vol 22 (8) ◽  
pp. 4111
Author(s):  
Anna Li Santi ◽  
Filomena Napolitano ◽  
Nunzia Montuori ◽  
Pia Ragno
Keyword(s):  
Proteolytic Activity ◽  
Cancer Cell ◽  
Cell Biology ◽  
Large Body ◽  
Supporting Cell ◽  
Therapeutic Implications ◽  
Cancer Hallmarks ◽  
Type Plasminogen Activator ◽  
Urokinase Type Plasminogen Activator ◽  
Anti Cancer

Proteolysis is a key event in several biological processes; proteolysis must be tightly controlled because its improper activation leads to dramatic consequences. Deregulation of proteolytic activity characterizes many pathological conditions, including cancer. The plasminogen activation (PA) system plays a key role in cancer; it includes the serine-protease urokinase-type plasminogen activator (uPA). uPA binds to a specific cellular receptor (uPAR), which concentrates proteolytic activity at the cell surface, thus supporting cell migration. However, a large body of evidence clearly showed uPAR involvement in the biology of cancer cell independently of the proteolytic activity of its ligand. In this review we will first describe this multifunctional molecule and then we will discuss how uPAR can sustain most of cancer hallmarks, which represent the biological capabilities acquired during the multistep cancer development. Finally, we will illustrate the main data available in the literature on uPAR as a cancer biomarker and a molecular target in anti-cancer therapy.

ANTICANCER EFFECT OF UVARIA GENUS

2014 ◽  
pp. 98-101
Author(s):  
Thi Bich Hien Le ◽  
Viet Duc Ho ◽  
Thi Hoai Nguyen
Keyword(s):  
Biological Activities ◽  
Current Trend ◽  
Healthcare Systems ◽  
Chemical Compositions ◽  
Cancer Therapies ◽  
Pharmacological Effects ◽  
Anticancer Effect ◽  
Anti Cancer ◽  
Tropical Areas ◽  
Cancer Activity

Nowadays, cancer treatment has been a big challenge to healthcare systems. Most of clinical anti-cancer therapies are toxic and cause adverse effects to human body. Therefore, current trend in science is seeking and screening of natural compounds which possess antineoplastic activities to utilize in treatment. Uvaria L. - Annonaceae includes approximately 175 species spreading over tropical areas of Asia, Australia, Africa and America. Studies on chemical compositions and pharmacological effects of Uvaria showed that several compound classes in this genus such as alkaloid, flavonoid, cyclohexen derivaties, acetogenin, steroid, terpenoid, etc. indicate considerable biological activities, for example anti-tumor, anti-cancer, antibacterial, antifungal, antioxidant, etc. Specifically, anti-cancer activity of fractions of extract and pure isolated compounds stands out for cytotoxicity against many cancer cell lines. This study provides an overview of anti-cancer activity of Uvaria and suggests a potential for further studies on seeking and developing novel anti-cancer compounds. Key words: Anti-cancer, Uvaria.

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