Knockdown of HuR represses osteosarcoma cells migration, invasion and stemness through inhibition of YAP activation and increases susceptibility to chemotherapeutic agents

Xu, Wei; Chen, Chao; Xu, Ruijun; Li, Yifan; Hu, Ruixi; Li, Zhikun; Zhu, Xiaodong

doi:10.1016/j.biopha.2018.03.098

Cited by 16 publications

(19 citation statements)

References 24 publications

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“…Mechanistically, we found that B4GALT1‐AS1 could recruit HuR via directly binding to HuR and further enhance YAP transcriptional activity. Since the HuR/YAP regulatory axis was previously confirmed by us in OS cells progression, our work elucidated that B4GALT1‐AS1 was a positive regulator of this axis. Importantly, overexpression of YAP rescued the inhibition of B4GALT1‐AS1 knockdown on OS cells progression, indicating that B4GALT1‐AS1 exerts its promotion dependent on YAP expression in OS cells.…”

Section: Discussionsupporting

confidence: 58%

“…YAP is regarded as the root and therapeutic target of cancer and acts as a critical factor in tumour stemness . Recent study has indicated that YAP activity is involved in osteosarcoma chemoresistance, and our work has demonstrated that HuR could directly bind to YAP and increase its activity in OS cells progression . However, it is still unclear whether lncRNAs are involved in HuR activity on YAP transcriptional activity in OS cells progression.…”

Section: Introductionmentioning

confidence: 66%

“…As our previous study has shown that RNA‐binding protein HuR represses OS cells migration, invasion and stemness, and increases susceptibility to chemotherapeutic agents via directly binding to YAP and promoting YAP activity, we wondered whether B4GALT1‐AS1 involved in HuR functions in OS cells progression. As shown in Figure A, HuR nuclear‐cytoplasmic translocation was suppressed in OS cells with B4GALT1‐AS1 knockdown.…”

Section: Resultsmentioning

confidence: 99%

“…In addition, HuR could stabilize MMP‐9 mRNA during seizure‐induced MMP‐9 expression in neurons . Our previous study demonstrated that HuR could increase osteosarcoma cells migration, invasion and stemness through activating YAP and decrease susceptibility to chemotherapeutic agents . However, the mechanisms by which HuR was regulated or whether lncRNAs facilitate HuR functions were unclear in OS.…”

Section: Introductionmentioning

confidence: 99%

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LncRNA B4GALT1‐AS1 recruits HuR to promote osteosarcoma cells stemness and migration via enhancing YAP transcriptional activity

Wang

et al. 2018

Cell Proliferation

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Section: Discussionsupporting

confidence: 58%

Section: Introductionmentioning

confidence: 66%

Section: Resultsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

LncRNA B4GALT1‐AS1 recruits HuR to promote osteosarcoma cells stemness and migration via enhancing YAP transcriptional activity

Wang

et al. 2018

Cell Proliferation

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“…AREs are signals for rapid RNA degradation, and by blocking these recognition sites HuR can stabilize its RNA interaction partners [71][72][73]. HuR is frequently upregulated in cancer cells and is known to be involved in many hallmarks of cancer, such as invasion, angiogenesis, and inflammation, by post-transcriptionally regulating various cancer-related mRNAs [71,72,[74][75][76]. HuR not only binds to protein-coding mRNA but also interacts with lncRNAs, thereby influencing their stability both in a positive and negative manner [55][56][57][58]77].…”

Section: Human Antigen R (Hur)mentioning

confidence: 99%

RNA-Binding Proteins as Important Regulators of Long Non-Coding RNAs in Cancer

Jonas

Calin

Pichler

2020

IJMS

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The majority of the genome is transcribed into pieces of non-(protein) coding RNA, among which long non-coding RNAs (lncRNAs) constitute a large group of particularly versatile molecules that govern basic cellular processes including transcription, splicing, RNA stability, and translation. The frequent deregulation of numerous lncRNAs in cancer is known to contribute to virtually all hallmarks of cancer. An important regulatory mechanism of lncRNAs is the post-transcriptional regulation mediated by RNA-binding proteins (RBPs). So far, however, only a small number of known cancer-associated lncRNAs have been found to be regulated by the interaction with RBPs like human antigen R (HuR), ARE/poly(U)-binding/degradation factor 1 (AUF1), insulin-like growth factor 2 mRNA-binding protein 1 (IGF2BP1), and tristetraprolin (TTP). These RBPs regulate, by various means, two aspects in particular, namely the stability and the localization of lncRNAs. Importantly, these RBPs themselves are commonly deregulated in cancer and might thus play a major role in the deregulation of cancer-related lncRNAs. There are, however, still many open questions, for example regarding the context specificity of these regulatory mechanisms that, in part, is based on the synergistic or competitive interaction between different RBPs. There is also a lack of knowledge on how RBPs facilitate the transport of lncRNAs between different cellular compartments. Compared to protein-coding genes, lncRNAs are poorly conserved between different species and their expression levels are rather low [7,8]. Initially, this led to the belief that they were nothing but transcriptional noise [6][7][8]. Soon, however, it was discovered that lncRNAs do exhibit considerable functionality, for example as regulators of transcription [6][7][8]. Mechanisms of transcriptional regulation by lncRNAs are multifarious and can occur either in cis or in trans, meaning either closer to or further away from the lncRNA's site of transcription, respectively [6,7]. A frequent mechanism of transcriptional regulation via lncRNAs is the recruitment, or prevention of such, of components of chromatin or histone-modifying complexes, like polycomb repressive complexes or histone deacetylase complexes [11][12][13]. LncRNAs can also direct transcription factors or cofactors to promoter regions of genes and facilitate the formation of chromatin loops between distant enhancers and promoters, as observed for some eRNAs [9,[14][15][16][17]. Another way that they can impact transcription is by interfering with the RNA polymerase II transcription machinery, thereby blocking transcriptional initiation or elongation [18]. LncRNAs are important regulators not only at the level of transcription but also at the post-transcriptional level [6,7]. They regulate pre-mRNA splicing by interacting with splicing factors or with the mRNA itself [19][20][21][22]. A well-studied example for this is metastasis-associated lung adenocarcinoma transcript 1 (MALAT1), an lncRNA that interacts with serine/arginine (SR) spl...

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Relationship between HuR and tumor drug resistance

Lei

et al. 2023

Clin Transl Oncol

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Knockdown of HuR represses osteosarcoma cells migration, invasion and stemness through inhibition of YAP activation and increases susceptibility to chemotherapeutic agents

Cited by 16 publications

References 24 publications

LncRNA B4GALT1‐AS1 recruits HuR to promote osteosarcoma cells stemness and migration via enhancing YAP transcriptional activity

LncRNA B4GALT1‐AS1 recruits HuR to promote osteosarcoma cells stemness and migration via enhancing YAP transcriptional activity

RNA-Binding Proteins as Important Regulators of Long Non-Coding RNAs in Cancer

Relationship between HuR and tumor drug resistance

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