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.

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Junction plakoglobin (JUP) is a critical cell adhesion molecule implicated in mediating cell-cell adhesion. Cancer, characterized by the loss of normal cellular regulation, results in unchecked proliferation and the breakdown of cell-cell junctions, facilitating malignant cell invasion into surrounding tissues. Recent studies have highlighted the involvement of JUP in the transduction of various intercellular signaling pathways, underscoring its significant role in tumor initiation, progression, and prognosis. In contrast to its homolog β-catenin, the interplay between JUP and cancer remains underexplored. To clarify JUP’s role and underlying mechanisms in cancer progression, this review examines recent advancements, focusing on JUP’s regulation of key cancer-related signaling pathways, such as Wnt/β-catenin, p53, and cadherin-mediated pathways. The review also investigates JUP’s relevance across various cancer types, including those of the reproductive, digestive, and urinary systems. Mechanistically, JUP exhibits context-dependent actions in different cancers, demonstrating dual roles in tumorigenesis. Lastly, the potential of JUP as a target for early diagnosis, effective treatment, and prognostic prediction in cancer is evaluated. In conclusion, targeting JUP offers a promising avenue for cancer therapy, providing valuable insights for future research.