RETRACTED: Ribosomal L22-like1 (RPL22L1) Promotes Ovarian Cancer Metastasis by Inducing Epithelial-to-Mesenchymal Transition
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Post-publication record
- Nature
- Retraction
- Reason
- Compromised Peer Review;Concerns/Issues about Data;Concerns/Issues about Peer Review;Contamination of Cell Lines/Tissues;Duplication of Data;Duplication of/in Image;Error in Image;Investigation by Journal/Publisher;Investigation by Third Party;Objections by Author(s);Unreliable Results and/or Conclusions;
- Date
- 2/9/2026 0:00
- Flagged by OpenAlex?
- Yes
Source: Retraction Watch, joined by DOI. OpenAlex records retraction as is_retracted, a boolean over a state space with at least four values, so it cannot express an expression of concern, a correction or a reinstatement — it reports them as false, which reads as “fine”.
Abstract
Double minute chromosomes (DMs) have important implications for cancer progression because oncogenes frequently amplified on them. We previously detected a functionally undefined gene amplified on DMs, Ribosomal L22-like1 (RPL22L1). The relationship between RPL22L1 and cancer progression is unknown. Here, RPL22L1 was characterized for its role in ovarian cancer (OC) metastasis and its underlying mechanism was examined. DNA copy number and mRNA expression of RPL22L1 in OC cells was analyzed using data obtained from The Cancer Genome Atlas and the Gene Expression Omnibus database. An immunohistochemical analysis of clinical OC specimens was performed and the relationships between expression level and clinicopathological factors were evaluated. Additionally, in vivo and in vitro assays were performed to understand the role of RPL22L1 in OC. RPL22L1 expression was higher in OC specimens than in normal tissues, and its expression level was highly positively correlated with invasion and lymph node metastasis (P < 0.05). RPL22L1 over-expression significantly enhanced intraperitoneal xenograft tumor development in nude mice and promoted invasion and migration in vitro. Additionally, RPL22L1 knockdown remarkably inhibited UACC-1598 cells invasion and migration. Further, RPL22L1 over-expression up-regulated the mesenchymal markers vimentin, fibronectin, and α-SMA, reduced expression of the epithelial markers E-cadherin, α-catenin, and β-catenin. RPL22L1 inhibition reduced expression of vimentin and N-cadherin. These results suggest that RPL22L1 induces epithelial-to-mesenchymal transition (EMT). Our data showed that the DMs amplified gene RPL22L1 is critical in maintaining the aggressive phenotype of OC and in triggering cell metastasis by inducing EMT. It could be employed as a novel prognostic marker and/or effective therapeutic target for OC.
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The record
- Venue
- PLoS ONE
- Topic
- RNA modifications and cancer
- Field
- Biochemistry, Genetics and Molecular Biology
- Canadian institutions
- University of Calgary
- Funders
- National Natural Science Foundation of ChinaHarbin Medical University
- Keywords
- VimentinEpithelial–mesenchymal transitionGene knockdownCancer researchMetastasisOvarian cancerBiologyCancerMesenchymal stem cellMolecular biologyImmunohistochemistryGeneImmunologyCell biologyGenetics
- Has abstract in OpenAlex
- yes