ArticleOncoTargets and therapy2019
Knockdown of EIF3C promotes human U-2OS cells apoptosis through increased CASP3/7 and Chk1/2 by upregulating SAPK/JNK.
Article in OncoTargets and therapy, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 6 citations in OpenAlex.
- Review of the role and potential clinical value of m6A methylation modifications in the biological process of osteosarcoma.Frontiers in genetics · 2025Review
- Role of eIF3C Overexpression in Predicting Prognosis of Intrahepatic Cholangiocarcinoma.Digestive diseases and sciences · 2022Article
- Targeting EIF3C to suppress the development and progression of nasopharyngeal carcinoma.Frontiers in bioengineering and biotechnology · 2022Article
- Downregulation of Diacylglycerol kinase zeta (DGKZ) suppresses tumorigenesis and progression of cervical cancer by facilitating cell apoptosis and cell cycle arrest.Bioengineered · 2021Article
- Novel application of single-cell next-generation sequencing for determination of intratumoral heterogeneity of canine osteosarcoma cell lines.Journal of veterinary diagnostic investigation : official publication of the American Association of Veterinary Laboratory Diagnosticians, Inc · 2021Article
- ZNF280A promotes lung adenocarcinoma development by regulating the expression of EIF3C.Cell death & disease · 2021Article
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundAs a component of the EIF3 complex, EIF3C is essential for several steps in protein synthesis initiation. Recently, it has been addressed that EIF3C is overexpressed in several human cancers and plays a pivotal role in cell proliferation and tumorigenesis. MATERIALS AND
methodsImmunohistochemistry, quantitative real-time PCR (qPCR), and Western blotting assays were employed to determine the expression of EIF3C in osteosarcoma (OsC) tissues obtained from 60 patients. The levels of EIF3C mRNA and protein were assessed by qPCR and Western blotting, respectively. The effect of EIF3C knockdown on OsC cell proliferation was detected by MTT and colony formation assays, respectively. Cell apoptosis induced by EIF3C silencing was analyzed by flow cytometric analysis. PathScan stress and apoptosis signaling antibody array kit was used to analyze the potential effects of EIF3C knockdown on OsC cells.
resultsThe levels of EIF3C were high in OsC tissues and cell lines. In addition, EIF3C knockdown by lentivirus-mediated shRNA targeting EIF3C significantly suppressed cell proliferation and colony formation and induced apoptosis in U-2OS cells. Moreover, EIF3C knockdown led to the upregulated expression of CASP3/7, Chk1/2, and SAPK/JNK, indicating that the downregulated expression of EIF3C might be associated with pro-apoptosis of U-2OS cells.
conclusionEIF3C may be a promising target for gene therapy of human OsC. However, the precise mechanisms behind the effect of EIF3C on OsC tumorigenesis require further analysis.
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