RBM15/IGF2BP1-mediated m 6A methylation of AKR1B10 promotes the progression of cervical squamous cell carcinoma
Abstract
Objective: RNA-binding motif protein 15 (RBM15) is a methyltransferase involved in N 6-methyladenosine (m 6A) modification and has been shown to be associated with the initiation and progression of various malignancies. This study aims to investigate the biological function and underlying mechanism by which RBM15 promotes the progression of cervical squamous cell carcinoma (CSCC) through in vitro and in vivo experiments.
Methods: The Cancer Genome Atlas (TCGA) and Gene Expression Omnibus (GEO) databases were used to analyze differences in the mRNA expression levels of RBM15, aldo-keto reductase family 1 member B10 ( AKR1B10), and insulin-like growth factor 2 mRNA-binding protein 1 ( IGF2BP1) between CSCC and adjacent non-tumor tissues, as well as the associations of RBM15, AKR1B10, and IGF2BP1 expression with overall survival in patients with CSCC. Real-time PCR and Western blotting (WB) were used to determine the expression levels of RBM15, AKR1B10, and IGF2BP1 in CSCC tissues and adjacent normal tissues. Cell Counting Kit-8 (CCK-8), colony formation, 5-ethynyl-2’-deoxyuridine (EdU) staining, wound-healing, and Transwell migration and invasion assays were performed to investigate the effects of RBM15 knockdown on the proliferation, migration, and invasion of CSCC cells. A nude mouse xenograft model was established to evaluate the effect of RBM15 knockdown on tumor growth. Methylated RNA immunoprecipitation (MeRIP) was performed to assess m6A modification of AKR1B10. RNA immunoprecipitation (RIP) and actinomycin D assays were used to analyze the interactions of RBM15 and IGF2BP1 with AKR1B10 mRNA. Small interfering RNAs (siRNAs), including si-IGF2BP1 and si-YTHDF1, were used to knock down IGF2BP1 or YTH N6-methyladenosine RNA-binding protein F1 ( YTHDF1), respectively, and their roles in regulating AKR1B10 mRNA stability were analyzed.
Results: Analysis of TCGA and GEO data showed that the mRNA and protein expression levels of RBM15, AKR1B10, and IGF2BP1 were significantly up-regulated in CSCC tissues (all P<0.05), and high expression of RBM15, AKR1B10, and IGF2BP1 was significantly associated with poor prognosis in patients with CSCC (all P<0.05). In vitro experiments showed that RBM15 knockdown inhibited the proliferation, invasion, and migration of CSCC cells, while in vivo experiments showed that RBM15 knockdown inhibited tumor growth (all P<0.05). MeRIP and actinomycin D assays showed that RBM15 knockdown significantly reduced the m 6A methylation level of AKR1B10 and decreased its mRNA stability. RIP assays showed that RBM15 knockdown significantly reduced the binding of RBM15 and IGF2BP1 to AKR1B10 mRNA (all P<0.05). IGF2BP1-dependency experiments showed that si-IGF2BP1 treatment significantly decreased AKR1B10 mRNA expression ( P<0.05), whereas no significant change was observed in the si-YTHDF1 group ( P>0.05).
Conclusion: RBM15-mediated m 6A modification promotes CSCC progression through the IGF2BP1-AKR1B10 axis. RBM15 may serve as a potential biomarker for predicting outcomes in patients with CSCC.
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BibTeX
@article{陈2026rbm15igf2bp1mediated,
title = {{RBM15/IGF2BP1-mediated m 6A methylation of AKR1B10 promotes the progression of cervical squamous cell carcinoma}},
author = {义波 陈 and 元娜 姜 and 前 王 and 周晓 何 and 轩昂 向 and 瑞琛 杨 and 兰琴 曹},
journal = {Journal of Central South University Medical Sciences},
year = {2026},
month = aug,
doi = {10.11817/j.issn.1672-7347.2026.250169},
url = {https://doi.org/10.11817/j.issn.1672-7347.2026.250169},
note = {CC BY-NC-ND 4.0},
}
RIS
TY - JOUR
TI - RBM15/IGF2BP1-mediated m 6A methylation of AKR1B10 promotes the progression of cervical squamous cell carcinoma
AU - 义波 陈
AU - 元娜 姜
AU - 前 王
AU - 周晓 何
AU - 轩昂 向
AU - 瑞琛 杨
AU - 兰琴 曹
PY - 2026
DA - 2026/08/28
JO - Journal of Central South University Medical Sciences
DO - 10.11817/j.issn.1672-7347.2026.250169
UR - https://doi.org/10.11817/j.issn.1672-7347.2026.250169
AB - Objective: RNA-binding motif protein 15 (RBM15) is a methyltransferase involved in N 6-methyladenosine (m 6A) modification and has been shown to be associated with the initiation and progression of various malignancies. This study aims to investigate the biological function and underlying mechanism by which RBM15 promotes the progression of cervical squamous cell carcinoma (CSCC) through in vitro and in vivo experiments. Methods: The Cancer Genome Atlas (TCGA) and Gene Expression Omnibus (GEO) databases were used to analyze differences in the mRNA expression levels of RBM15, aldo-keto reductase family 1 member B10 ( AKR1B10), and insulin-like growth factor 2 mRNA-binding protein 1 ( IGF2BP1) between CSCC and adjacent non-tumor tissues, as well as the associations of RBM15, AKR1B10, and IGF2BP1 expression with overall survival in patients with CSCC. Real-time PCR and Western blotting (WB) were used to determine the expression levels of RBM15, AKR1B10, and IGF2BP1 in CSCC tissues and adjacent normal tissues. Cell Counting Kit-8 (CCK-8), colony formation, 5-ethynyl-2’-deoxyuridine (EdU) staining, wound-healing, and Transwell migration and invasion assays were performed to investigate the effects of RBM15 knockdown on the proliferation, migration, and invasion of CSCC cells. A nude mouse xenograft model was established to evaluate the effect of RBM15 knockdown on tumor growth. Methylated RNA immunoprecipitation (MeRIP) was performed to assess m6A modification of AKR1B10. RNA immunoprecipitation (RIP) and actinomycin D assays were used to analyze the interactions of RBM15 and IGF2BP1 with AKR1B10 mRNA. Small interfering RNAs (siRNAs), including si-IGF2BP1 and si-YTHDF1, were used to knock down IGF2BP1 or YTH N6-methyladenosine RNA-binding protein F1 ( YTHDF1), respectively, and their roles in regulating AKR1B10 mRNA stability were analyzed. Results: Analysis of TCGA and GEO data showed that the mRNA and protein expression levels of RBM15, AKR1B10, and IGF2BP1 were significantly up-regulated in CSCC tissues (all P<0.05), and high expression of RBM15, AKR1B10, and IGF2BP1 was significantly associated with poor prognosis in patients with CSCC (all P<0.05). In vitro experiments showed that RBM15 knockdown inhibited the proliferation, invasion, and migration of CSCC cells, while in vivo experiments showed that RBM15 knockdown inhibited tumor growth (all P<0.05). MeRIP and actinomycin D assays showed that RBM15 knockdown significantly reduced the m 6A methylation level of AKR1B10 and decreased its mRNA stability. RIP assays showed that RBM15 knockdown significantly reduced the binding of RBM15 and IGF2BP1 to AKR1B10 mRNA (all P<0.05). IGF2BP1-dependency experiments showed that si-IGF2BP1 treatment significantly decreased AKR1B10 mRNA expression ( P<0.05), whereas no significant change was observed in the si-YTHDF1 group ( P>0.05). Conclusion: RBM15-mediated m 6A modification promotes CSCC progression through the IGF2BP1-AKR1B10 axis. RBM15 may serve as a potential biomarker for predicting outcomes in patients with CSCC.
SN - 1672-7347
ER -