Epigenetic modification regulates tumor progression and metastasis through EMT (Review)

Tan, Tingshan; Shi, Pengfei; Abbas, Muhammad Nadeem; Wang, Yi; Xu, Jie; Chen, Yu; Cui, Hongjuan

doi:10.3892/ijo.2022.5360

Cited by 23 publications

(16 citation statements)

References 238 publications

(238 reference statements)

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“…Furthermore, this growing body of evidence has demonstrated that histone deacetylases (HDACs) are linked to the initiation and/or maintenance of repression for DNA hypermethylated genes, and studies have revealed that the simultaneous targeting of both DNA methylation and histone deacetylation leads to additive or synergistic effects to reactivate the aberrantly silenced genes ( Arrowsmith et al, 2012 ). Meanwhile, it has been observed that in the case of histone methylation, methylation of histones H3 and H4 is a very common feature of cancer cells ( Tan et al, 2022 ). Notably, it was reported that DNMT demethylating agents and histone deacetylase inhibitors could be combined to exert antitumor effects ( Zahnow et al, 2016 ; Myasoedova et al, 2019 ).…”

Section: Future Outlookmentioning

confidence: 99%

Emerging role of different DNA methyltransferases in the pathogenesis of cancer

et al. 2022

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DNA methylation is one of the most essential epigenetic mechanisms to regulate gene expression. DNA methyltransferases (DNMTs) play a vital role in DNA methylation in the genome. In mammals, DNMTs act with some elements to regulate the dynamic DNA methylation patterns of embryonic and adult cells. Conversely, the aberrant function of DNMTs is frequently the hallmark in judging cancer, including total hypomethylation and partial hypermethylation of tumor suppressor genes (TSGs), which improve the malignancy of tumors, aggravate the ailment for patients, and significantly exacerbate the difficulty of cancer therapy. Since DNA methylation is reversible, currently, DNMTs are viewed as an important epigenetic target for drug development. However, the impression of DNMTs on cancers is still controversial, and therapeutic methods targeting DNMTs remain under exploration. This review mainly summarizes the relationship between the main DNMTs and cancers as well as regulatory mechanisms and clinical applications of DNMTs in cancer and highlights several forthcoming strategies for targeting DNMTs.

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Section: Future Outlookmentioning

confidence: 99%

Emerging role of different DNA methyltransferases in the pathogenesis of cancer

et al. 2022

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“…DNA methylation, as one of the common epigenetic events, plays a key role in the diagnosis and treatment of tumors ( 40 ). In contrast to other CGRs, ATP7B, NLRP3, and ATP7A were distinctly hypomethylated in multiple cancers, such as BRCA, LUSC, and LUAD.…”

Section: Resultsmentioning

confidence: 99%

Regulation, genomics, and clinical characteristics of cuproptosis regulators in pan-cancer

Zhou

Zheng

et al. 2022

Front. Oncol.

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BackgroundCuproptosis, a copper-dependent controlled cell death, is a novel form of cell death that differs from known cell death mechanisms; however, its overall regulation in cancer remains elusive.MethodsMultiple open-source bioinformatic platforms were used to comprehensively elucidate the expression levels, prognostic efficiency, potential biological functions, genomic and epigenetic characteristics, immune microenvironment, and drug sensitivity of cuproptosis regulators (ATP7A, ATP7B, DLAT, DLD, FDX1, GLS, LIAS, LIPT1, MTF1, NLRP3, PDHA1, PDHB, and SLC31A1) in pan-cancer.ResultsCuproptosis-related genes (CRGs) were upregulated in most cancers tested. In KIRC, KIRP, LGG, MESO, and PCPG, most highly expressed CRGs predicted a better prognosis but poorer prognosis in patients with ACC, LIHC, and UCEC. Pathway analysis confirmed that cuproptosis regulators were associated with the metabolism-related pathways. The expression of MTF1, NLRP3, and SLC31A1 was positively related with ImmuneScore, StromalScore, and ESTIMATEScore in almost all types of tumor, whereas ATP7B, DLAT, DLD, LIAS, PDHA1, and PDHB were significantly negatively correlated with the scores. In addition, CRGs were significantly correlated with RNA stemness score, DNA stemness score, microsatellite instability, and tumor mutational burden. The expression of ATP7A, ATP7B, LIAS, and DLAT was significantly positively correlated with the drug sensitivity of Docetaxel. ATP7A, LIAS, and FDX1 were significantly negatively correlated with the drug sensitivity of UNC0638, XMD13−2, YM201636, and KIN001−260.ConclusionsThe altered genomic and clinical characteristics of cuproptosis regulators were comprehensively elucidated, providing a preliminary basis for understanding the functions of cuproptosis in pan-cancer.

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“…The overall prognosis for patients with OS is poor because of its high metastatic potential [ 28 ]. EMT is a key mechanism of tumor metastasis, inhibition of which may attenuate cancer metastasis [ 29 ]. In this study, we found that silencing ZCCHC12 slowed down migration of OS cells.…”

Section: Discussionmentioning

confidence: 99%

ZCCHC12 promotes the progression of osteosarcoma via PI3K/AKT pathway

Cui

Dong

2022

Aging

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Researchers have reported that zinc finger CCHC domain containing 12 gene (ZCCHC12) plays a role in the progression and tumorigenesis of papillary thyroid cancer. However, the biological role of ZCCHC12 in osteosarcoma (OS) remains unknown. ZCCHC12 was highly upregulated in OS cell lines according to our present study. Also, our subsequent assays demonstrated that ZCCHC12 enhanced the proliferation, tumor growth and migration of OS cells. Moreover, the epithelial-mesenchymal transition (EMT) of OS cells was also promoted by ZCCHC12. In addition, downregulation of ZCCHC12 induced apoptosis and S-phase arrest in OS cells. Then, our study indicated that ZCCHC12 exerts its oncogenic function in OS cells by activating the PI3K/AKT pathway. Inhibition of the PI3K/AKT pathway greatly limits the oncogenic function of ZCCHC12 in OS cells. Also, overexpression of ZCCHC12 promotes tumor growth in vivo. Altogether, our study suggests ZCCHC12 promotes OS cells progression by activating the PI3K/AKT pathway. The ZCCHC12 gene may be a novel diagnostic and therapeutic target for OS.

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Epigenetic modification regulates tumor progression and metastasis through EMT (Review)

Cited by 23 publications

References 238 publications

Emerging role of different DNA methyltransferases in the pathogenesis of cancer

Emerging role of different DNA methyltransferases in the pathogenesis of cancer

Regulation, genomics, and clinical characteristics of cuproptosis regulators in pan-cancer

ZCCHC12 promotes the progression of osteosarcoma via PI3K/AKT pathway

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