LincROR promotes tumor growth of colorectal cancer through the miR-145/WNT2B/WNT10A/Wnt/β-catenin regulatory axis
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View abstract on PubMed
Summary
This summary is machine-generated.This study reveals long intergenic non-protein coding RNA (lincROR) promotes colorectal cancer (CRC) by sponging miR-145, activating WNT2B/WNT10A, and the Wnt/β-catenin pathway. Targeting lincROR offers a potential therapeutic strategy for CRC.
Area Of Science
- Oncology
- Molecular Biology
- Genetics
Background
- Colorectal cancer (CRC) presents significant clinical challenges, necessitating novel therapeutic targets.
- Long intergenic non-protein coding RNAs (lincRNAs) are implicated in various cancers, but their role in CRC tumorigenesis is not fully understood.
Purpose Of The Study
- To elucidate the molecular mechanism of lincROR in colorectal cancer (CRC) progression.
- To investigate lincROR as a potential therapeutic target for CRC.
Main Methods
- Investigated the effect of lincROR knockdown and overexpression on CRC cell viability and tumor growth in vitro and in vivo.
- Utilized miRNA sponge assays to determine the interaction between lincROR and miR-145.
- Analyzed the downstream effects on WNT2B, WNT10A expression, and Wnt/β-catenin pathway activation.
Main Results
- Knockdown of lincROR inhibited CRC cell viability, while overexpression promoted tumor growth.
- lincROR functions as a miRNA sponge for miR-145, leading to increased WNT2B and WNT10A expression.
- Overexpression of WNT2B and WNT10A activated the Wnt/β-catenin pathway, promoting CRC tumorigenesis.
Conclusions
- lincROR acts as an oncogenic lincRNA in CRC by sponging miR-145 and activating the Wnt/β-catenin pathway via WNT2B/WNT10A.
- lincROR represents a promising therapeutic target for colorectal cancer treatment.
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