ReferenceID 4832

Cantharidin inhibits osteosarcoma proliferation and metastasis by directly targeting miR-214-3p/DKK3 axis to inactivate β-catenin nuclear translocation and LEF1 translation

Int J Biol Sci

Background: As the leading primary bone cancer in adolescents and children, osteosarcoma patients with metastasis show a five-year-survival-rate of 20-30%, without improvement over the past 30 years. Wnt/beta-catenin is

Back to Browse

Relationship Network

Interactive first-hop connections across herbs, ingredients, formulas, targets, diseases, symptoms, syndromes, evidence, and monographs.

Click a node to open it in a new tab
Ingredient: 1Reference: 1Links: 1
Arranging relationship network...

Record Fields

Scalar fields from the final reference record.

Reference Id
4832
Evidence Id
21422
Core Evidence Id
21422
Source Reference Id
2916
Herb2 Reference Id
HBREF003713
Subject Paper Key
HBIN019611_34326690
Pubmed Id
34326690
Doi
10.7150/ijbs.51638
Paper Title
Cantharidin inhibits osteosarcoma proliferation and metastasis by directly targeting miR-214-3p/DKK3 axis to inactivate β-catenin nuclear translocation and LEF1 translation
Paper Abstract
Background: As the leading primary bone cancer in adolescents and children, osteosarcoma patients with metastasis show a five-year-survival-rate of 20-30%, without improvement over the past 30 years. Wnt/beta-catenin is important in promoting osteosarcoma development. DKK3 is a Wnt/beta-catenin antagonist and predicted to have the specific binding site in 3'-UTR with miR-214-3p. Methods: miR-214-3p and DKK3 levels were investigated in human osteosarcoma tissues and cells by RT-qPCR; the prognostic importance of DKK3 level in osteosarcoma patients was determined with Log-rank test; direct binding between DKK3 with miR-214-3p was identified with targetscan; anti-osteosarcoma mechanism of cantharidin was investigated by miR-214-3p silence/over-expression with or without cantharidin treatment, and nuclear/cytoplasmic protein assay in osteosarcoma cells. Results: Down-regulated DKK3 indicated poor prognosis of osteosarcoma patients. Up-regulated miR-214-3p promoted proliferation and migration, while suppressed apoptosis of osteosarcoma cells by increasing beta-catenin nuclear translocation and LEF1 translation via degradation of DKK3. Cantharidin suppressed viabilities, migration and invasion, while promoted cell cycle arrest and apoptosis in 143B and U-2 OS cells via down-regulating miR-214-3p to up-regulate DKK3, thus inhibited p-GSK-3beta expression, beta-catenin nuclear translocation and LEF1 translation. Meanwhile, cantharidin inhibited tumor growth in xenograft-bearing mice with 143B cell injection in tibia. Conclusion: miR-214-3p mediated Wnt/beta-catenin/LEF1 signaling activation by targeting DKK3 to promote oncogenesis of osteosarcoma; cantharidin inhibited proliferation and metastasis of osteosarcoma cells via down-regulating miR-214-3p to up-regulate DKK3 and decrease beta-catenin nuclear translocation, indicating that cantharidin may be a prospective candidate for osteosarcoma treatment by targeting miR-214-3p/DKK3/beta-catenin signaling.
Journal
Int J Biol Sci
Publish Year
2021
Experiment Subject
mouse; human; patient; 143b and u-2 os cells; children
Experiment Type
Cell Experiment
Phenotype Related
Tumor; Osteosarcoma; Bone Cancer
Paper Title Cn
Paper Title En
Cantharidin inhibits osteosarcoma proliferation and metastasis by directly targeting miR-214-3p/DKK3 axis to inactivate β-catenin nuclear translocation and LEF1 translation
Bilingual Status
semi_complete