Disruption of LINC00265/miR-101-3p axis using siRNA suppresses growth and promotes apoptosis in laryngeal cancer cells

Laryngeal cancer is a prevalent malignancy of the head and neck, often associated with poor prognosis due to late diagnosis and therapeutic resistance. Emerging evidence highlights the important role of long non-coding RNAs (lncRNAs) in cancer progression, including LINC00265, which has been implicated in promoting tumor growth and metastasis in various cancers. Conversely, miR-101 functions as a tumor suppressor by targeting oncogenic pathways. Understanding the regulatory interaction between LINC00265 and miR-101 can provide new insights into disease biology. We evaluated LINC00265 expression in 30 paired LSCC and adjacent normal tissues using qRT-PCR, which was followed by analyzing its correlation with clinicopathological features. To investigate LINC00265 functional effects, HN5 cells were transfected with LINC00265-specific siRNA, and afterward, cell viability and apoptosis were assessed through MTT assay and Annexin V/PI flow cytometry, respectively. Our results showed that LINC00265 was significantly overexpressed in LSCC tissues (2.52-fold increase, p < 0.0129), which was correlated with larger tumor size and lymph node metastasis. Moderate diagnostic accuracy for metastasis detection was demonstrated by ROC analysis (AUC = 0.74, p = 0.0276). Moreover, the knockdown of LINC00265 in HN5 cells significantly reduced cell viability by 30 %, and increased apoptosis up to 36.03 % potentially through upregulation of miR-101 (1.53-fold, p = 0.0012). Our study proposes that LINC00265 might exert an oncogenic effect in LSCC by promoting tumor progression, potentially through miR-101 suppression. Its association with metastasis and larger tumor size suggests clinical relevance as a prognostic biomarker. The knockdown of LINC00265 demonstrated anti-proliferative and pro-apoptotic effects that could suggest its therapeutic potential for LSCC treatment. • LINC00265 is significantly overexpressed in LSCC tissues (2.52-fold, p < 0.01). • LINC00265 overexpression correlates with aggressive LSCC features. • LINC00265 knockdown significantly reduces cell viability and induces apoptosis. • LINC00265 inversely regulates tumor suppressor miR-101-3p expression. • First study identifying LINC00265 oncogenic role in laryngeal cancer.