Cervical cancer (CC) is considered to be the most prevalent female malignancies across the globe and a prime cause of mortality among women. RNA-binding motif protein 15 (RBM15) has been elucidated to participate in tumorigenesis in various cancers by regulating RNA N6-methyladenosine (m6A) methylation. However, its significance and detailed molecular mechanisms remain uncertain in CC. Using CGA database and qRT-PCR, the RBM15 expression was found to be elevated in CC tissues. After performing EdU, wound healing, Transwell migration, and xenograft tumor assays, RBM15 knockdown inhibited the malignant properties of CC cells along with the tumor development of CC cells in vivo. Moreover, qRT-PCR, MeRIP, and western blotting experiments were also confirmed that decorin (DCN) downregulated in CC was a direct substrate of RBM15 m6A methylation, and RBM15 knockdown could enhance DCN expression in CC cells. The anti-tumor effects of RBM15 knockdown could be abolished by DCN silencing. Overall, RBM15 knockdown lowered the tumorigenesis of CC both in vitro and in vivo, and it does so via mediating m6A modification of DCN mRNA in CC cells.
Download full-text PDF |
Source |
---|---|
http://dx.doi.org/10.1007/s10528-024-10757-x | DOI Listing |
Mol Med
December 2024
Department of Respiratory Medicine, The First Affiliated Hospital of Jilin University, 1 Xinmin Street, Changchun, 130021, Jilin, China.
Background: Non-small cell lung cancer (NSCLC) is the predominant form of lung cancer, contributing significantly to global health and economic challenges. This study elucidated the role of RBM15 in NSCLC progression through its involvement in m6A modifications.
Methods: RBM15 levels in NSCLC tissues and cells were assessed via RT-qPCR and Western blotting.
Am J Cancer Res
November 2024
Department of Central Laboratory, The Affiliated Huai'an No. 1 People's Hospital of Nanjing Medical University Huai'an 223001, Jiangsu, China.
Background: Collagen, a primary protein component of the extracellular matrix (ECM), undergoes a notable series of alterations concomitant with the growth of the tumor. Procollagen-lysine,2-oxoglutarate 5-dioxygenase 3 (PLOD3) is involved in the synthesis of collagen and has been associated with a variety of cancers. However, it is unclear how PLOD3 functions in esophageal squamous cell carcinoma (ESCC).
View Article and Find Full Text PDFMol Biotechnol
November 2024
Department of Geriatrics, Huanggang Central Hospital, No.126, Huangzhou District, Huanggang, 438000, Hubei, China.
The promotive effect of P53 apoptosis effector related to PMP-22 (PERP) on lung adenocarcinoma (LUAD) has been confirmed. However, the N6-methyladenosine (m6A) modification of PERP to regulate LUAD progression have not been revealed. Bioinformatic analysis predicted the mechanism of PERP interacting with RBM15 and p53 pathway using GEPIA and The Cancer Genome Atlas (TCGA) databases.
View Article and Find Full Text PDFMol Cell Biochem
November 2024
Orthopedic Center, Haikou Affiliated Hospital of Central South University Xiangya School of Medicine, No. 43, Haidian Island Peoples Avenue, Meilan District, Haikou, 570208, China.
Methionine adenosyltransferase 2 A (MAT2A) has been found to mediate osteosarcoma (OS) progression. Therefore, more roles and mechanisms of MAT2A in the development of OS deserve further exploration. The mRNA and protein levels of MAT2A and RNA binding motif protein 15 (RBM15) were tested by quantitative real-time PCR and western blot (WB).
View Article and Find Full Text PDFCurr Eye Res
November 2024
Department of Ophthalmology, Jiujiang City Key Laboratory of Cell Therapy, JiuJiang NO.1 People's Hospital, Jiujiang, Jiangxi, China.
Purpose: Diabetic cataract (DC) is a major cause of blindness worldwide. Prion protein (PRNP) was proved to be up-regulated and hypomethylated in DC samples. Here, we investigated whether PRNP was involved in DC progression in N6-methyladenosine (m6A)-dependent manner, and its potential mechanisms.
View Article and Find Full Text PDFEnter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!