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Obesity has for decades been recognised as one of the major health concerns. Recently accumulated evidence has established that obesity or being overweight is strongly linked to an increased risk of cancer. However, it is still not completely clear how adipose tissue (fat), along with other stromal connective tissues and cells, contribute to tumour initiation and progression. In the tumour microenvironment, the adipose tissue cells, in particular the adipocytes, secrete a number of adipokines, including growth factors, hormones, collagens, fatty acids, and other metabolites as well as extracellular vesicles to shape and condition the tumour and its microenvironment. In fact, the adipocytes, through releasing these factors and materials, can directly and indirectly facilitate cancer cell proliferation, apoptosis, metabolism, angiogenesis, metastasis and even chemotherapy resistance. In this chapter, the multidimensional role played by adipocytes, a major and functional component of the adipose tissue, in promoting cancer development and progression within the tumour microenvironment will be discussed.Dysregulated metabolism is a key hallmark of cancer cells and an enticing target for cancer treatment. Since the last 10 years, research on cancer metabolism has moved from pathway attention to network consideration. This metabolic complexity continuously adapt to new constraints in the tumor microenvironment. In this review, we will highlight striking changes in cancer cell metabolism compared to normal cells. Understanding this tumor metabolic plasticity suggests potential new targets and innovative combinatorial treatments for fighting cancer.Cancer develops in multicellular organisms from cells that ignore the rules of cooperation and escape the mechanisms of anti-cancer surveillance. Tumorigenesis is jointly encountered by the host and microbiota, a vast collection of microorganisms that live on the external and internal epithelial surfaces of the body. AEVI-006 The largest community of human microbiota resides in the gastrointestinal tract where commensal, symbiotic and pathogenic microorganisms interact with the intestinal barrier and gut mucosal lymphoid tissue, creating a tumor microenvironment in which cancer cells thrive or perish. Aberrant composition and function of the gut microbiota (dysbiosis) has been associated with tumorigenesis by inducing inflammation, promoting cell growth and proliferation, weakening immunosurveillance, and altering food and drug metabolism or other biochemical functions of the host. However, recent research has also identified several mechanisms through which gut microbiota support the host in the fight against cancer. These mechanisms include the use of antigenic mimicry, biotransformation of chemotherapeutic agents, and other mechanisms to boost anti-cancer immune responses and improve the efficacy of cancer immunotherapy. Further research in this rapidly advancing field is expected to identify additional microbial metabolites with tumor suppressing properties, map the complex interactions of host-microbe ‘transkingdom network’ with cancer cells, and elucidate cellular and molecular pathways underlying the impact of specific intestinal microbial configurations on immune checkpoint inhibitor therapy.Several aspects of the human physiology are controlled by the microbiota that plays a key role in health and disease. In fact, microbial dysbiosis is associated with numerous diseases, including several types of cancer such as colon, gastric, esophageal, pancreatic, laryngeal, breast and gallbladder carcinomas.Metabolic symbiosis between non-malignant cells and the resident microbita is crucial for the host homeostasis. However, cancer cells are able to repurpose the pre-existing metabolic symbiosis, being able to recycle those relations and also create novel metabolic symbiosis, leading to profound alterations on the local microenvironment.In here we will explore some of these symbiotic metabolic interactions between bacteria and non-malignant cells in two different contexts colon and uterine cervix. The way malignant cells are able to recycle these normal interactions and also create novel types of symbiotic metabolic relations will also be discussed.The knowledge of these complex interactions and recycling mechanisms is of extreme importance for cancer treatment, as new therapeutic targets could be developed.Reprogramming of energy metabolism is a key hallmark of cancer. Most cancer cells display a glycolytic phenotype, with increased glucose consumption and glycolysis rates, and production of lactate as the end product, independently of oxygen concentrations. This phenomenon, known as “Warburg Effect”, provides several survival advantages to cancer cells and modulates the metabolism and function of neighbour cells in the tumour microenvironment. However, due to the presence of metabolic heterogeneity within a tumour, cancer cells can also display an oxidative phenotype, and corruptible cells from the microenvironment become glycolytic, cooperating with oxidative cancer cells to boost tumour growth. This phenomenon is known as “Reverse Warburg Effect”. In either way, lactate is a key mediator in the metabolic crosstalk between cancer cells and the microenvironment, and lactate transporters are expressed differentially by existing cell populations, to support this crosstalk.In this review, we will focus on lactate and on lactate transporters in distinct cells of the tumour microenvironment, aiming at a better understanding of their role in the acquisition and maintenance of the direct/reverse “Warburg effect” phenotype, which modulate cancer progression.In 2018, 9.6 million deaths from cancer were estimated, being this disease the second leading cause of death worldwide. Notwithstanding all the efforts developed in prevention, diagnosis and new treatment approaches, chemoresistance seems to be inevitable, leading to cancer progression, recurrence and affecting the outcome of the disease. As more and more evidence support that cancer is an evolutionary and ecological process, this concept is rarely applied in the clinical context. In fact, cancer cells emerge and progress within an ecological niche – the tumor microenvironment – that is shared with several other cell types and that is continuously changing. Therefore, the tumor microenvironment imposes several selective pressures on cancer cells such as acidosis, hypoxia, competition for space and resources, immune predation and anti-cancer therapies, that cancer cells must be able to adapt to or will face extinction.In here, the role of the tumor microenvironment selective pressures on cancer progression will be discussed, as well as the targeting of its features/components as strategies to fight cancer.