Liang Ying, Cheng Gang, Huang Denggao, Yuan Feng
Department of Radiation Oncology, Affiliated Haikou Hospital of Xiangya Medical College, Central South University Haikou, Hainan Province, China.
Central Laboratory, Affiliated Haikou Hospital of Xiangya Medical College, Central South University Haikou, Hainan Province, China.
Am J Transl Res. 2021 Jun 15;13(6):6248-6259. eCollection 2021.
To explore the invasion and apoptosis of head and neck squamous cell carcinoma (HNSCC) regulated by Linc00467 through the miR-1285-3p/TFAP2A axis.
qRT-PCR was used to detect the expressions of Linc00467, miR-1285-3p, and TFAP2A in tissues and cells of HNSCC patients. The targeting relationships between Linc00467 and miR-1285-3p, miR-1285-3p, and TFAP2A were verified by dual-luciferase reporter assay. Transfection and grouping were carried out, after HNSCC cell lines were screened. Transwell assay and flow cytometry were used to test cell invasion and apoptosis, respectively.
Compared with normal tissues adjacent to the tumor, the expressions of Linc00467 and TFAP2A increased significantly in cancer tissues, while the expression of miR-1285-3p decreased (all P<0.05). Compared with the si-NC group, the invasion of the si-Linc00467 group decreased and the apoptosis rate increased (both P<0.05). In HNSCC cells, over-expression of Linc00467 promoted increased cell invasion and decreased apoptosis rate, which could be partially rescued by over-expression of miR-1285-3p (all P<0.05). Over-expression of miR-1285-3p caused decreased cell invasion and increased apoptosis rate, which was partially reversed by over-expression of TFAP2A (all P<0.05).
Linc00467 can be used as ceRNA to adsorb miR-1285-3p to regulate the expression of TFAP2A, promote invasion and inhibit apoptosis of HNSCC cells. Linc00467 inhibitors may become one of the targeted therapeutic drugs for HNSCC.
探讨长链非编码RNA 00467(Linc00467)通过微小RNA - 1285 - 3p(miR - 1285 - 3p)/转录因子AP - 2α(TFAP2A)轴调控头颈部鳞状细胞癌(HNSCC)侵袭和凋亡的机制。
采用实时定量聚合酶链反应(qRT - PCR)检测HNSCC患者组织及细胞中Linc00467、miR - 1285 - 3p和TFAP2A的表达。通过双荧光素酶报告基因实验验证Linc00467与miR - 1285 - 3p、miR - 1285 - 3p与TFAP2A之间的靶向关系。筛选HNSCC细胞系后进行转染和分组。分别采用Transwell实验和流式细胞术检测细胞侵袭和凋亡情况。
与肿瘤旁正常组织相比,癌组织中Linc00467和TFAP2A的表达显著升高,而miR - 1285 - 3p的表达降低(均P<0.05)。与小干扰RNA阴性对照(si - NC)组相比,小干扰RNA沉默Linc00467(si - Linc00467)组细胞侵袭能力降低,凋亡率升高(均P<0.05)。在HNSCC细胞中,过表达Linc00467促进细胞侵袭增加,凋亡率降低,而过表达miR - 1285 - 3p可部分逆转上述作用(均P<0.05)。过表达miR - 1285 - 3p导致细胞侵袭减少,凋亡率增加,而过表达TFAP2A可部分逆转这一现象(均P<0.05)。
Linc00467可作为竞争性内源RNA吸附miR - 1285 - 3p,调控TFAP2A的表达,促进HNSCC细胞的侵袭并抑制其凋亡。Linc00467抑制剂可能成为HNSCC的靶向治疗药物之一。