LncRNA CASC11 Promotes Hepatocellular Carcinoma Progression via Upregulation of UBE2T in a m6A-Dependent Manner

Chen, Fei; Li, Meijun; Wang, Liang

doi:10.3389/fonc.2021.772671

Cited by 21 publications

(19 citation statements)

References 44 publications

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“…The two mechanisms underlying this process of tumor development involve the ubiquitin-conjugating enzyme E2T (UBE2T) and an m6A reader protein YT521-B homology domain family 2 (YTHDF2), respectively. CASC11 lowers the m6A level of UBE2T and thus stabilizes it by recruiting an increased amount of human AlkB homolog H5 (Chen et al, 2021). The RNA METTL16, similar to METTL3, serves as a link between m6A modification and the development of HCC.…”

Section: Non-coding Rnas Suppress the Progression Of Hepatitis B Viru...mentioning

confidence: 99%

A double-edged sword: The HBV-induced non-coding RNAs alterations in hepatocellular carcinoma

LIU¹,

Diao²

2023

Biocell

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Non-coding RNAs are speculated to exert important regulatory functions at the level of gene expression, oncogenesis, and many other pathologies. Hepatitis B virus (HBV) infection is a leading cause of hepatocellular carcinoma (HCC), and some studies have shown that the expression of non-coding RNAs has an assignable effect on the development of HBV-induced HCC. In this context, the functions and molecular mechanisms of the HBVinduced non-coding RNA expression in the development of hepatoma have attracted increasing attention. This review covers the progress in the exploration of the relationship between HBV-induced hepatoma and non-coding RNA expression, cataloging the recent reports about the roles of non-coding RNAs in HBV-induced hepatoma into five classes, including (1) modulation of metabolism in hepatic cancer, (2) aggravation of inflammation and hepatic fibrosis, (3) alteration of the tumor immune microenvironment, (4) non-coding RNA N6-methyladenosine modification, and a seemingly opposite process, (5) the suppression of the progression of HBV-related HCC. All evidence supports non-coding RNAs as promising novel targets for the early diagnosis and treatments for HCC.

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Section: Non-coding Rnas Suppress the Progression Of Hepatitis B Viru...mentioning

confidence: 99%

A double-edged sword: The HBV-induced non-coding RNAs alterations in hepatocellular carcinoma

LIU¹,

Diao²

2023

Biocell

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“…In laryngeal squamous cell carcinoma (LSCC), increased expression of ALKBH5 can promote tumorigenesis in an m 6 A‐YTHDF2‐dependent manner by promoting the lncRNA KCNQ1OT1‐HOXA9 signaling axis [ 281 ]. In HCC, the lncRNA CASC11 is upregulated and associated with poor survival and metastasis [ 282 ]. CASC11 stabilizes UBE2T mRNA by recruiting ALKBH5 m 6 A activity and also by inhibiting UBE2T mRNA association with YTHDF2 [ 282 ].…”

Section: Molecular Alterations In Cancer Metastasismentioning

confidence: 99%

Cancer metastasis under the magnifying glass of epigenetics and epitranscriptomics

Janin

Dávalos

Esteller

2023

Cancer Metastasis Rev

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Most of the cancer-associated mortality and morbidity can be attributed to metastasis. The role of epigenetic and epitranscriptomic alterations in cancer origin and progression has been extensively demonstrated during the last years. Both regulations share similar mechanisms driven by DNA or RNA modifiers, namely writers, readers, and erasers; enzymes responsible of respectively introducing, recognizing, or removing the epigenetic or epitranscriptomic modifications. Epigenetic regulation is achieved by DNA methylation, histone modifications, non-coding RNAs, chromatin accessibility, and enhancer reprogramming. In parallel, regulation at RNA level, named epitranscriptomic, is driven by a wide diversity of chemical modifications in mostly all RNA molecules. These two-layer regulatory mechanisms are finely controlled in normal tissue, and dysregulations are associated with every hallmark of human cancer. In this review, we provide an overview of the current state of knowledge regarding epigenetic and epitranscriptomic alterations governing tumor metastasis, and compare pathways regulated at DNA or RNA levels to shed light on a possible epi-crosstalk in cancer metastasis. A deeper understanding on these mechanisms could have important clinical implications for the prevention of advanced malignancies and the management of the disseminated diseases. Additionally, as these epi-alterations can potentially be reversed by small molecules or inhibitors against epi-modifiers, novel therapeutic alternatives could be envisioned.

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“…Ubiquitin-conjugating enzyme E2 T (UBE2T, also known as E2 ubiquitin-conjugating enzyme T, FANCT, PIG50 and HSPC150) belongs to the UBE2 superfamily, which plays a fundamental role in the second step of ubiquitination. Following previous studies that reported that UBE2T was involved in the regulation of DNA repair in Fanconi anaemia (FA), it was recently molecularly identified as a risk factor closely associated with oncogenesis, metastasis, survival and prognosis in human patients or mammal animals with cancer (1)(2)(3)(4)(5)(6)(7)(8)(9)(10)(11).…”

Section: Introductionmentioning

confidence: 99%

Diverse roles of UBE2T in cancer (Review)

Yan

et al. 2023

Oncol Rep

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As a leading cause of mortalities worldwide, cancer results from accumulation of both genetic and epigenetic alterations. Disruption of epigenetic regulation in cancer, particularly aberrant ubiquitination, has drawn increasing interest in recent years. The present study aimed to review the roles of ubiquitin-conjugating enzyme E2 T (UBE2T) and its associated pathways in the pathogenesis of pan-cancer, and the development of small-molecule modulators to regulate ubiquitination for treatment strategies. The current study comprehensively investigated the expression landscape and functional significance of UBE2T, as well as its correlation with cancer cell sensitivity to chemotherapy/radiotherapy. Multiple levels of evidence suggested that aberrant UBE2T played important roles in pan-cancer. Information was collected from 16 clinical trials on ubiquitin enzymes, and it was found that these molecules had an important role in the ubiquitin-proteasome system. Further studies are necessary to explore their feasibility and effectiveness as diagnostic and prognostic biomarkers, or as up/down-stream and therapeutic targets for cancer treatment.

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LncRNA CASC11 Promotes Hepatocellular Carcinoma Progression via Upregulation of UBE2T in a m6A-Dependent Manner

Cited by 21 publications

References 44 publications

A double-edged sword: The HBV-induced non-coding RNAs alterations in hepatocellular carcinoma

A double-edged sword: The HBV-induced non-coding RNAs alterations in hepatocellular carcinoma

Cancer metastasis under the magnifying glass of epigenetics and epitranscriptomics

Diverse roles of UBE2T in cancer (Review)

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