Back to Search
Start Over
SP1-induced circ_0017552 modulates colon cancer cell proliferation and apoptosis via up-regulation of NET1.
- Source :
-
Cancer genetics [Cancer Genet] 2024 Aug; Vol. 286-287, pp. 1-10. Date of Electronic Publication: 2024 May 12. - Publication Year :
- 2024
-
Abstract
- Colon cancer (CC) is a common malignancy over the world and its morbidity and mortality significantly went up in China in recent years. Molecular functions in cancers have gradually been the pivot subject in cancer research. Neuroepithelial cell transforming 1 (NET1) was reported to contribute to prostate cancer and gastric cancer. Our study figured out that NET1 was overexpressed in CC cells. Then, loss-of-function assays revealed that NET1 facilitated CC cell proliferation and repressed CC cell apoptosis. Next, miR-338-3p was confirmed to target NET1. After that, we verified that circ&#95;0017552 which originates from NET1 could positively modulate NET1 expression. Besides, circ&#95;0017552 was a sponge of miR-338-3p. Rescue assays' results demonstrated that circ&#95;0017552 could regulate CC cell proliferation and apoptosis through up-regulation of NET1. A transcription factor named Sp1 (SP1) was found to be present in circ&#95;0017552. SP1 induced transcription of circ&#95;0017552 to facilitate CC cell proliferation and inhibit CC cell apoptosis. In a word, SP1-induced circ&#95;0017552 regulated CC cell proliferation and apoptosis through miR-338-3p/NET1 axis.<br />Competing Interests: Declaration of competing interest The authors declare that they have no conflict of interest.<br /> (Copyright © 2024. Published by Elsevier Inc.)
- Subjects :
- Humans
Cell Line, Tumor
Gene Expression Regulation, Neoplastic
Up-Regulation
Apoptosis
Cell Proliferation
Colonic Neoplasms genetics
Colonic Neoplasms pathology
MicroRNAs genetics
Oncogene Proteins metabolism
RNA, Circular genetics
Sp1 Transcription Factor metabolism
Sp1 Transcription Factor genetics
Subjects
Details
- Language :
- English
- ISSN :
- 2210-7762
- Volume :
- 286-287
- Database :
- MEDLINE
- Journal :
- Cancer genetics
- Publication Type :
- Academic Journal
- Accession number :
- 38810361
- Full Text :
- https://doi.org/10.1016/j.cancergen.2024.05.002