LncRNA MIR205HG accelerates cell proliferation, migration and invasion in hepatoblastoma through the activation of MAPK signaling pathway and PI3K/AKT signaling pathway

Zhang, Wei; Feng, Liang; Li, Qingfeng; Sun, Huizhen; Li, Fēi; Jiao, Zhibo; Lei, Jie

doi:10.1186/s13062-021-00309-3

Cited by 14 publications

(10 citation statements)

References 34 publications

(26 reference statements)

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“… Cui et al (2019) found that miR-193a-5p directly targets DPEP1 and participates in Hepatoblastoma progression by regulating the expression of the PI3K/Akt/mTOR signaling pathway. The lncRNA MIR205HG has also been reported to accelerate cell proliferation, migration, and invasion in Hepatoblastoma by activating the MAPK and PI3K/AKT signaling pathways ( Zhang et al, 2022 ). Yamamoto et al (2007) suggested that reduced expression of the tumor suppressor p53 could confer resistance to oxidative stress in Hepatoblastoma, partly contributing to its development.…”

Section: Genetics and Hepatoblastomamentioning

confidence: 99%

“…The lncRNA MIR205HG is significantly overexpressed in Hepatoblastoma and competitively binds to miRNA-514a-5p to activate the mitogen-activated protein kinase signaling pathway. It also activates the PI3K/AKT signaling pathway, and lncRNA MIR205HG promotes the proliferation, migration, and invasion of Hepatoblastoma by activating both pathways ( Zhang et al, 2022 ). The lncRNA OIP5-AS1 can activate β-catenin signaling by promoting binding between PTBP1 and β-catenin, thereby promoting Hepatoblastoma proliferation and silencing.…”

Section: Epigenetics and Hepatoblastomamentioning

confidence: 99%

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Epigenetics and genetics of hepatoblastoma: Linkage and treatment

et al. 2022

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Hepatoblastoma is a malignant embryonal tumor with multiple differentiation modes and is the clearest liver malignancy in children. However, little is known about genetic and epigenetic events in Hepatoblastoma. Increased research has recently demonstrated, unique genetic and epigenetic events in Hepatoblastoma, providing insights into its origin and precise treatment. Some genetic disorders and congenital factors are associated with the risk of Hepatoblastoma development, such as the Beckwith-Wiedemann syndrome, Familial Adenomatous polyposis, and Hemihypertrophy. Epigenetic modifications such as DNA modifications, histone modifications, and non-coding RNA regulation are also essential in the development of Hepatoblastoma. Herein, we reviewed genetic and epigenetic events in Hepatoblastoma, focusing on the relationship between these events and cancer susceptibility, tumor growth, and prognosis. By deciphering the genetic and epigenetic associations in Hepatoblastoma, tumor pathogenesis can be clarified, and guide the development of new anti-cancer drugs and prevention strategies.

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Section: Genetics and Hepatoblastomamentioning

confidence: 99%

Section: Epigenetics and Hepatoblastomamentioning

confidence: 99%

Epigenetics and genetics of hepatoblastoma: Linkage and treatment

et al. 2022

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“…Meanwhile, MIR205HG also serves as a sponge for miR-205-5p to activate the PI3K/AKT signaling pathway. Taken together, MIR205HG accelerates cell proliferation, migration and invasion in HB through MAPK and PI3K/AKT signaling pathways (118). The expression of NBR2 is significantly increased within HB samples; moreover, under glucose starvation, NBR2 expression is significantly upregulated.…”

Section: Hepatoblastoma (Hb)mentioning

confidence: 88%

Roles of lncRNAs in childhood cancer: Current landscape and future perspectives

et al. 2023

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According to World Health Organization (WHO), cancer is the leading cause of death for children and adolescents. Leukemias, brain cancers, lymphomas and solid tumors, such as neuroblastoma, ostesarcoma and Wilms tumors are the most common types of childhood cancers. Approximately 400,000 children and adolescents between the ages of 0 and 19 are diagnosed with cancer each year worldwide. The cancer incidence rates have been rising for the past few decades. Generally, the prognosis of childhood cancers is favorable, but the survival rate for many unresectable or recurring cancers is substantially worse. Although random genetic mutations, persistent infections, and environmental factors may serve as contributing factors for many pediatric malignancies, the underlying mechanisms are yet unknown. Long non-coding RNAs (lncRNAs) are a group of transcripts with longer than 200 nucleotides that lack the coding capacity. However, increasing evidence indicates that lncRNAs play vital regulatory roles in cancer initiation and development in both adults and children. In particular, many lncRNAs are stable in cancer patients’ body fluids such as blood and urine, suggesting that they could be used as novel biomarkers. In support of this notion, lncRNAs have been identified in liquid biopsy samples from pediatric cancer patients. In this review, we look at the regulatory functions and underlying processes of lncRNAs in the initiation and progression of children cancer and discuss the potential of lncRNAs as biomarkers for early detection. We hope that this article will help researchers explore lncRNA functions and clinical applications in pediatric cancers.

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“…Similar effects have been observed in ubiquitin specific peptidase 7 (UPS7), an essential component for LC progression and regulation of p53, in that miR-205 acts as an inhibitor of UPS7 and helps channeling p53 into check of cell’s proliferation levels [ 25 ]. Furthermore, when the expression of miR-205 host gene role was investigated, it showed that miR-205-5p activates the pathway signaling of PI3K/AKT and helps in the suppression, migration, proliferation and invasion of hepatoblastoma cells [ 26 ].…”

Section: Role Of Mir-205 In Liver Diseasesmentioning

confidence: 99%