Converting "cold" to "hot": epigenetics strategies to improve immune therapy effect by regulating tumor-associated immune suppressive cells.

Significant developments in cancer treatment have been made since the advent of immune therapies. However, there are still some patients with malignant tumors who do not benefit from immunotherapy. Tumors without immunogenicity are called "cold" tumors which are unresponsive to immunotherapy, and the opposite are "hot" tumors. Immune suppressive cells (ISCs) refer to cells which can inhibit the immune response such as tumor-associated macrophages (TAMs), myeloid-derived suppressor cells (MDSCs), regulatory T (Treg) cells and so on. The more ISCs infiltrated, the weaker the immunogenicity of the tumor, showing the characteristics of "cold" tumor. The dysfunction of ISCs in the tumor microenvironment (TME) may play essential roles in insensitive therapeutic reaction. Previous studies have found that epigenetic mechanisms play an important role in the regulation of ISCs. Regulating ISCs may be a new approach to transforming "cold" tumors into "hot" tumors. Here, we focused on the function of ISCs in the TME and discussed how epigenetics is involved in regulating ISCs. In addition, we summarized the mechanisms by which the epigenetic drugs convert immunotherapy-insensitive tumors into immunotherapy-sensitive tumors which would be an innovative tendency for future immunotherapy in "cold" tumor.

Immune infiltration related CENPI associates with the malignant features and drug resistance of lung adenocarcinoma.

Centromere protein I (CENPI) is an important member of centromeric proteins family, which is crucial to chromosome alignment and segregation. Nevertheless, the interrelation between CENPI expression and tumor progression is in the shadows. In this reserch, we carried out a panoramic bioinformatic analysis about CENPI with TCGA, Timer 2.0, Oncomine, GEPIA, Cbioportal, LinkedOmics and CancerSEA databases. Besides, our bioinformatic results have been further confirmed through in vitro experiments, including Real-Time quantitative PCR (RT-qPCR), immunofluorescence (IF), immunohistochemistry (IHC), western blotting (WB), cell proliferation assays, EdU, cell cycle and apoptosis test. Our results suggested that CENPI was increased in most of the cancers, and may serve as a potential biomarker. What's more, the knock down of CENPI inhibited the expression of CDK2 in lung adenocarcinoma (LUAD), and resulted in the arrest of G0/G1 phase and apoptosis. Besides, CENPI was related to immune cells infiltration and drug sensitivity in pan-cancer, and can act as a potential treatment target to cure cancer patients.

Corrigendum: Role and mechanism of DNA methylation and its inhibitors in hepatic fibrosis.

[This corrects the article DOI: 10.3389/fgene.2023.1124330.].

Role and mechanism of DNA methylation and its inhibitors in hepatic fibrosis.

Liver fibrosis is a repair response to injury caused by various chronic stimuli that continually act on the liver. Among them, the activation of hepatic stellate cells (HSCs) and their transformation into a myofibroblast phenotype is a key event leading to liver fibrosis, however the mechanism has not yet been elucidated. The molecular basis of HSC activation involves changes in the regulation of gene expression without changes in the genome sequence, namely, via epigenetic regulation. DNA methylation is a key focus of epigenetic research, as it affects the expression of fibrosis-related, metabolism-related, and tumor suppressor genes. Increasing studies have shown that DNA methylation is closely related to several physiological and pathological processes including HSC activation and liver fibrosis. This review aimed to discuss the mechanism of DNA methylation in the pathogenesis of liver fibrosis, explore DNA methylation inhibitors as potential therapies for liver fibrosis, and provide new insights on the prevention and clinical treatment of liver fibrosis.