Tao Qingyuan, Li Xiaojin, Xia Yanyan, Zheng Bin, Yan Yijun, Wang Songrun, Jia Li
The Affiliated Hospital of Yunnan University (Yunnan Second People's Hospital), Nuclear Medicine, Kunming, Yunnan, 650021, China.
The Affiliated Hospital of Yunnan University (Yunnan Second People's Hospital), Central Laboratory, Kunming, Yunnan, 650021, China.
Biochem Biophys Rep. 2024 Oct 30;40:101858. doi: 10.1016/j.bbrep.2024.101858. eCollection 2024 Dec.
Long-chain non-coding RNA (LINC00261) in the treatment of papillary thyroid carcinoma (PTC) with I is still unknown despite its proven anti-tumour effect in thyroid cancer (TC) and other types of cancer.
The database and RT-qPCR were used to analyze the expression level of LINC00261 in PTC and cell lines. PTC cells resistant to I (TPC-1/R) were created through ongoing exposure to a lethal dose of I, 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.
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 I-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 I-resistant PTC cells by LINC00261.
LINC00261 activates DNA damage in I-resistant PTC cells caused by miR-23a-3p/CELF2 axis, improving the progression of cancer cells of PTC.
长链非编码RNA（LINC00261）在甲状腺癌（TC）和其他类型癌症中已被证实具有抗肿瘤作用，但其在碘（I）治疗乳头状甲状腺癌（PTC）中的作用仍不清楚。
利用数据库和RT-qPCR分析LINC00261在PTC及细胞系中的表达水平。通过持续暴露于致死剂量的I建立对I耐药的PTC细胞（TPC-1/R），并利用PTC小鼠建立皮下异种移植模型。生物信息学分析和双荧光素酶测定证实了LINC00261、miR-23a-3p和CELF2之间的相互作用。采用RT-qPCR和蛋白质免疫印迹法检测LINC00261、miR-23a-3p和CELF2的表达。此外，使用CCK-8、流式细胞术、免疫荧光（IF）、蛋白质免疫印迹法和彗星试验来测量细胞活力水平和DNA损伤。
PTC细胞系中LINC00261表达降低。LINC00261抑制TPC-1/R细胞的生长及S期进程，导致细胞凋亡增加和DNA损伤。LINC00261的作用靶点是调控miR-23a-3p/CELF2轴。下调LINC00261通过激活miR-23a-3p/CELF2途径增强I耐药细胞在S期的生长和进程，同时抑制细胞死亡和DNA损伤。LINC00261通过miR-23a-3p/CELF2轴激活I耐药PTC细胞中的DNA损伤。
LINC00261通过miR-23a-3p/CELF2轴激活I耐药PTC细胞中的DNA损伤，促进PTC癌细胞进展。
