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Updated: Oct 1, 2025
In Vivo Inhibition of MicroRNA to Decrease Tumor Growth in Mice
Published on: August 23, 2019
LINC00472 suppresses oral squamous cell carcinoma growth by targeting miR-455-3p/ELF3 axis
Xiu Liu1, Xinrong Ma1, Hongyu Li1
1Beijing Institute of Dental Research, Beijing Stomatological Hospital, Capital Medical University, Beijing, China.
Abstract:
LINC00472 is reported to play a role in suppressing tumors in cancers such as lung cancer and hepatocellular carcinoma, among others. We made investigations into the effects of LINC00472 in oral squamous cell carcinoma (OSCC) progression to explore the underlying molecular mechanisms. By qRT-PCR, we assessed the LINC00472 expression in OSCC tissues and cells and performed functional analysis to investigate how LINC00472/miR-455-3p/ELF3 impacts OSCC cell proliferation, apoptosis, and cell cycle. The role that LINC00472 plays in OSCC tumor growth was examined by establishing a xenograft model. Down-regulation of LINC00472 occurred in tissues and cells of an OSCC tumor. LINC00472 overexpression caused OSCC cell proliferation to be inhibited, cell apoptosis to be promoted, and cell cycle arrest to be induced. As a competing endogenous RNA (ceRNA), LINC00472 can block miR-455-3p function and further promote ELF3 expression. The overexpression of miR-455-3p or ELF3 knockdown was shown to be capable of reversing the anti-tumor effects of LINC00472 in OSCC. In vivo experiments confirmed the tumor-suppressing role of LINC00472 in the progression of OSCC. In short, we found that the novel LINC00472 inhibits OSCC growth via the miR-455-3p/ELF3 axis. LINC00472 and its targeted miR-455-3p/ELF3 axis may represent valuable targets for treating OSCC.
Insights
Long non-coding RNA LINC00472 suppresses oral squamous cell carcinoma (OSCC) growth by regulating the miR-455-3p/ELF3 pathway. This finding highlights LINC00472 as a potential therapeutic target for OSCC treatment.
Area of Science:
- Oncology
- Molecular Biology
- Genetics
Background:
- Long non-coding RNAs (lncRNAs) are increasingly recognized for their roles in cancer.
- LINC00472 has demonstrated tumor-suppressive functions in various cancers.
- Its specific role and mechanism in oral squamous cell carcinoma (OSCC) remain underexplored.
Purpose of the Study:
- To investigate the function of LINC00472 in oral squamous cell carcinoma (OSCC) progression.
- To elucidate the molecular mechanisms underlying LINC00472's effects in OSCC.
- To evaluate LINC00472 as a potential therapeutic target for OSCC.
Main Methods:
- Quantitative reverse transcription polymerase chain reaction (qRT-PCR) to assess LINC00472 expression.
- In vitro functional assays (proliferation, apoptosis, cell cycle) in OSCC cells.
- Xenograft models to examine in vivo tumor growth.
- Analysis of the LINC00472/miR-455-3p/ELF3 axis interactions.
Main Results:
- LINC00472 expression was significantly down-regulated in OSCC tissues and cells.
- Overexpression of LINC00472 inhibited OSCC cell proliferation, induced apoptosis, and caused cell cycle arrest.
- LINC00472 functions as a competing endogenous RNA (ceRNA), sponging miR-455-3p to upregulate ELF3 expression.
- Overexpression of miR-455-3p or knockdown of ELF3 reversed the anti-tumor effects of LINC00472.
- In vivo studies confirmed LINC00472's tumor-suppressive role in OSCC progression.
Conclusions:
- LINC00472 acts as a tumor suppressor in oral squamous cell carcinoma (OSCC).
- The novel LINC00472/miR-455-3p/ELF3 axis plays a critical role in regulating OSCC growth.
- LINC00472 and its associated axis represent promising therapeutic targets for OSCC treatment.
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