Post-translational modifications (PTMs) are chemical modifications that occur on specific amino acid residues after protein biosynthesis, which can affect protein function by altering protein structure, localization and activity, thus expanding protein diversity. Extensive research has demonstrated that PTMs can regulate various metabolic processes, such as glucose and lipid metabolism, as well as immune modulation in tumor cells, thereby promoting tumor initiation, progression, and metastasis. In this article, we systematically review a class of emerging PTMs whose roles in tumor metabolism and immune regulation have gradually been recognized in recent years, including six types: lactylation, palmitoylation, SUMOylation, succinylation, crotonylation, and myristoylation. First, we summarized the occurrence process and biological behavior of these six PTMs. Next, we elaborate the relationship between these PTMs and tumorigenesis and progression from the perspectives of metabolism and immune regulation of tumor cells. Finally, we summarize recent research progress in targeting these six types of PTMs for cancer therapy. This paper aims to provide directions for related researchers, and to provide a theoretical basis for targeting PTMs to treat tumors and make it possible.

Bone metastasis is the primary cause of death in patients with prostate cancer (PCa). In this study, we aimed to explore the mechanism by which MS4A8 mediates bone metastasis via exosomes. First, exosome proteome sequencing and detection of exosome MS4A8 expression revealed that MS4A8 was highly expressed in PCa exosomes and closely related to bone metastasis. Then, in vitro and in vivo experiments further showed that exosome MS4A8 could trigger osteolytic destruction in PCa bone metastases by enhancing the activity of osteoclasts. Furthermore, techniques such as ScRNA-seq, multicolour immunofluorescence, and co-immunoprecipitation (Co-IP) further revealed that exosome MS4A8 activates the nuclear factor kappa B (NF-κB) and phosphoinositide 3-kinase (PI3K)/protein kinase B (AKT) pathways in osteoclasts of PCa bone metastases through receptor activator of nuclear factor-κB ligand (RANKL) and promoted osteoclast differentiation, resulting in a vicious cycle. Our study could provide a theoretical basis for clarifying the underlying mechanism of the occurrence and development of PCa bone metastasis and for future development of therapeutic strategies.