JARID2 and EZH2, the eminent epigenetic drivers in human cancer.

Cancer has become a prominent cause of death, accounting for approximately 10 million deaths worldwide as per the World Health Organization report 2020. Epigenetics deal with the alterations of heritable phenotypes, except for DNA alterations. Currently, we are trying to comprehend the role of utmost significant epigenetic genes involved in the burgeoning of human cancer. A sundry of studies have reported the Enhancer of Zeste Homologue2 (EZH2) as a prime catalytic subunit of Polycomb Repressive Complex2, which is involved in several pivotal activities, including embryogenesis. In addition, EZH2 has detrimental effects leading to the onset and metastasis of several cancers. Jumonji AT Rich Interacting Domain2 (JARID2), an undebated crucial nuclear factor, has strong coordination with the PRC2 family. In this review, we discuss various epigenetic entities, primarily focusing on the possible role and mechanism of EZH2 and the significant contribution of JARID2 in human cancers.

Comprehending the crosstalk between Notch, Wnt and Hedgehog signaling pathways in oral squamous cell carcinoma - clinical implications.

BACKGROUND: Oral squamous cell carcinoma (OSCC) is a malignant oral cavity neoplasm that affects many people, especially in developing countries. Despite several advances that have been made in diagnosis and treatment, the morbidity and mortality rates due to OSCC remain high. Accumulating evidence indicates that aberrant activation of cellular signaling pathways, such as the Notch, Wnt and Hedgehog pathways, occurs during the development and metastasis of OSCC. In this review, we have articulated the roles of the Notch, Wnt and Hedgehog signaling pathways in OSCC and their crosstalk during tumor development and progression. We have also examined possible interactions and associations between these pathways and treatment regimens that could be employed to effectively tackle OSCC and/or prevent its recurrence. CONCLUSIONS: Activation of the Notch signaling pathway upregulates the expression of several genes, including c-Myc, ß-catenin, NF-κB and Shh. Associations between the Notch signaling pathway and other pathways have been shown to enhance OSCC tumor aggressiveness. Crosstalk between these pathways supports the maintenance of cancer stem cells (CSCs) and regulates OSCC cell motility. Thus, application of compounds that block these pathways may be a valid strategy to treat OSCC. Such compounds have already been employed in other types of cancer and could be repurposed for OSCC.