The long non-coding RNA 91H increases aggressive phenotype of breast cancer cells and up-regulates H19/IGF2 expression through epigenetic modifications

Vennin, Constance; Spruyt, Nathalie; Robin, Y.; Chassat, Thierry; Bourhis, Xuefen Le; Adriaenssens, Éric

doi:10.1016/j.canlet.2016.10.023

Cited by 64 publications

(51 citation statements)

References 24 publications

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“…Particularly, IGF2, a neighbouring gene expressed from the paternal allele, encodes for a protein of 7.5 kDa involved in embryonic growth, is commonly upregulated in CRC [9,10]. Early studies had showed that lncRNA 91H could up-regulate IGF2 expression by epigenetic modifications which could further promote breast cancer development [5,11].…”

Section: Introductionmentioning

confidence: 99%

RETRACTED ARTICLE: Long non-coding RNA 91H regulates IGF2 expression by interacting with IGF2BP2 and promotes tumorigenesis in colorectal cancer

Gao

Liu

et al. 2020

Artificial Cells, Nanomedicine, and Biotechnology

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91H, a long non-coding antisense transcripts located on the position of the H19/IGF2 locus had been suggested to play a critical role in tumour development. However, little study had proved the mechanism in colorectal cancer (CRC). Hence, we performed this study to deeply explore the mechanism of lncRNA 91H in tumour progression. The expression of lncRNA 91H was first detected in CRC tissues and cells which was higher in vitro and in vivo than normal cells or tissues and CRC patients with high lncRNA 91H expression usually had a high risk in tumour metastasis (p < .05). Then, monodansylcadaverine (MDC) staining, scratch wound, migration and invasion assays were conducted which showed to that reduced lncRNA 91H would greatly affect tumour migration, invasion and autophagy. Finally, by RNA pull down and RNA-binding protein immunoprecipitation (RIP) assay, a significant interaction was found between lncRNA 91H and IGF2BP2 which was proved to play an important role in CRC IGF2 expression. All these results suggested lncRNA 91H promotes IGF2 expression by interacting with IGF2BP2 which would provide a new strategy in finding potential CRC diagnostic biomarkers and therapeutic targets.

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Section: Introductionmentioning

confidence: 99%

RETRACTED ARTICLE: Long non-coding RNA 91H regulates IGF2 expression by interacting with IGF2BP2 and promotes tumorigenesis in colorectal cancer

Gao

Liu

et al. 2020

Artificial Cells, Nanomedicine, and Biotechnology

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“…These findings indicated that interact with IGF2, which played an important role in multiple diseases. [48][49][50] Besides, rs326049 showed significant association with CCDC127 expression, a significantly upregulated gene in lung tumor tissues. Furthermore, co-expression genes with RP11-43F13.3 mainly enriched in DNA replication, homologous recombination, spliceosome pathways.…”

Section: Discussionmentioning

confidence: 92%

“…In addition, the expression of RP11‐43F13.3 was significantly decreased in tumor tissues compared with adjacent normal tissues, indicating that RP11‐43F13.3 might play as a tumor inhibitor. According to lncRNome database, the RP11‐43F13.3 was an antisense and could interact with IGF2 , which played an important role in multiple diseases . Besides, rs326049 showed significant association with CCDC127 expression, a significantly upregulated gene in lung tumor tissues.…”

Section: Discussionmentioning

confidence: 99%

Fine mapping in TERT‐CLPTM1L region identified three independent lung cancer susceptibility signals: A large‐scale multi‐ethnic population study

Fan

et al. 2018

Molecular Carcinogenesis

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Genome-wide association studies (GWAS) and fine mapping studies have identified multiple lung cancer susceptibility variants in TERT-CLPTM1L region. However, it is still unclear about the relationship between these risk variants and the independent lung cancer risk signals in this region. Therefore, we evaluated the independent susceptibility signals for lung cancer and explored the potential functional variants in this region. Sequential conditional analysis was used to detect the independent susceptibility loci based on four lung cancer GWAS datasets with 12 843 lung cases and 12 639 controls. Comprehensively functional annotations were performed for each independent signal. Three independent susceptibility signals were identified in multi-ethnic population. For the first signal, rs2736100 showed the most significant association with lung cancer risk (C > A, OR = 0.82, 95%CI: 0.79-0.85, P = 1.98 × 10 ). Rs36019446 was the top-ranked site (A > G, OR = 0.88, 95%CI: 0.84-0.92, P = 1.74 × 10 ) in the second signal. For the third signal, rs326048 was the leading SNP (A > G, OR = 0.91, 95%CI: 0.87-0.95, P = 1.38 × 10 ). The following subgroup analysis found the same three loci among Asian population. Further, we compared the difference between various subgroup populations. Functional annotations revealed that rs2736100, rs27996 (r = 0.85 with rs36019446) and rs326049 (r = 0.73 with rs326048) could be potential functional variants in these three risk signals, respectively. In conclusion, although multiple variants have been found associated with lung cancer risk in TERT-CLPTM1L region, our findings indicated that there are three independent lung cancer susceptibility signals in this region.

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“…Knockdown studies have shown that 91H contributes to IGF2 expression at the paternal allele [28]. 91H is also responsible for maintaining H19/IGF2 imprinting and preventing DNA methylation on the H19/IGF2 locus ( ICR and H19 promoter) on the maternal allele, potentially by binding and masking these sites, driving H19 and IGF2 expression [108]. Outside of controlling imprinting, 91H can also directly activate a promoter of IGF2 .…”

Section: Further Considerations At the H19 Locus 91h And Hotsmentioning

confidence: 99%

Targeting H19, an Imprinted Long Non-Coding RNA, in Hepatic Functions and Liver Diseases

et al. 2017

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H19 is a long non-coding RNA regulated by genomic imprinting through methylation at the locus between H19 and IGF2. H19 is important in normal liver development, controlling proliferation and impacting genes involved in an important network controlling fetal development. H19 also plays a major role in disease progression, particularly in hepatocellular carcinoma. H19 participates in the epigenetic regulation of many processes impacting diseases, such as activating the miR-200 pathway by histone acetylation to inhibit the epithelial-mesenchymal transition to suppress tumor metastasis. Furthermore, H19's normal regulation is disturbed in diseases, such as hepatocellular carcinoma. In this disease, aberrant epigenetic maintenance results in biallelic expression of IGF2, leading to uncontrolled cellular proliferation. This review aims to further research utilizing H19 for drug discovery and the treatment of liver diseases by focusing on both the epigenetic regulation of H19 and how H19 regulates normal liver functions and diseases, particularly by epigenetic mechanisms.

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The long non-coding RNA 91H increases aggressive phenotype of breast cancer cells and up-regulates H19/IGF2 expression through epigenetic modifications

Cited by 64 publications

References 24 publications

RETRACTED ARTICLE: Long non-coding RNA 91H regulates IGF2 expression by interacting with IGF2BP2 and promotes tumorigenesis in colorectal cancer

RETRACTED ARTICLE: Long non-coding RNA 91H regulates IGF2 expression by interacting with IGF2BP2 and promotes tumorigenesis in colorectal cancer

Fine mapping in TERT‐CLPTM1L region identified three independent lung cancer susceptibility signals: A large‐scale multi‐ethnic population study

Targeting H19, an Imprinted Long Non-Coding RNA, in Hepatic Functions and Liver Diseases

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