Ferroptosis suppressor protein 1 (FSP1) is one of the main regulatory molecules of ferroptosis. FSP1 functions through the FSP1-coenzyme Q10 (CoQ10)-NAD(P)H axis and the vitamin K redox cycle. FSP1 is regulated by upstream factors, including transcription factors and noncoding RNA (ncRNA), and is subject to epigenetic modifications, which affect the progress of FSP1-related diseases. FSP1 is closely associated with the poor prognosis of malignant tumors and plays an important role in disease treatment. This review aims to provide a comprehensive understanding of the role of FSP1 in ferroptosis regulation by summarizing regulatory pathways, possible mechanisms involving FSP1, and the relationship between FSP1 and disease prognosis and treatment.

CD8⁺ T cells are an important component of the body’s adaptive immune response. During viral or intracellular bacterial infections, CD8⁺ T cells are rapidly activated and differentiated to exert their immune function by producing cytokines. Alterations in the glycolysis of CD8⁺ T cells have an important effect on their activation and function, while glycolysis is important for CD8⁺ T cell functional failure and recovery. This paper summarizes the importance of CD8⁺ T cell glycolysis in the immune system. We discuss the link between glycolysis and CD8⁺ T cell activation, differentiation, and proliferation, and the effect of altered glycolysis on CD8⁺ T cell function. In addition, potential molecular targets to enhance and restore the immune function of CD8⁺ T cells by affecting glycolysis and the link between glycolysis and CD8⁺ T cell senescence are summarized. This review provides new insights into the relationship between glycolysis and CD8⁺ T cell function, and proposes novel strategies for immunotherapy by targeting glycolysis.

Pericytes are a type of mural cell located between the endothelial cells of capillaries and the basement membrane, which function to regulate the capillary vasomotor and maintain normal microcirculation of local tissues and organs and have been identified as a significant component in the tumor microenvironment (TME). Pericytes have various interactions with different components of the TME, such as constituting the pre-metastatic niche, promoting the growth of cancer cells and drug resistance through paracrine activity, and inducing M2 macrophage polarization. While changes in the TME can affect the number, phenotype, and molecular markers of pericytes. For example, pericyte detachment from endothelial cells in the TME facilitates tumor cells in situ to invade the circulating blood and is beneficial to local capillary basement membrane enzymatic hydrolysis and endothelial cell proliferation and budding, which contribute to tumor angiogenesis and metastasis. In this review, we discuss the emerging role of pericytes in the TME, and tumor treatment related to pericytes. This review aimed to provide a more comprehensive understanding of the function of pericytes and the relationship between pericytes and tumors and to provide ideas for the treatment and prevention of malignant tumors.

Interest in cancer metabolism has increased in recent years. The pentose phosphate pathway (PPP) is a major glucose catabolism pathway that directs glucose flux to its oxidative branch and leads to the production of a reduced form of nicotinamide adenine dinucleotide phosphate and nucleic acid. The PPP serves a vital role in regulating cancer cell growth and involves many enzymes. The aim of the present review was to describe the recent discoveries associated with the deregulatory mechanisms of the PPP and glycolysis in malignant tumors, particularly in hepatocellular carcinoma, breast and lung cancer.

Metabolic reprogramming is one of the main characteristics of malignant tumors. The metabolic reprogramming of tumors is not only related to the characteristics of cancer cells, but also closely related to the tumor microenvironment (TME). ‘Aerobic glycolysis’ is considered to be the classic metabolic mode of tumor cells. However, recent experiments have shown that the TME plays a key role in carcinogenesis and epithelial‑mesenchymal transition. Cancer‑associated fibroblasts (CAFs) dominate in the microenvironment and affect the homeostasis of the TME. The interaction between cancer cells and the surrounding CAFs markedly affects the growth, metabolism, metastasis, and progression of cancer. Based on this, a ‘dual‑chamber’ model, also known as the ‘Reverse Warburg effect’, is proposed. Specifically, cancer cells secrete hydrogen peroxide into the TME to induce oxidative stress in neighboring stromal cells. CAFs undergo aerobic glycolysis and produce high levels of energy‑rich ‘fuels’ (such as pyruvate, ketone bodies, fatty acids, and lactic acid). In turn, these energy‑rich ‘fuels’ then ‘feed’ cancer cells. The mitochondrial oxidative phosphorylation system produces a large quantity of ATP, such that tumor cells have a higher proliferation ability. The proposed ‘Reverse Warburg effect’ redefines the tumor cell microenvironment and tumor metabolic reprogramming. Therefore, understanding the ‘Reverse Warburg effect’ of CAFs and its related mechanisms will help us to understand the association between the microenvironment, the matrix, and cancer cells, and may lead to new treatment strategies and targets.

Mitochondria are vital organelles in cells, regulating energy metabolism and apoptosis. Mitochondrial transcellular transfer plays a crucial role during physiological and pathological conditions, such as rescuing recipient cells from bioenergetic deficit and tumorigenesis. Studies have shown several structures that conduct transcellular transfer of mitochondria, including tunneling nanotubes (TNTs), extracellular vesicles (EVs), and Cx43 gap junctions (GJs). The intra- and intercellular transfer of mitochondria is driven by a transport complex. Mitochondrial Rho small GTPase (MIRO) may be the adaptor that connects the transport complex with mitochondria, and myosin XIX is the motor protein of the transport complex, which participates in the transcellular transport of mitochondria through TNTs. In this review, the roles of TNTs, EVs, GJs, and related transport complexes in mitochondrial transcellular transfer are discussed in detail, as well as the formation mechanisms of TNTs and EVs. This review provides the basis for the development of potential clinical therapies targeting the structures of mitochondrial transcellular transfer.