Biochimica et biophysica acta. Reviews on cancer最新文献

Colorectal cancer (CRC) ranks among the leading cancers in terms of incidence and mortality in the Western world. Currently, there are no sufficient diagnostic markers that would enable an early diagnosis and efficient therapy. Unfortunately, a significant number of new CRC cases is detected in late stages, with distant metastases, therefore, new therapeutic approaches, which would alleviate the prognosis for advanced stages of CRC, are highly in demand.

SNHG6 belongs to the group of long non-coding RNAs, which are a larger entity of RNAs consisting of >200 nucleotides. SNHG6 is expressed mainly in the cell cytoplasm, where it acts as a regulator of numerous processes: modulation of crucial protein hubs; sponging miRNAs and upregulating the expression of their target mRNAs; and interacting with various cellular pathways including TGF-β/Smad and Wnt/β-catenin. SNHG6 is an oncogene, substantially overexpressed in CRC tissues and cancerous cell lines as compared to healthy samples. Its overexpression is associated with higher grade, lymphovascular invasion and tumor size.

Taking into consideration the role of SNHG6 in the colorectal tumorigenesis, invasion and metastasis, we summarized its role in CRC and conclude that it could serve as a potential biomarker in CRC diagnosis and prognosis assessment.

The composition and pattern of dietary intake have emerged as key factors influencing aging, regeneration, and consequently, healthspan and lifespan. Cancer is one of the major diseases more tightly linked with aging, and age-related mortality. Although the role of nutrition in cancer incidence is generally well established, we are far from a consensus on how diet influences tumour development in different tissues. In this review, we will discuss how diet and dietary restrictions affect cancer risk and the molecular mechanisms potentially responsible for their effects. We will cover calorie restriction, intermittent fasting, prolonged fasting, fasting-mimicking diet, time-restricted eating, ketogenic diet, high protein diet, Mediterranean diet, and the vegan and vegetarian diets.

Cancer vaccines, designed to activate the body's own immune system to fight against tumors, are a current trend in cancer treatment and receiving increasing attention. Cancer vaccines mainly include oncolytic virus vaccine, cell vaccine, peptide vaccine and nucleic acid vaccine. Over the course of decades of research, oncolytic virus vaccine T-VEC, cellular vaccine sipuleucel-T, various peptide vaccines, and DNA vaccine against HPV positive cervical cancer have brought encouraging results for cancer therapy, but are losing momentum in development due to their respective shortcomings. In contrast, the advantages of mRNA vaccines such as high safety, ease of production, and unmatched efficacy are on full display. In addition, advances in technology such as pseudouridine modification have cracked down the bottleneck for developing mRNA vaccines including instability, innate immunogenicity, and low efficiency of in vivo delivery. Several cancer mRNA vaccines have achieved promising results in clinical trials, and their usage in conjunction with other immune checkpoint inhibitors (ICIs) has further boosted the efficiency of anti-tumor immune response. We expect a rapid development of mRNA vaccines for cancer immunotherapy in the near future. This review provides a brief overview of the current status of mRNA vaccines, highlights the action mechanism of cancer mRNA vaccines, their recent advances in clinical trials, and prospects for their clinical applications.

Pancreatic cancer (PC) remains a leading cause of mortality worldwide due to the absence of early detection methods and the low success rates of traditional therapeutic strategies. Drug resistance in PC is driven by its desmoplastic stroma, which creates a barrier that shields cancer niches and prevents the penetration of drugs. The PC stroma comprises heterogeneous cellular populations and non-cellular components involved in aberrant ECM deposition, immunosuppression, and drug resistance. These components can influence PC development through intricate and complex crosstalk with the PC cells. Understanding how stromal components and cells interact with and influence the invasiveness and refractoriness of PC cells is thus a prerequisite for developing successful stroma-modulating strategies capable of remodeling the PC stroma to alleviate drug resistance and enhance therapeutic outcomes. In this review, we explore how non-cellular and cellular stromal components, including cancer-associated fibroblasts and tumor-associated macrophages, contribute to the immunosuppressive and tumor-promoting effects of the stroma. We also examine the signaling pathways underlying their activation, tumorigenic effects, and interactions with PC cells. Finally, we discuss recent pre-clinical and clinical work aimed at developing and testing novel stroma-modulating agents to alleviate drug resistance and improve therapeutic outcomes in PC.

The tumour microenvironment (TME) is usually defined as a cell environment associated with tumours or cancerous stem cells where conditions are established affecting tumour development and progression through malignant cell interaction with non-malignant cells. The TME is made up of endothelial, immune and non-immune cells, extracellular matrix (ECM) components and signalling molecules acting specifically on tumour and non-tumour cells. Breast cancer (BC) is the commonest malignant neoplasm worldwide and the main cause of mortality in women globally; advances regarding BC study and understanding it are relevant for acquiring novel, personalised therapeutic tools. Studying canine mammary gland tumours (CMGT) is one of the most relevant options for understanding BC using animal models as they share common epidemiological, clinical, pathological, biological, environmental, genetic and molecular characteristics with human BC. In-depth, detailed investigation regarding knowledge of human BC-related TME and in its canine model is considered extremely relevant for understanding changes in TME composition during tumour development. This review addresses important aspects concerned with different methods used for studying BC- and CMGT-related TME that are important for developing new and more effective therapeutic strategies for attacking a tumour during specific evolutionary stages.

Prostate cancer (PC) is the second most frequently diagnosed cancer and the fifth leading cause of cancer-related deaths in male population worldwide. Since the growth and progression of PC highly depend on the androgen pathway, androgen deprivation therapy (ADT) is the mainstay of systemic treatment. Enzalutamide is a second-generation antiandrogen, which is widely used for the treatment of advanced and metastatic PC. However, treatment failure and disease progression, caused by the emergence of enzalutamide resistant phenotypes, remains an important clinical challenge. MicroRNAs (miRNAs) are key regulators of gene expression and have recently emerged as potential biomarkers for being stable and easily analysed in several biological fluids. Several miRNAs that exhibit dysregulated expression patterns in enzalutamide-resistant PC have recently been identified, including miRNAs that modulate critical signalling pathways and genes involved in PC growth, survival and in the acquisition of enzalutamide phenotype. The understanding of molecular mechanisms by which miRNAs promote the development of enzalutamide resistance can provide valuable insights into the complex interplay between miRNAs, gene regulation, and treatment response in PC. Moreover, these miRNAs could serve as valuable tools for monitoring treatment response and disease progression during enzalutamide administration. This review summarises the miRNAs associated with enzalutamide resistance in PC already described in the literature, focusing on their biological roles and on their potential as biomarkers.

Decitabine's early successful therapeutic outcomes in hematologic malignancies have led to regulatory approvals from the Food and Drug Administration (FDA) and the European Medicines Agency (EMA) for addressing myelodysplastic syndromes (MDS) and acute myeloid leukemia (AML). These approvals have sparked keen interest in exploring the potential of decitabine for treating solid tumors. Continuous preclinical and clinical trials have proved that low doses of decitabine also bring benefits in treating solid tumors, and various proposed mechanisms attempt to explain the potential efficacy. It is important to note that the application of decitabine in solid tumors is still considered investigational. This article reviews the application mechanism and current status of decitabine in the treatment of solid tumors.

Several clinical trials and experimental studies have recently shown that vitamin K (VK) supplementation benefits the human body. Specifically, VK participates in coagulation and is associated with cellular senescence and cancer. VK has a potential anticancer effect in various cancers, such as pancreatic and prostate cancers. Through anti-inflammatory and antioxidant effects, VK can prevent senescence and inhibit cancer metastasis. Therefore, cancer prognosis can be improved by preventing cellular senescence. In addition, VK can inhibit the proliferation, growth, and differentiation of cancer cells through various mechanisms, including induction of c-myc and c-fos genes, regulation of B-cell lymphoma-2 (Bcl-2) and p21 genes, and angiogenesis inhibition. This review aims to discuss the relationship among VK, cellular senescence, and cancer metastasis and thus may improve comprehension of the specific functions of VK in human health. The potential application of VK as an adjuvant therapy for cancer (or in combination with traditional chemotherapy drugs or other vitamins) has also been highlighted.

Renewed interest in tumor metabolism sparked an enthusiasm for dietary interventions to prevent and treat cancer. Changes in diet impact circulating nutrient levels in the plasma and the tumor microenvironment, and preclinical studies suggest that dietary approaches, including caloric and nutrient restrictions, can modulate tumor initiation, progression, and metastasis. Cancers are heterogeneous in their metabolic dependencies and preferred energy sources and can be addicted to glucose, fructose, amino acids, or lipids for survival and growth. This dependence is influenced by tumor type, anatomical location, tissue of origin, aberrant signaling, and the microenvironment.

This review summarizes nutrient dependencies and the related signaling pathway activations that provide targets for nutritional interventions. We examine popular dietary approaches used as adjuvants to anticancer therapies, encompassing caloric restrictions, including time-restricted feeding, intermittent fasting, fasting-mimicking diets (FMDs), and nutrient restrictions, notably the ketogenic diet. Despite promising results, much of the knowledge on dietary restrictions comes from in vitro and animal studies, which may not accurately reflect real-life situations. Further research is needed to determine the optimal duration, timing, safety, and efficacy of dietary restrictions for different cancers and treatments. In addition, well-designed human trials are necessary to establish the link between specific metabolic vulnerabilities and targeted dietary interventions. However, low patient compliance in clinical trials remains a significant challenge.

Cancer and its metastases arise from mutations of genes, drivers that promote a tumor's growth. Analyses of driver events provide insights into cancer cell history and may lead to a better understanding of oncogenesis. We reviewed 27 metastatic research studies, including pan-cancer studies, individual cancer studies, and phylogenetic analyses, and summarized our current knowledge of metastatic drivers. All of the analyzed studies had a high level of consistency of driver mutations between primary tumors and metastasis, indicating that most drivers appear early in cancer progression and are maintained in metastatic cells. Additionally, we reviewed data from around 50,000 metastatic cancer patients and compiled a list of genes altered in metastatic lesions. We performed Gene Ontology analysis and confirmed that the most significantly enriched processes in metastatic lesions were the epigenetic regulation of gene expression, signal transduction, cell cycle, programmed cell death, DNA damage, hypoxia and EMT. In this review, we explore the most recent discoveries regarding genetic factors in the advancement of cancer, specifically those that drive metastasis.