Published online Dec 15, 2023. doi: 10.4251/wjgo.v15.i12.2120
Peer-review started: July 27, 2023
First decision: August 8, 2023
Revised: September 22, 2023
Accepted: October 16, 2023
Article in press: October 16, 2023
Published online: December 15, 2023
Processing time: 140 Days and 1.9 Hours
Colorectal carcinoma (CRC) is the most frequent-occurring malignant tumour in the United States. Curcumin exerts anti-tumor activity in CRC, but the underlying mechanism needs further elucidation. Meanwhile, over the last decade, circular RNAs (circRNAs) is correlated with the initiation and development of various tumors, containing CRC. Also, the increasing focus on the competing endogenous RNAs hypothesis is that circRNAs serve as microRNA sponges to derepress target mRNAs’ levels.
Clinically, it is urgent to find a more effective therapy, which has high clinical significance for CRC patients. Currently, the chemo-preventive properties of traditional Chinese medicine have drawn great attention in cancer therapeutics. As a naturally occurring medicine, curcumin is derived from the medical plant Curcuma longa L. However, it needs further investigation regarding the mechanism through which curcumin affects CRC development.
This study aims at illuminating whether hsa_circ_0136666 involvement on curcumin-triggered CRC progression was mediated via sponging miR-1301-3p.
CRC cells were adopted and treated with 20 μM curcumin for 24 h. Then, for hsa_circ_0136666 stably upregulation, CRC cells were treated with hsa_circ_0136666 overexpression vector transfection or miR-1301-3p mimic and inhibitor. Real-time quantitative PCR was used to quantified the expression of hsa_circ_0136666, miR-1301-3p and CXCL1. 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. The relationship between hsa_circ_0136666, miR-1301-3p and CXCL1 were validated by RNA pull-down, RIP, and dual-luciferase reporter assay. In vivo experiments were implemented by the murine xenograft model.
Curcumin treatment could distinctly reduce the colony number of SW480 and SW620 cells relative to their control groups. Furthermore, the apoptosis rate in the curcumin group was markedly improved in comparison with other groups Interestingly, curcumin treatment significantly decreased hsa_circ_0136666 in SW480 and SW620 but had no effect on hsa_circ_0000392 and hsa_circ_0000896 expression. These data indicated the suppressive role of curcumin on CRC development. hsa_circ_0136666 upregulation could abolish the impacts of curcumin on CRC cell growth and apoptosis. Meanwhile, miR-1301-3p acted as a direct target of hsa_circ_0136666 and miR-1301-3p directly targeted CXCL1. Hsa_circ_0136666 could reverse curcumin-triggered CRC cell proliferation and apoptosis by interacting with miR-1301-3p while miR-1301-3p knockdown overturned curcumin-induced increase in CRC cell growth and decrease in apoptosis by targeting CXCL1. Curcumin repressed CRC cell growth via regulating hsa_circ_0136666 in vivo.
Curcumin repressed CRC cell proliferation and boosted apoptosis, and first verified it was associated with the regulatory network of the hsa_circ_0136666/miR-1301-3p/CXCL1. Hsa_circ_0136666 relieves curcumin-induced CRC cell growth and apoptosis partly via the miR-1301-3p/CXCL1 signaling.
This study elucidates a new mechanism of curcumin and sheds light on developing a new therapeutic for CRC treatment.