ArticleMolecular biotechnology2022
Long Non-coding RNA TPT1-AS1 Suppresses APC Transcription in a STAT1-Dependent Manner to Increase the Stemness of Colorectal Cancer Stem Cells.
Article in Molecular biotechnology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
6 citing papers in PubMed, 10 citations in OpenAlex.
- Nuclear adenomatous polyposis coli elevates STAT1 and reduces CXCL1,2, and 3 expression and inhibits neutrophil recruitment.Cellular signalling · 2025Article
- Exploring the interplay of natural products and long non-coding RNAs in colorectal cancer: pathogenesis, diagnosis, and overcoming drug resistance.Naunyn-Schmiedeberg's archives of pharmacology · 2025Review
- Interplay between JAK/STAT pathway and non-coding RNAs in different cancers.Non-coding RNA research · 2024Review
- High OCT4 Expression Might Be Associated with an Aggressive Phenotype in Rectal Cancer.Cancers · 2023Article
- Article
- Wnt signaling in colorectal cancer: pathogenic role and therapeutic target.Molecular cancer · 2022Review
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Cancer stem cells (CSCs) are the major culprits leading to a new level of complexity and the consequential therapy resistance and disease recurrence in colorectal cancer (CRC). This study focuses on the effect of long non-coding RNA (lncRNA) TPT1-AS1 and its associated molecules on the stemness maintenance of CRC stem cells. TPT1-AS1 was identified as a significantly upregulated gene in CRC using the GSE146587 dataset. Stem cells from CRC HCT116 and CACO2 cells were isolated. TPT1-AS1 was significantly highly expressed in the CSCs compared to non-stem cells. Downregulation of TPT1-AS1 reduced the stemness of the CRC stem cells. TPT1-AS1 recruited STAT1 to the promoter region of APC to suppress APC transcription. Further upregulation of STAT1 or downregulation of APC blocked the role of TPT1-AS1 silencing and restored the malignant behaviors of CSC stem cells. APC inactivated the Wnt/β-catenin pathway. Overexpression of STAT1 restored the levels of cyclin D1 and β-catenin in cells suppressed by TPT1-AS1 silencing. In summary, this work demonstrates that TPT1-AS1 recruits STAT1 to suppress APC transcription and increase the stemness of colorectal CSCs via Wnt/β-catenin activation.
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Registered trials
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