Background
Long-chain non-coding RNA (LINC00261) in the treatment of papillary thyroid carcinoma (PTC) with 131I is still unknown despite its proven anti-tumour effect in thyroid cancer (TC) and other types of cancer.
Conclusions
LINC00261 activates DNA damage in 131I-resistant PTC cells caused by miR-23a-3p/CELF2 axis, improving the progression of cancer cells of PTC.
Methods
The database and RT-qPCR were used to analyze the expression level of LINC00261 in PTC and cell lines. PTC cells resistant to 131I (TPC-1/R) were created through ongoing exposure to a lethal dose of 131I, and a subcutaneous xenotransplantation model was developed using PTC mice. Bioinformatics analysis and dual-luciferase assays demonstrated the interaction between LINC00261, miR-23a-3p, and CELF2. RT-qPCR and Western blot were used to detect the expression of LINC00261, miR-23a-3p, and CELF2. Additionally, CCK-8, flow cytometry, immunofluorescence (IF), Western blot, and comet assay were employed to measure cell viability level and DNA damage.
Results
PTC cell lines exhibited a decrease in the expression of LINC00261. The growth and progression through the S-phase of TPC-1/R cells were suppressed by LINC00261, leading to increased apoptosis and DNA damage. The objective of LINC00261 was to regulate the axis of miR-23a-3p/CELF2. Downregulating LINC00261 enhances the growth and advancement of 131I-resistant cells in the S-phase by activating the miR-23a-3p/CELF2 pathway while suppressing cell death and DNA harm. The miR-23a-3p/CELF2 axis activates DNA damage in 131I-resistant PTC cells by LINC00261. Conclusions: LINC00261 activates DNA damage in 131I-resistant PTC cells caused by miR-23a-3p/CELF2 axis, improving the progression of cancer cells of PTC.