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Published on: May 1, 2020
IGF2BP2 regulates DANCR by serving as an N6-methyladenosine reader
Xiaoge Hu1,2, Wan-Xin Peng2,3, Huaixiang Zhou1
1Key Laboratory of Tumor Molecular Diagnosis and Individualized Medicine of Zhejiang Province, Zhejiang Provincial People's Hospital, People's Hospital of Hangzhou Medical College, Hangzhou, 310014, Zhejiang, China.
Abstract:
The major function of Insulin-like growth factor 2 mRNA-binding protein 2 (IGF2BP2) is to regulate cell metabolism. However, emerging evidence indicates that IGF2BP2 plays a role in cancer, but the underlying mechanism is largely unknown. Here we showed that upregulation of IGF2BP2 is associated with poor outcomes of pancreatic cancer patients and suppression of IGF2BP2 inhibits cell proliferation. We further showed that IGF2BP2 regulates lncRNA DANCR. Ectopic expression IGF2BP2 enhances, whereas knockdown (KD) or knockout (KO) of IGF2BP2 suppresses DANCR expression. Moreover, in vivo RNA precipitation and reciprocal RNA immunoprecipitation revealed that IGF2BP2 interacts with DANCR. DANCR promotes cell proliferation and stemness-like properties. Experiments with xenograft models revealed that while ectopic expression of DANCR promotes, DANCR KO suppresses tumor growth. Mechanistically, DANCR is modified at N6-methyladenosine (m6A) and mutagenesis assay identified that adenosine at 664 of DANCR is critical to the interaction between IGF2BP2 and DANCR where IGF2BP2 serves a reader for m6A modified DANCR and stabilizes DANCR RNA. Together, these results suggest that DANCR is a novel target for IGF2BP2 through m6A modification, and IGF2BP2 and DANCR work together to promote cancer stemness-like properties and pancreatic cancer pathogenesis.
Insights
Insulin-like growth factor 2 mRNA-binding protein 2 (IGF2BP2) promotes pancreatic cancer by stabilizing the lncRNA DANCR. Targeting this interaction may offer new therapeutic strategies for pancreatic cancer.
Area of Science:
- Oncology
- Molecular Biology
- RNA Biology
Background:
- Insulin-like growth factor 2 mRNA-binding protein 2 (IGF2BP2) is known to regulate cell metabolism.
- Emerging evidence suggests a role for IGF2BP2 in cancer, but the mechanisms remain unclear.
- Upregulation of IGF2BP2 correlates with poor outcomes in pancreatic cancer patients.
Purpose of the Study:
- To investigate the role and mechanism of IGF2BP2 in pancreatic cancer pathogenesis.
- To elucidate the interaction between IGF2BP2 and long non-coding RNAs (lncRNAs).
- To explore the potential of targeting the IGF2BP2-lncRNA axis for cancer therapy.
Main Methods:
- Analysis of IGF2BP2 expression in pancreatic cancer patient data.
- Cell proliferation assays following IGF2BP2 knockdown (KD) or knockout (KO).
- RNA immunoprecipitation (RIP) and RNA pull-down assays to confirm IGF2BP2-lncRNA interaction.
- Xenograft models to assess the impact of DANCR on tumor growth.
- N6-methyladenosine (m6A) modification analysis and mutagenesis assays.
Main Results:
- IGF2BP2 upregulation is linked to poor prognosis in pancreatic cancer and its suppression inhibits cell proliferation.
- IGF2BP2 directly interacts with and stabilizes the lncRNA DANCR, enhancing its expression.
- DANCR promotes pancreatic cancer cell proliferation and stemness-like properties.
- IGF2BP2 acts as an m6A reader for DANCR, stabilizing the RNA.
- Knockdown or knockout of DANCR suppresses tumor growth in vivo.
Conclusions:
- IGF2BP2 promotes pancreatic cancer progression by stabilizing the m6A-modified lncRNA DANCR.
- The IGF2BP2-DANCR axis plays a critical role in promoting cancer stemness and pancreatic cancer pathogenesis.
- Targeting the IGF2BP2-DANCR interaction represents a potential therapeutic strategy for pancreatic cancer.
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