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Long Non-Coding RNA RAB11B-AS1 Suppresses Cervical Cancer Progression by Upregulating RPL26 Expression
Xuemin Gu1, Yuanyuan Yang1, Zhixia Zhang1
1Department of Obstetrics and Gynaecology, Shanghai Tongji Hospital of Tongji University, Tongji University School of Medicine, 200065 Shanghai, China.
Background:
Cervical cancer (CC) is one of the most prevalent gynecological malignancies. The expression and functional role of the long non-coding RNA (lncRNA) Ras-related protein Rab-11B antisense RNA 1 (RAB11B-AS1) in CC remain poorly understood.
Methods:
The expression profile of lncRNA RAB11B-AS1 across multiple cancer types was initially assessed using data from The Cancer Genome Atlas. Its expression in CC tissues and lesions of varying pathological grades was subsequently validated via RNA in situ hybridization. To investigate its functional role in CC, a combination of transcriptomic, proteomic, and functional assays was employed to delineate the molecular role of RAB11B-AS1. The effects of alterations in RAB11B-AS1 expression on cervical cancer growth were ultimately validated in vivo.
Results:
LncRNA RAB11B-AS1 was downregulated in CC and associated with a favorable patient prognosis. Functionally, RAB11B-AS1 promoted apoptosis while suppressing proliferation, migration, and invasion of CC cells in vitro, and inhibited tumor growth in vivo. Mechanistically, RAB11B-AS1 upregulated ribosomal protein L26 (RPL26) expression. Notably, RAB11B-AS1 suppressed cervical cancer progression by activating the p53 pathway via RPL26. Critically, in vitro and in vivo experiments confirmed that RPL26 knockdown abrogates the tumor-suppressive functions of RAB11B-AS1, establishing RPL26 as a pivotal downstream effector of RAB11B-AS1 in CC.
Conclusions:
Our findings demonstrate that lncRNA RAB11B-AS1 suppresses cervical cancer progression primarily through upregulation of RPL26 and suggest that RAB11B-AS1 may serve as a potential biomarker and therapeutic target in cervical cancer.
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