ArticleCancer biology & therapy2020
Long non-coding RNA FALEC promotes colorectal cancer progression via regulating miR-2116-3p-targeted PIWIL1.
Article in Cancer biology & therapy, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 15 citations in OpenAlex.
- Cuproptosis: the mechanisms of copper-induced cell death and its implication in colorectal cancer.Naunyn-Schmiedeberg's archives of pharmacology · 2025Review
- Dysregulated miRNA Expression and Androgen Receptor Loss in Racially Distinct Triple-Negative Breast Cancer.International journal of molecular sciences · 2024Article
- Novel roles of PIWI proteins and PIWI-interacting RNAs in human health and diseases.Cell communication and signaling : CCS · 2023Review
- Article
- Comprehensive analysis of cuproptosis-related long noncoding RNA for predicting prognostic and diagnostic value and immune landscape in colorectal adenocarcinoma.Human genomics · 2023Article
- Roles of circRNA dysregulation in esophageal squamous cell carcinoma tumor microenvironment.Frontiers in oncology · 2023Review
- Long non-coding RNA (FALEC) promotes malignant behaviors of gastric cancer cells by regulating miR-203b/PIM3 axis.Annals of translational medicine · 2022Article
- Long non-coding RNA LINC00997 silencing inhibits the progression and metastasis of colorectal cancer by sponging miR-512-3p.Bioengineered · 2021Article
- Critical Roles of PIWIL1 in Human Tumors: Expression, Functions, Mechanisms, and Potential Clinical Implications.Frontiers in cell and developmental biology · 2021Review
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundColorectal cancer (CRC) is one of the most common digestive malignant tumors globally. Focally amplified lncRNA on chromosome 1 (FALEC) is a novel lncRNA that has been reported to be involved in many biological processes during carcinogenesis. However, its role in CRC remains poorly understood.
methodsGene expression at mRNA or protein level was measured by qRT-PCR or western blot, respectively. In vitro experiments including EdU, colony formation, flow cytometry, wound-healing and transwell assays, as well as in vivo xenograft experiment, were utilized to determine the functional role of FALEC in CRC. Relevant mechanical assays were performed to investigate the underlying molecular mechanism.
resultsFALEC was aberrantly up-regulated in CRC. FALEC knockdown could impair CRC cell proliferation, migration and invasion, whereas facilitate cell apoptosis. MiR-2116-3p was revealed to be sponged by FALEC. PIWIL1 was identified as the target of miR-2116-3p. Mechanically, FALEC restored the expression of PIWIL1 via absorbing miR-2116-3p. MiR-2116-3p inhibition and PIWIL1 enrichment could counteract the anti-tumor impact induced by silenced FALEC on the oncogenic behaviors of CRC cells.
conclusionOur study revealed that FALEC promoted CRC progression via restoring the expression of miR-2116-3p-targeted PIWIL1, suggesting the potential application of targeting FALEC in the treatment of CRC.
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