Background: This study investigate the anti-tumor effect of curcumin and whether its mediated by hsa_circ_0136666 through miR-1301-3p/ in colorectal carcinoma (CRC). Through multiple experiments, we have drawn the conclusion that curcumin inhibited CRC development through the hsa_circ_0136666/miR-1301-3p/ axis, hinting at a novel treatment option for curcumin to prevent CRC development.
Aim: To determine whether hsa_circ_0136666 involvement in curcumin-triggered CRC progression was mediated by sponging miR-1301-3p.
Methods: Cell counting kit-8, colony-forming cell, 5-ethynyl-2'-deoxyuridine, and flow cytometry assays were carried out to determine cell proliferation, apoptosis, and cell cycle progression. Real-time quantitative polymerase chain reaction quantified hsa_circ_0136666, miR-1301-3p, and chemokine (C-X-C motif) ligand 1 (), and western blot analysis determined , B-cell lymphoma-2 (Bcl-2), and Bcl-2 related X protein (Bax) protein levels. CircBank or starbase software was first used for the prediction of miR-1301-3p binding with hsa_circ_0136666 and , followed by RNA pull-down, RNA immunoprecipitation, and dual-luciferase reporter assay validation. experiments were implemented in a murine xenograft model.
Results: Curcumin blocked CRC cell proliferation but boosted apoptosis. Moreover, elevated hsa_circ_0136666 Levels were observed in CRC cells, which were reduced by curcumin. , hsa_circ_0136666 overexpression abolished the antitumor activity of CRC cells. Mechanical analysis revealed the ability of hsa_circ_0136666 to sponge miR-1301-3p to modulate levels.
Conclusion: Curcumin inhibited CRC development through the hsa_circ_0136666/miR-1301-3p/ axis, hinting at a novel treatment option for curcumin to prevent CRC development.
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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC10758645 | PMC |
http://dx.doi.org/10.4251/wjgo.v15.i12.2120 | DOI Listing |
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