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Role of the NKILA-miR-889-3p Axis in Regulating Proliferation Migration and Invasion of Oral Squamous Cell Carcinoma Cells |
YANG Shuo, et al |
Shijiazhuang People's Hospital, Hebei Shijiazhuang 050000, China |
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Abstract Objective: To analyze the expression and clinical significance of the long non-coding RNA NKILA in oral squamous cell carcinoma (OSCC), investigate the regulatory mechanism between NKILA and its potential target miRNA, and elucidate its role in OSCC development.Methods: Eighty OSCC patients confirmed by pathology and corresponding adjacent normal oral mucosa tissue samples were collected. The expression level of NKILA and its correlation with prognosis were detected using qRT-PCR. The effects of NKILA on OSCC cell proliferation, migration, and invasion were evaluated through colony formation assays and Transwell assays. Subcellular fractionation experiments were conducted to determine the subcellular localization of NKILA. LncBase was used to predict potential target miRNAs of NKILA. AGO2 immunoprecipitation experiments were performed to validate the interaction between miR-889-3p and NKILA.Results: NKILA expression was significantly downregulated in OSCC tissues compared to adjacent normal tissues (P<0.0001). Low expression of NKILA was significantly associated with advanced TNM stage, lymph node metastasis, and distant metastasis in OSCC patients (P=0.001, P=0.046, P=0.011). Cell experiments demonstrated that knockdown of NKILA significantly promoted OSCC cell migration and invasion (P<0.05), while overexpression of NKILA significantly inhibited these cellular functions (P<0.05). Subcellular localization experiments showed that NKILA primarily localized in the cytoplasm. miR-889-3p was identified as a potential target of NKILA, and overexpression of NKILA significantly upregulated miR-889-3p expression (P<0.05), and vice versa. AGO2 immunoprecipitation experiments further confirmed that miR-889-3p specifically binds to and regulates NKILA (P<0.05).Conclusion: This study elucidates the downregulation of NKILA in OSCC development and its potential functional mechanisms. It reveals an important regulatory interaction between NKILA and miR-889-3p, providing new insights for the study and treatment of OSCC.
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