ArticleEuropean journal of medical research2025
LINC00704 boosts the immunologic escape of colorectal cancer cells by upregulating TLR4 by binding with miR- 203a- 3p.
Article in European journal of medical research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
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Who cites it
1 citing paper in PubMed.
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5 authors.
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Abstract
backgroundColorectal cancer (CRC) is a common malignant tumor and is the second most common cause of cancer-related deaths worldwide. Immune escape suppresses anti-tumor immunity and facilitates tumor cells to proliferate. MiR- 203a- 3p regulates cancer progression and LINC00704 may bind with miR- 203a- 3p to inhibit its effects.
methodsIn this study, the levels of miR- 203a- 3p and LINC00704 were tested in tumor tissue and non-cancer tissues in vivo. In further in vitro experiments, transfection, cell vitality, apoptosis, and proliferation ability were detected. The expression level of TLR4 was also examined. Finally, a luciferase assay was conducted to detect whether LINC00704 could bind with miR- 203a- 3p.
resultsA rise in LINC00704 mRNA was observed in CRC tissues while miR- 203a- 3p was reduced. LINC00704 boosts the proliferation of cells and inhibits cell apoptosis. LINC00704 regulates Toll- 1ike receptor- 4 (TLR4) expression through miR- 203a- 3p, thereby modulating cell viability. CRC cell immune escape was facilitated by LINC00704 via miR- 203a- 3p.
conclusionLINC00704 promotes CRC cell immunologic escape by upgrading TLR4 by binding with miR- 203a- 3p.
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