Knockdown of LINC00702 inhibits the growth and induces apoptosis of breast cancer through the Wnt/β-catenin pathway
Long non-coding RNAs (lncRNAs) are essential in many biological areas like cell growth and apoptosis. The role of recently discovered LINC00702 is yet to be explored. Therefore, we wanted to elucidate its role in breast cancer (BC) with bioinformatic and various methods. LINC00702 expression was pre...
Saved in:
Published in: | Heliyon Vol. 9; no. 10; p. e20651 |
---|---|
Main Authors: | , , , , , , |
Format: | Journal Article |
Language: | English |
Published: |
Elsevier Ltd
01-10-2023
Elsevier |
Subjects: | |
Online Access: | Get full text |
Tags: |
Add Tag
No Tags, Be the first to tag this record!
|
Summary: | Long non-coding RNAs (lncRNAs) are essential in many biological areas like cell growth and apoptosis. The role of recently discovered LINC00702 is yet to be explored. Therefore, we wanted to elucidate its role in breast cancer (BC) with bioinformatic and various methods. LINC00702 expression was predicted using bioinformatic analysis and confirmed by RT-qPCR. Furthermore, the impact of LINC00702 knockdown on BC progression was evaluated. High LINC00702 level could lead to a worse outcome in BC patients. Additionally, CCK-8, EdU,and Annexin V-APC7/AAD experiments showed that LINC00702 knockdown inhibited the growth of BT-474 and T-47D cells and promoted their apoptosis. Moreover, in vivo experiments showed that shLINC00702-2 significantly reduced tumor sizes and suppressed c-Myc and β-catenin expressions. On the contrary, a rescue assay showed that HLY78, an activator of the Wnt/β-catenin pathway, reversed the cell-inhibiting impact of LINC00702 knockdown. LINC00702 is an oncogenic lncRNA that promotes BC progression by stimulating the Wnt/β-catenin pathway and downstream proteins, making it a promising target for further research on BC treatment. |
---|---|
Bibliography: | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 These authors contributed equally. |
ISSN: | 2405-8440 2405-8440 |
DOI: | 10.1016/j.heliyon.2023.e20651 |