ArticleBiochemical genetics2022
CircPLK1 Acts as a Carcinogenic Driver to Promote the Development of Malignant Pleural Mesothelioma by Governing the miR-1294/HMGA1 Pathway.
Article in Biochemical genetics, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
11 citing papers in PubMed, 16 citations in OpenAlex.
- Tumor-associated macrophages derived exosomal circPLK1 promotes resistance to EGFR inhibitor osimertinib in non-small cell lung cancer.Discover oncology · 2025Article
- CircPLK1 upregulates ETS1 to confer anthracycline resistance in triple-negative breast cancer.Journal of translational internal medicine · 2025Article
- Complicated crosstalk between HMGA and non-coding RNAs modulates hallmarks of cancer.Cancer cell international · 2025Review
- The Dual Roles of Circular RNAs in Breast Cancer Distant Metastasis and Their Clinical Applications.Journal of Cancer · 2025Review
- Article
- Regulatory mechanisms and clinical applications of tumor-driven exosomal circRNAs in cancers.International journal of medical sciences · 2023Review
- The tumor suppressor role and ceRNA network of miR-1294 in cancer.Oncology research · 2023Review
- CircCRIM1 promotes nasopharyngeal carcinoma progression via the miR-34c-5p/FOSL1 axis.European journal of medical research · 2022Article
- Promising therapeutic potential of tumor suppressor microRNAs for malignant pleural mesothelioma.Journal of cancer metastasis and treatment · 2022Article
- HMGA1 As a Potential Prognostic and Therapeutic Biomarker in Breast Cancer.Disease markers · 2022Article
- Circ0038632 modulates MiR-186/DNMT3A axis to promote proliferation and metastasis in osteosarcoma.Frontiers in oncology · 2022Article
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
The deregulation of circular RNAs (circRNAs) is involved in cancer development. CircRNA polo-like kinase 1 (circPLK1) was reported to promote breast cancer development. However, the role of circPLK1 in malignant pleural mesothelioma (MPM) is unclear. The expression of circPLK1, miR-1294, and high mobility group AT-hook 1 (HMGA1) mRNA was measured by quantitative real-time PCR (qPCR). Cell viability was detected by CCK-8 assay. Colony formation ability was monitored by colony formation assay. Cell proliferation was detected by EdU assay. Cell migration and cell invasion were monitored by transwell assay. Cancer cell stemness was investigated by sphere formation assay. The protein levels of marker proteins and HMGA1 expression were measured by western blot analysis. The binding relationship between miR-1294 and circPLK1 or HMGA1 was validated by pull-down assay, dual-luciferase reporter assay or RIP assy. Animal study was performed to disclose the role of circPLK1 in vivo. Exosomes were identified by transmission electron microscopy (TEM) and nanoparticle tracking analysis (NTA). CircPLK1 was upregulated in MPM tumor tissues and cell lines. CircPLK1 knockdown suppressed the proliferation, migration, invasion and stemness of MPM cells. CircPLK1 contained a binding site for miR-1294 and thus bound to miR-1294 to sequester its expression. Inhibition of miR-1294 reversed the effects of circPLK1 knockdown. HMGA1 was a target of miR-1294, and circPLK1 bound to miR-1294 to increase the expression of HMGA1. MiR-1294 restoration also suppressed the proliferation, migration, invasion and stemness of MPM cells, while these effects were abolished by HMGA1 overexpression. In addition, circPLK1 knockdown inhibited tumor growth in vivo. CircPLK1 was overexpressed in exosomes derived from serum of MPM patients. CircPLK1 knockdown inhibited MPM cell proliferation, migration, invasion and stemness by targeting the miR-1294/HMGA1 pathway.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.