IGF2BP2 knockdown suppresses thyroid cancer progression by reducing the expression of long non-coding RNA HAGLR

Liu, Dong; Geng, Zushi; Liu, Zheng; Mei, Tao; Pan, Mengjiao; Lu, Xiaoyan

doi:10.1016/j.prp.2021.153550

Cited by 22 publications

(16 citation statements)

References 37 publications

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“…Based on the TGCA database, IGF2BP2 expression was notably up-regulated in thyroid cancer relative to normal tissues ( Wang et al, 2020 ). IGF2BP2 knockdown suppressed cell proliferation, migration, invasion, and induced cell apoptosis of thyroid cancer via by reducing the expression of long non-coding RNA HAGLR ( Dong et al, 2021 ). In this study, differentiation of PTC was enhanced after IGF2BP2 knockdown which was shown as increase of 125 I uptake and NIS expression.…”

Section: Discussionmentioning

confidence: 99%

AhR Antagonist Promotes Differentiation of Papillary Thyroid Cancer via Regulating circSH2B3/miR-4640-5P/IGF2BP2 Axis

Guo

Liu

et al. 2021

Front. Pharmacol.

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Abnormally high expression of aryl hydrocarbon receptor (AhR) has been implicated in dedifferentiation of radioiodine-refractory papillary thyroid cancer (RR-PTC). This study aimed to evaluate the differentiation effect of AhR antagonist in PTC, and to explore the potential mechanism of it. Results showed that AhR antagonists promoted differentiation of PTC, as shown as increase in 125I uptake and Na/I symporter (NIS) expression level. CircRNA microarray in K1 cells treated with StemRegenin 1(SR1) revealed that hsa_circ_0006741 (circSH2B3) was down-regulated in SR1 treated K1 cells. Downregulation of circSH2B3 increased 125I uptake and NIS expression levels. CircSH2B3 acted as an endogenous sponge of hsa-miR-4640-5p and modulated IGF2BP2 expression. IGF2BP2 overexpression induced dedifferentiation of PTC, while silencing IGF2BP2 accelerated differentiation of PTC cells. Rescue studies showed that the dedifferentiation activity of AhR was modulated by the circSH2B3/miR-4640-5p/IGF2BP2 axis. Our findings confirmed for the first time that AhR antagonists promote differentiation of PTC via inhibiting the circSH2B3/miR-4640-5p/IGF2BP2 axis, offering a novel therapeutic approach and a potential marker for differentiation of PTC.

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Section: Discussionmentioning

confidence: 99%

AhR Antagonist Promotes Differentiation of Papillary Thyroid Cancer via Regulating circSH2B3/miR-4640-5P/IGF2BP2 Axis

Guo

Liu

et al. 2021

Front. Pharmacol.

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“…There is no current evidence of a direct role of IGF2BP2 in the response against viral infections, but recent data connected its function to the lncRNAs. In thyroid cancer, IGF2BP2 is an oncogenic factor since it enhances the expression of the HAGLR lncRNA and the cellular proliferation [100]. Also, in non-small-cell lung cancer, IGF2BP2 enhances the proliferation of tumor cells by binding to the oncogenic MALAT1 lncRNA and increasing its stability [101].…”

Section: Discussionmentioning

confidence: 99%

The interplay between lncRNAs, RNA-binding proteins and viral genome during SARS-CoV-2 infection reveals strong connections with regulatory events involved in RNA metabolism and immune response

Enguita

Leitão

McDonald

et al. 2022

Preprint

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Viral infections are complex processes based on an intricate network of molecular interactions. The infectious agent hijacks components of the cellular machinery for its profit, circumventing the natural defense mechanisms triggered by the infected cell. The successful completion of the replicative viral cycle within a cell depends on the function of viral components versus the cellular defenses. Non-coding RNAs (ncRNAs) are important cellular modulators, either promoting or preventing the progression of viral infections. Among these ncRNAs, the long non-coding RNA (lncRNA) family is especially relevant due to their intrinsic functional properties and ubiquitous biological roles. Specific lncRNAs have been recently characterized as modulators of the cellular response during infection of human host cells by single stranded RNA viruses. However, the role of host lncRNAs in the infection by human RNA coronaviruses such as SARS-CoV-2 remains uncharacterized. In the present work, we have performed a transcriptomic study of a cohort of patients with different SARS-CoV-2 viral load. Our results revealed the existence of a SARS-CoV-2 infection-dependent pattern of transcriptional up-regulation in which specific lncRNAs are an integral component. To determine the role of these lncRNAs, we performed a functional correlation analysis complemented with the study of the validated interactions between lncRNAs and RNA-binding proteins (RBPs). This combination of in silico functional association studies and experimental evidence allowed us to identify a lncRNA signature composed of six elements - NRIR, BISPR, MIR155HG, FMR1-IT1, USP30-AS1, and U62317.2 - associated with the regulation of SARS-CoV-2 infection. We propose a competition mechanism between the viral RNA genome and the regulatory lncRNAs in the sequestering of specific RBPs that modulates the interferon response and the regulation of RNA surveillance by nonsense-mediated decay (NMD).

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“…Recent studies revealed that IGF2BP1 bound to the 3’UTR m6A site of SOX2 mRNA and inhibited the degradation of SOX2 mRNA, which in turn led to the proliferation and metastasis of endometrial cancer cells [ 134 ]. IGF2BP protein family gene products have been found to be overexpressed in a variety of tumors and to regulate the stability of PEG10 [ 135 ], SOX2 [ 134 ], FSCN1 [ 7 ], MYC [ 7 , 136 ], HMGA1 [ 137 ], YAP [ 138 ], LEF1 [ 139 ], FOXM1 [ 140 ], ABCB1 [ 141 ], CCND1 [ 142 ], VEGF [ 142 ], HIF1A [ 143 ], TMBIM6 [ 144 ], and lncRNA HAGLR [ 145 ] expression in an m6A-dependent manner to promote tumor progression.…”

Section: Writers Erasers Readersmentioning

confidence: 99%

“…However, another study found that METTL3 cooperates with YTHDF2 to regulate downstream c-Rel and RelA, participates in the inactivation of the NF-κB pathway, and plays a key tumor-suppressing role in papillary thyroid cancer [ 269 ]. IGF2BP2 can regulate the expression of MYC [ 136 ], lncRNA HAGLR [ 145 ], and IGF2 [ 270 ] in a m6A-dependent manner and promote the progression of thyroid cancer.…”

Section: M6a and Cancersmentioning

confidence: 99%

Role of m6A writers, erasers and readers in cancer

et al. 2022

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The N(6)-methyladenosine (m6A) modification is the most pervasive modification of human RNAs. In recent years, an increasing number of studies have suggested that m6A likely plays important roles in cancers. Many studies have demonstrated that m6A is involved in the biological functions of cancer cells, such as proliferation, invasion, metastasis, and drug resistance. In addition, m6A is closely related to the prognosis of cancer patients. In this review, we highlight recent advances in understanding the function of m6A in various cancers. We emphasize the importance of m6A to cancer progression and look forward to describe future research directions.

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IGF2BP2 knockdown suppresses thyroid cancer progression by reducing the expression of long non-coding RNA HAGLR

Cited by 22 publications

References 37 publications

AhR Antagonist Promotes Differentiation of Papillary Thyroid Cancer via Regulating circSH2B3/miR-4640-5P/IGF2BP2 Axis

AhR Antagonist Promotes Differentiation of Papillary Thyroid Cancer via Regulating circSH2B3/miR-4640-5P/IGF2BP2 Axis

The interplay between lncRNAs, RNA-binding proteins and viral genome during SARS-CoV-2 infection reveals strong connections with regulatory events involved in RNA metabolism and immune response

Role of m6A writers, erasers and readers in cancer

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