LncRNA MACC1-AS1 facilitates the cell growth of small cell lung cancer by sequestering miR-579-3p and mediating NOTCH1-pathway.

Autor: Hong J; Department of Thoracic Surgery, Changhai Hospital, Naval Medical University, Shanghai 200433, China., Gu R; Department of Thoracic Surgery, Third Affiliated Hospital of Naval Medical University, Shanghai 200438, China., Cheng W; Department of Thoracic Surgery, Changhai Hospital, Naval Medical University, Shanghai 200433, China., Lu C; Department of Thoracic Surgery, Changhai Hospital, Naval Medical University, Shanghai 200433, China. Electronic address: luchaojing@126.com., Wang X; Department of Thoracic Surgery, Changhai Hospital, Naval Medical University, Shanghai 200433, China. Electronic address: xiaoweiwang@genopub.com.
Jazyk: angličtina
Zdroj: International journal of biological macromolecules [Int J Biol Macromol] 2024 Nov; Vol. 281 (Pt 4), pp. 136579. Date of Electronic Publication: 2024 Oct 13.
DOI: 10.1016/j.ijbiomac.2024.136579
Abstrakt: As reported, long non-coding RNAs (lncRNAs) have been confirmed to be of great importance in regulating the progression of diseases, especially of cancers. LncRNA MACC1 antisense RNA 1 (MACC1-AS1) has been studied in some cancers, whereas its biological role and underlying mechanism is still unclear in small cell lung cancer (SCLC). In the current research, we found high level of MACC1-AS1 in SCLC cells. Subsequently, it was discovered that MACC1-AS1 knockdown considerably restrained the proliferative and migratory ability of SCLC cells by inducing the apoptosis. Importantly, the knockdown of MACC1-AS1 inhibited protein levels of genes of NOTCH pathway, and NOTCH pathway activator (Jagged1) countervailed the inhibition of MACC1-AS1 depletion on SCLC cell growth. Further, the deficiency of NOTCH1 hampered SCLC cell growth. More importantly, miR-579-3p was identified as a downstream gene of MACC1-AS1 and thereby targeted to NOTCH1. In addition, miR-579-3p repression recovered the suppressive role of MACC1-AS1 knockdown in NOTCH1 expression. Rescue assays indicated that repressed SCLC cell growth caused by MACC1-AS1 knockdown could be reserved by miR-579-3p repression or NOTCH1 overexpression. In brief, lncRNA MACC1-AS1 boosted SCLC cell growth via sequestering miR-579-3p and mediating NOTCH1-pathway.
Competing Interests: Declaration of competing interest The authors declare no competing interests.
(Copyright © 2024 Elsevier B.V. All rights reserved.)
Databáze: MEDLINE
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