ArticleOncology research2019
Silencing of lncRNA AFAP1-AS1 Inhibits Cell Growth and Metastasis in Clear Cell Renal Cell Carcinoma.
Article in Oncology research, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers, 1 of them a synthesis that pooled it.
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The trial behind it
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Who cites it
8 citing papers in PubMed, 1 synthesis or guideline pooled it, 18 citations in OpenAlex.
- Roles of AFAP1-AS1 in Gynecology and Urogenital System.Current pharmaceutical design · 2024Pooled it
- Identification of a combined lncRNA prognostic signature and knockdown of lncRNA MANCR to inhibit progression of clear cell renal cell carcinoma by bioinformatics analysis.Translational andrology and urology · 2022Article
- AFAP1-AS1: a rising star among oncogenic long non-coding RNAs.Science China. Life sciences · 2021Review
- A Review on the Role of AFAP1-AS1 in the Pathoetiology of Cancer.Frontiers in oncology · 2021Review
- Dysregulation of Long Non-coding RNAs and mRNAs in Plasma of Clear Cell Renal Cell Carcinoma Patients Using Microarray and Bioinformatic Analysis.Frontiers in oncology · 2020Article
- HDAC10 Is Positively Associated With PD-L1 Expression and Poor Prognosis in Patients With NSCLC.Frontiers in oncology · 2020Article
- Prognostic Value of YTHDF2 in Clear Cell Renal Cell Carcinoma.Frontiers in oncology · 2020Article
- Article
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The lncRNA AFAP1-AS1, oriented from an antisense direction to the protein-coding gene AFAP1 in the opposite strand, was upregulated in a variety of tumors and associated with poor prognosis, including lung cancer, breast cancer, ovarian cancer, and so on. However, the biological role of AFAP1-AS1 in clear cell renal cell carcinoma (ccRCC) is still unknown. We observed that AFAP1-AS1 expression was significantly upregulated in ccRCC tissues and that patients with high-level expression of AFAP1-AS1 had a shorter overall survival. Knockdown of AFAP1-AS1 markedly suppressed the progression of proliferation, invasion, migration, and EMT in ccRCC cells. Downregulation of AFAP1-AS1 resulted in an increase in E-cadherin and a decrease in vimentin. Noticeably, we found that PTEN has a negative correlation with the lncRNA AFAP1-AS1 expression. Further studies verified that PTEN deficiency effectively attenuated the ability of AFAP1-AS1 in promoting ccRCC cell proliferation, invasion, migration, and EMT. Moreover, the similar biological response of silencing AFAP1-AS1 was observed in our ccRCC mice model. Knockdown of AFAP1-AS1 evidently suppressed tumor growth. Taken together, our results provide the evidences that silencing of AFAP1-AS1 inhibits cell proliferation, EMT, and metastasis through PTEN-dependent signaling, and our findings elucidate a novel potential therapeutic target or biomarker for the treatment of ccRCC.
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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.