NOP2‐Mediated m5C Methylation Modification of LMNB2 mRNA Facilitates Colorectal Cancer Progression

ABSTRACT Background Colorectal cancer (CRC) is a leading cause of cancer‐related mortality globally, yet current therapies exhibit suboptimal efficacy with limited prognostic improvement. RNA 5‐methylcytosine (m5C), a posttranscriptional modification, has been implicated in tumorigenesis and progres...

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Main Authors: Jinling Bi, Yong Huang, Wentao Hu, Yulong Liu
Format: Article
Language:English
Published: Wiley 2025-05-01
Series:Cancer Medicine
Subjects:
Online Access:https://doi.org/10.1002/cam4.70970
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author Jinling Bi
Yong Huang
Wentao Hu
Yulong Liu
author_facet Jinling Bi
Yong Huang
Wentao Hu
Yulong Liu
author_sort Jinling Bi
collection DOAJ
description ABSTRACT Background Colorectal cancer (CRC) is a leading cause of cancer‐related mortality globally, yet current therapies exhibit suboptimal efficacy with limited prognostic improvement. RNA 5‐methylcytosine (m5C), a posttranscriptional modification, has been implicated in tumorigenesis and progression across malignancies. In our previous study, the m5C methyltransferase NOP2 has been shown to promote proliferation, migration, and invasion of CRC cells, however, the underlying mechanism is still elusive. Methods An integrated multi‐omics strategy was employed, combining transcriptomic sequencing, RNA immunoprecipitation sequencing (RIP‐seq), and methylated RNA immunoprecipitation sequencing (MeRIP‐seq) to explore NOP2‐regulated downstream genes mediating CRC progression via m5C methylation. Functional validation included in vitro and in vivo assays to assess tumor growth and metastasis. Rescue experiments were performed by overexpressing LMNB2 in NOP2‐silenced CRC cells. Results NOP2‐dependent m5C modification of LMNB2 mRNA enhanced its stability, leading to elevated LMNB2 protein levels. This mechanism drove CRC tumor growth and metastasis both in vitro and in vivo. Overexpression of LMNB2 effectively rescued the suppressed malignant phenotypes induced by NOP2 knockdown, confirming LMNB2 as a critical downstream effector. Conclusion NOP2 catalyzes the m5C modification of LMNB2 mRNA to facilitate its stability, which contributes to the elevated LMNB2 protein level and CRC progression, suggesting the potential of NOP2 as a therapeutic target in the development of novel CRC treatment.
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spelling doaj-art-06b108eaa0d044109456dec8c7f344eb2025-08-20T02:30:05ZengWileyCancer Medicine2045-76342025-05-011410n/an/a10.1002/cam4.70970NOP2‐Mediated m5C Methylation Modification of LMNB2 mRNA Facilitates Colorectal Cancer ProgressionJinling Bi0Yong Huang1Wentao Hu2Yulong Liu3Department of Oncology The Second People's Hospital of Hefei Hefei ChinaDepartment of Oncology The Second People's Hospital of Hefei Hefei ChinaState Key Laboratory of Radiation Medicine and Protection, School of Radiation Medicine and Protection, Collaborative Innovation Center of Radiological Medicine of Jiangsu Higher Education Institutions Soochow University Suzhou ChinaDepartment of Oncology The Second Affiliated Hospital of Soochow University Suzhou ChinaABSTRACT Background Colorectal cancer (CRC) is a leading cause of cancer‐related mortality globally, yet current therapies exhibit suboptimal efficacy with limited prognostic improvement. RNA 5‐methylcytosine (m5C), a posttranscriptional modification, has been implicated in tumorigenesis and progression across malignancies. In our previous study, the m5C methyltransferase NOP2 has been shown to promote proliferation, migration, and invasion of CRC cells, however, the underlying mechanism is still elusive. Methods An integrated multi‐omics strategy was employed, combining transcriptomic sequencing, RNA immunoprecipitation sequencing (RIP‐seq), and methylated RNA immunoprecipitation sequencing (MeRIP‐seq) to explore NOP2‐regulated downstream genes mediating CRC progression via m5C methylation. Functional validation included in vitro and in vivo assays to assess tumor growth and metastasis. Rescue experiments were performed by overexpressing LMNB2 in NOP2‐silenced CRC cells. Results NOP2‐dependent m5C modification of LMNB2 mRNA enhanced its stability, leading to elevated LMNB2 protein levels. This mechanism drove CRC tumor growth and metastasis both in vitro and in vivo. Overexpression of LMNB2 effectively rescued the suppressed malignant phenotypes induced by NOP2 knockdown, confirming LMNB2 as a critical downstream effector. Conclusion NOP2 catalyzes the m5C modification of LMNB2 mRNA to facilitate its stability, which contributes to the elevated LMNB2 protein level and CRC progression, suggesting the potential of NOP2 as a therapeutic target in the development of novel CRC treatment.https://doi.org/10.1002/cam4.70970colorectal cancerLMNB2m5CmethyltransferaseNOP2
spellingShingle Jinling Bi
Yong Huang
Wentao Hu
Yulong Liu
NOP2‐Mediated m5C Methylation Modification of LMNB2 mRNA Facilitates Colorectal Cancer Progression
Cancer Medicine
colorectal cancer
LMNB2
m5C
methyltransferase
NOP2
title NOP2‐Mediated m5C Methylation Modification of LMNB2 mRNA Facilitates Colorectal Cancer Progression
title_full NOP2‐Mediated m5C Methylation Modification of LMNB2 mRNA Facilitates Colorectal Cancer Progression
title_fullStr NOP2‐Mediated m5C Methylation Modification of LMNB2 mRNA Facilitates Colorectal Cancer Progression
title_full_unstemmed NOP2‐Mediated m5C Methylation Modification of LMNB2 mRNA Facilitates Colorectal Cancer Progression
title_short NOP2‐Mediated m5C Methylation Modification of LMNB2 mRNA Facilitates Colorectal Cancer Progression
title_sort nop2 mediated m5c methylation modification of lmnb2 mrna facilitates colorectal cancer progression
topic colorectal cancer
LMNB2
m5C
methyltransferase
NOP2
url https://doi.org/10.1002/cam4.70970
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AT yonghuang nop2mediatedm5cmethylationmodificationoflmnb2mrnafacilitatescolorectalcancerprogression
AT wentaohu nop2mediatedm5cmethylationmodificationoflmnb2mrnafacilitatescolorectalcancerprogression
AT yulongliu nop2mediatedm5cmethylationmodificationoflmnb2mrnafacilitatescolorectalcancerprogression