LncOCMRL1 promotes oral squamous cell carcinoma growth and metastasis via the RRM2/EMT pathway
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Updated: Jun 11, 2025

Induction of Mesenchymal-Epithelial Transitions in Sarcoma Cells
Published on: April 7, 2017
Nan Lu1,2,3, Qiming Jiang1,3,4,5, Tianshu Xu1,3,4,6
1Guangdong Provincial Key Laboratory of Malignant Tumor Epigenetics and Gene Regulation, Guangdong-Hong Kong Joint Laboratory for RNA Medicine, Medical Research Center, Sun Yat-Sen Memorial Hospital, Sun Yat-Sen University, Guangzhou, 510120, PR China.
Background:
Long noncoding RNAs (lncRNAs) are widely involved in cancer development and progression, but the functions of most lncRNAs have not yet been elucidated. Metastasis is the main factor restricting the therapeutic outcomes of various cancer types, including oral squamous cell carcinoma (OSCC). Therefore, exploring the key lncRNAs that regulate OSCC metastasis and elucidating their molecular mechanisms will facilitate the development of new strategies for effective OSCC therapy.
Methods:
We analyzed the lncRNA expression profiles of tumor tissues from OSCC patients with and without cervical lymph node metastasis, and OSCC cell lines. We revealed high expression of oral squamous cell carcinoma metastasis-related lncRNA 1 (lncOCMRL1) in OSCC patient tumor tissues with lymph node metastasis and highly metastatic OSCC cell lines. The effects of lncOCMRL1 knockdown on the invasion, migration and proliferation abilities of OSCC cells were explored through qRT-PCR, Transwell, colony formation, and cell proliferation experiments. The mechanism by which lncOCMRL1 promotes OSCC metastasis and proliferation was explored through RNA pull-down, silver staining, mass spectrometry, RIP, and WB experiments. To increase its translational potential, we developed a reduction-responsive nanodelivery system to deliver siRNA for antitumor therapy.
Results:
We determined that lncOCMRL1 is highly expressed in OSCC metastatic tumor tissues and cells. Functional studies have shown that high lncOCMRL1 expression can promote the growth and metastasis of OSCC cells both in vivo and in vitro. Mechanistically, lncOCMRL1 could induce epithelial-mesenchymal transition (EMT) via the suppression of RRM2 ubiquitination and thereby promote the proliferation, invasion, and migration of OSCC cells. We further constructed reduction-responsive nanoparticles (NPs) for the systemic delivery of siRNAs targeting lncOCMRL1 and demonstrated their high efficacy in silencing lncOCMRL1 expression in vivo and significantly inhibited OSCC tumor growth and metastasis.
Conclusions:
Our results suggest that lncOCMRL1 is a reliable target for blocking lymph node metastasis in OSCC.
Insights
Oral squamous cell carcinoma metastasis-related lncRNA 1 (lncOCMRL1) promotes cancer growth and metastasis. Targeting lncOCMRL1 with nanoparticles effectively inhibits oral cancer progression and metastasis.
Area of Science:
- Oncology
- Molecular Biology
- Biotechnology
Background:
- Long noncoding RNAs (lncRNAs) play roles in cancer, but their functions are often unknown.
- Metastasis limits treatment outcomes in cancers like oral squamous cell carcinoma (OSCC).
- Identifying key lncRNAs in OSCC metastasis is crucial for developing new therapies.
Purpose of the Study:
- To investigate the role of oral squamous cell carcinoma metastasis-related lncRNA 1 (lncOCMRL1) in OSCC metastasis.
- To elucidate the molecular mechanisms by which lncOCMRL1 promotes OSCC progression.
- To develop a targeted nanodelivery system for lncOCMRL1-based therapy.
Main Methods:
- Analyzed lncRNA expression profiles in OSCC tissues and cell lines.
- Performed functional assays (Transwell, colony formation) to assess OSCC cell invasion, migration, and proliferation after lncOCMRL1 knockdown.
- Utilized molecular techniques (RNA pull-down, mass spectrometry, RIP, WB) to explore the underlying mechanisms.
- Developed and tested reduction-responsive nanoparticles for siRNA delivery.
Main Results:
- lncOCMRL1 expression is elevated in metastatic OSCC tissues and cells.
- High lncOCMRL1 expression promotes OSCC growth and metastasis in vitro and in vivo.
- lncOCMRL1 induces epithelial-mesenchymal transition (EMT) by suppressing RRM2 ubiquitination, enhancing proliferation and metastasis.
- Nanoparticle-mediated delivery of siRNA targeting lncOCMRL1 effectively inhibited OSCC tumor growth and metastasis in vivo.
Conclusions:
- lncOCMRL1 is a key driver of OSCC metastasis.
- lncOCMRL1 is a potential therapeutic target for blocking lymph node metastasis in OSCC.
- Nanoparticle-based delivery of lncOCMRL1 siRNA shows promise for OSCC treatment.
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