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LncRNA MALAT1 expression inhibition suppresses tongue squamous cell carcinoma proliferation, migration and invasion
1Department of Stomatology, The Third Affiliated Hospital of Sun Yat-sen University, Guangzhou City, Guangdong Province, China. exl4qdesd5wj@163.com.
Objective:
LncRNA MALAT1 has been proved to be involved in the development of various types of human cancers while the involvement of MALAT1 in tongue squamous cell carcinoma has not been reported. In view of this, our study aimed to investigate the functionality of MALAT1 in tongue squamous cell carcinoma.
Patients And Methods:
The expression of MALAT1 in tumor tissues and adjacent healthy tissues of tongue cancer patients, and the serum from tongue cancer patients as well as healthy controls, were detected by quantitative Real Time-PCR (qRT-PCR). ROC curve analysis was performed to analyze the diagnostic value of plasma MALAT1 for tongue cancer. Survival curves were plotted using the Kaplan-Meier method to evaluate the prognostic value of plasma MALAT1 for tongue cancer. CCK-8 assay, transwell migration and invasion assay were performed to investigate the effects of MALAT1 knockdown on the proliferation, migration and invasion of tongue cancer cells, respectively. The effects of MALAT1 overexpression on the PI3K/Akt pathway and MMP-9 expression were detected by Western blot.
Results:
The expression level of MALAT1 was remarkably higher in tumor tissues than that in adjacent healthy tissues. Serum MALAT1 was significantly higher in tongue cancer patients than in healthy controls. MALAT1 knockdown markedly inhibits the proliferation, migration and invasion of tongue cancer cells. MALAT1 knockdown also reduced the phosphorylation level of Akt as well as the expression level of MMP-9. It showed no significant effects on Akt expression, while PI3K activator treatment reduced the inhibitory effects of MALAT1 knockdown on the proliferation, migration and invasion of tongue cancer cells.
Conclusions:
LncRNA MALAT1 expression inhibition can inhibit the proliferation, migration and invasion of tongue cancer cells by inactivating the PI3K/Akt pathway and downregulating MMP-9. MALAT1 may serve as a target for the treatment of tongue squamous cell carcinoma.
Insights
Long non-coding RNA MALAT1 is elevated in tongue cancer, promoting cell proliferation, migration, and invasion. Inhibiting MALAT1 may offer a therapeutic strategy for tongue squamous cell carcinoma by affecting the PI3K/Akt pathway.
Area of Science:
- Oncology
- Molecular Biology
- Biochemistry
Background:
- Long non-coding RNA MALAT1 is implicated in various human cancers.
- The role of MALAT1 in tongue squamous cell carcinoma (TSCC) remains uninvestigated.
Purpose of the Study:
- To investigate the functional role of MALAT1 in tongue squamous cell carcinoma.
- To explore MALAT1 as a potential diagnostic marker and therapeutic target for TSCC.
Main Methods:
- Quantitative Real-Time PCR (qRT-PCR) to assess MALAT1 expression in tissues and serum.
- Receiver Operating Characteristic (ROC) curve analysis for diagnostic value.
- Kaplan-Meier survival analysis for prognostic value.
- Cell proliferation, migration, and invasion assays (CCK-8, Transwell).
- Western blot to analyze PI3K/Akt pathway and MMP-9 expression.
Main Results:
- MALAT1 expression is significantly upregulated in TSCC tissues and serum compared to healthy controls.
- MALAT1 knockdown inhibits TSCC cell proliferation, migration, and invasion.
- MALAT1 knockdown reduces Akt phosphorylation and MMP-9 expression, impacting the PI3K/Akt pathway.
- PI3K activation partially reverses the inhibitory effects of MALAT1 knockdown.
Conclusions:
- Inhibition of MALAT1 suppresses TSCC progression by inactivating the PI3K/Akt pathway and downregulating MMP-9.
- MALAT1 represents a promising therapeutic target for tongue squamous cell carcinoma.
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