Long non-coding RNA colon cancer-associated transcript 1 - Vimentin axis promoting the migration and invasion of HeLa cells

Sep 24, 2026

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Long non-coding RNA CCAT1 is implicated in malignant transformation across multiple cancers, yet how CCAT1-protein interactions drive tumor metastasis remains unclear. This study aimed to identify proteome-wide CCAT1 partners and define CCAT1-mediated interactions relevant to metastasis. CCAT1-protein complexes were analyzed by RAP-MS and validated using RNA pull-down and RNA immunoprecipitation. Functional effects on migration and invasion were assessed in HeLa cells.

LanguageEnglish

CategoryHealthcare

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Pages11

Reading Time28 min

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Abstract

Background

Methods

Results

Conclusion

Introduction

RNA binding proteins (RBPs)

Vimentin

Long non-coding RNA colon cancer-associated transcript 1-Vimentin axis promoting the migration and invasion of HeLa cells Zhangfu Li1, Jiangbei Yuan1, Qingen Da1,2, Zilong Yan1, Jianhua Qu3, Dan Li4, Xu Liu3, Qimin Zhan4,5, Jikui Liu3 1 Department of Hepato-Pancreato-Biliary Surgery, Peking University Shenzhen Hospital, Shenzhen Peking University-The Hong Kong University of Science and Technology Medical Center, Shenzhen, Guangdong 518036, China; 2 Department of Cardiovascular Surgery, Peking University Shenzhen Hospital, Shenzhen Peking University-The Hong Kong University of Science and Technology Medical Center, Shenzhen, Guangdong 518036, China; 3 Department of Hepato-Pancreato-Biliary Surgery, Peking University Shenzhen Hospital, Shenzhen, Guangdong 518036, China; 4State Key Laboratory of Molecular Oncology, National Cancer Institute and Cancer Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing 100021, China; 5 Key Laboratory of Carcinogenesis and Translational Research (Ministry of Education/Beijing), Laboratory of Molecular Oncology, Peking University Cancer Hospital & Institute, Beijing 100142, China. Abstract Background: Long non-coding RNA colon cancer-associated transcript 1 (CCAT1) is involved in transforming multiple cancers into malignant cancer types. Previous studies underlining the mechanisms ofthe functions of CCAT1 primarily focused on its decoy for miRNAs (micro RNAs). However, the regulatory mechanism of CCAT1–protein interaction associated with tumor metastasis is still largely unknown. The present study aimed to identify proteome-wide CCAT1 partners and explored the CCAT1–protein interaction mediated tumor metastasis. Methods: CCAT1–proteins complexes were puriﬁed and identiﬁed using RNA antisense puriﬁcation coupled with the mass spectrometry (RAP-MS) method. The database for annotation, visualization, and integrated discovery and database for eukaryotic RNA binding proteins (EuRBPDB) websites were used to bioinformatic analyzing CCAT1 binding proteins. RNA pull-down and RNA immunoprecipitation were used to validate CCAT1–Vimentin interaction. Transwell assay was used to evaluate the migration and invasion abilities of HeLa cells. Results: RAP-MS method worked well by culturing cells with nucleoside analog 4-thiouridine, and cross-linking was performed using 365 nm wavelength ultraviolet. There were 631 proteins identiﬁed, out of which about 60% were RNA binding proteins recorded by the EuRBPDB database. Vimentin was one of the CCAT1 binding proteins and participated in the tumor metastasis pathway. Knocked down vimetin (VIM) and rescued the downregulation by overexpressing CCAT1 demonstrated that CCAT1 could enhance tumor migration and invasion abilities by stabilizing Vimentin protein. Conclusion: CCAT1 may bind with and stabilize Vimentin protein, thus enhancing cancer cell migration and invasion abilities. Keywords: lncRNA CCAT1; RAP-MS; RNA binding protein; Vimentin; Migration; Invasion Introduction Colon cancer-associated transcript 1 (CCAT1) is anoncogenic long non-coding RNA (lncRNA) located at 8q24.21, a commonly ampliﬁed genomic area in various human cancers. [1] Consistent with this, multiple human cancer tissues show a higher CCAT1 expression than the corresponding adjacent normal tissues. [2] Studies have identiﬁed that CCAT1 is highly involved in migration, invasion, proliferation, and chemoresistance in cancer development. [3-5] Mechanistically, CCAT1 may regulate | Access this article online | | | --- | --- | | Quick Response Code:
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[www.cmj.org](www.cmj.org) | | | DOI:
10.1097/CM9.0000000000002373 | gene expression by binding with transcriptional factors that inﬂuence the promoter activity of target genes. [6,7] CCAT1 also serves as a competing endogenous RNA to sponge miRNAs that affect kinase signaling regulatory pathways. [4,8,9] Recently, several studies have focused on lncRNA–protein interactio

FAQs

What is the main goal of the study on CCAT1?

To identify proteome-wide CCAT1 partners and clarify how CCAT1-protein interactions mediate tumor metastasis.

How were CCAT1-protein partners identified?

CCAT1-protein complexes were purified and identified using RNA antisense purification coupled with mass spectrometry (RAP-MS), with bioinformatic analysis of CCAT1 binding proteins.

How did CCAT1 affect HeLa cell migration and invasion?

CCAT1 increased migration and invasion abilities by stabilizing Vimentin protein; knockdown of VIM reduced effects and was rescued by CCAT1 overexpression.

Sep 24, 2026

Uploaded by Cipher