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Updated: Mar 14, 2026

In Vivo Inhibition of MicroRNA to Decrease Tumor Growth in Mice
Published on: August 23, 2019
Poly r(C) binding protein (PCBP) 1 is a negative regulator of thyroid carcinoma
Mingpeng Zhang1, Xin Wang1, Jin Tan1
1Department of Geriatrics, Tianjin Medical University General Hospital, Tianjin Geriatrics Institute Tianjin 300052, China.
Abstract:
Poly r(C) binding protein (PCBP) 1 or heterogeneous ribonucleoprotein (hnRNP) E1 is a RNA binding protein functional in multiple biological processes. PCBP1 has been shown to function as a tumor suppressor by negatively regulating translation of EMT inducer proteins in different cancers. Loss of PCBP1 expression or its Akt2-mediated phosphorylation at serine residue 43 has both been indicated to de-repress its regulation of EMT inducer proteins. However, its role in thyroid carcinoma has not been elucidated. Here we report that PCBP1 expression is significantly downregulated in thyroid carcinoma patients. In vitro kinase assay revealed that immunoprecipitated PCBP1 from transient or stably transfected thyroid carcinoma cells can be phosphorylated by recombinant Akt2 kinase. In situ analysis revealed that PCBP1 is a putative target of miR-490-3p, which was further confirmed by PCBP1 3'UTR-based reporter assays using the wild-type or a miR-490 seed mutant 3'UTR. The endogenous regulation of the PCBP1 3'UTR reporter by miR-490-3p could be rescued by transfection of miR-490 antagomir in WRO and BCPAP cells. Stably overexpressing PCBP1 BCPAP cells attenuated tumor formation completely as compared to empty vector overexpressing cells in xenograft assay. Cumulatively, our results indicate that PCBP1 functions as a tumor suppressor in thyroid carcinoma and that its expression is down regulated by high expression of the miR-490-3p observed in thyroid carcinoma patients.
Insights
Poly r(C) binding protein 1 (PCBP1) acts as a tumor suppressor in thyroid cancer. Its downregulation by miR-490-3p promotes cancer progression, but restoring PCBP1 inhibits tumor formation.
Area of Science:
- Molecular Biology
- Oncology
- RNA Biology
Background:
- Poly r(C) binding protein 1 (PCBP1), also known as heterogeneous ribonucleoprotein E1, is an RNA-binding protein involved in various biological processes.
- PCBP1 functions as a tumor suppressor in several cancers by inhibiting the translation of proteins that induce epithelial-mesenchymal transition (EMT).
- Loss of PCBP1 expression or its phosphorylation can de-repress EMT inducers, but its specific role in thyroid carcinoma was previously unknown.
Purpose of the Study:
- To investigate the role of PCBP1 in thyroid carcinoma.
- To elucidate the regulatory mechanisms of PCBP1 expression in thyroid cancer.
- To assess the therapeutic potential of PCBP1 in thyroid carcinoma.
Main Methods:
- Analysis of PCBP1 expression in thyroid carcinoma patients.
- In vitro kinase assays to assess Akt2-mediated phosphorylation of PCBP1.
- In situ analysis and 3'UTR-based reporter assays to identify microRNA regulation.
- Xenograft assays in mice to evaluate the tumor-suppressive function of PCBP1.
Main Results:
- PCBP1 expression is significantly downregulated in thyroid carcinoma.
- PCBP1 can be phosphorylated by Akt2 kinase in thyroid carcinoma cells.
- PCBP1 is a target of miR-490-3p, which is highly expressed in thyroid carcinoma.
- Overexpression of PCBP1 in thyroid cancer cells completely attenuated tumor formation in vivo.
Conclusions:
- PCBP1 acts as a tumor suppressor in thyroid carcinoma.
- Downregulation of PCBP1 in thyroid cancer is mediated by high expression of miR-490-3p.
- Restoring PCBP1 expression holds potential for thyroid carcinoma therapy.
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