ArticleTranslational oncology2022
Long non-coding FAM201A accelerates the tumorigenesis and progression of colorectal cancer through miR-3163/MACC1 axis.
Article in Translational oncology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 11 citations in OpenAlex.
- Long non-coding RNA POC1B-AS1 depletion represses colorectal cancer progression through the microRNA-625-5p/FOXK1 axis.American journal of translational research · 2025Article
- Longitudinal analysis of hsa-miR-3163, hsa-miR-124-3p, hsa-miR-548c-3p, and hsa-miR-27a-3p as prognostic biomarkers in HIV-infected patients.Frontiers in immunology · 2025Article
- MiRNA-3163 limits ovarian cancer stem-like cells via targeting SOX-2 transcription factor.Non-coding RNA research · 2024Article
- MACC1 revisited - an in-depth review of a master of metastasis.Biomarker research · 2024Review
- miRNA and leptin signaling in metabolic diseases and at extreme environments.Pharmacology research & perspectives · 2024Review
- Article
- The functions and mechanisms of long non-coding RNA in colorectal cancer.Frontiers in oncology · 2024Review
- Circular RNA circFBXO7 attenuates non-small cell lung cancer tumorigenesis by sponging miR-296-3p to facilitate KLF15-mediated transcriptional activation of CDKN1A.Translational oncology · 2023Article
- Editorial: Metabolic reprogramming and cancer progression.Translational oncology · 2023Article
- LncRNA PRRT3-AS1 exerts oncogenic effects on nonsmall cell lung cancer by targeting microRNA-507/homeobox B5 axis.Oncology research · 2021Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Colorectal cancer (CRC) is the leading contributor to cancer-relevant deaths worldwide with severe incidence and mortality. An extensive body of evidence has demonstrated that lncRNA plays a critical role in the oncogenicity of CRC. Despite the oncogenic function of FAM201A in esophageal squamous cell cancer and non-small-cell lung cancer, the potential of FAM201A in CRC progression remains unknown. FAM201A expression level was significantly enhanced in CRC cells compared with normal cells. Further, functional experiments illustrated that knockdown of FAM201A restrained cell growth, stemness and promoted chemoresistance of CRC cells. By exploring molecular mechanism of FAM201A, we found that FAM201A acted as a sponge of miR-3163. More importantly, oncogene MACC1 was confirmed to be a direct target of miR-3163 and FAM201A modulated MACC1 expression level via competing for miR-3163. Subsequently, we testified that FAM201A exerted its role in the tumorigenesis and development of CRC through targeting miR-3163/MACC1. Animal assay certified that FAM201A expedited CRC cell growth in vivo. In conclusion, our study was the first to unveil that FAM201A promoted cell proliferation and CSC characteristics in CRC via regulation of the miR-3163/MACC1 axis, which provided clues for the clinical treatment of patients with this disease.
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