Department of Nuclear Medicine, Hunan Provincial People's Hospital, First Affiliated Hospital of Hunan Normal University, Changsha, Hunan Province, China.
Department of Breast Nail Surgery, Hunan Provincial People's Hospital, First Affiliated Hospital of Hunan Normal University, Changsha, Hunan Province, China.
Cell Cycle. 2021 Dec;20(24):2619-2637. doi: 10.1080/15384101.2021.1995129. Epub 2021 Nov 16.
Long non-coding RNA LIFR-AS1 is low-expressed in many cancers, but its functions in papillary thyroid carcinoma (PTC) were not defined and require further study. The relationship between LIFR-AS1 expression and clinicopathological characteristics of patients with PTC was statistically analyzed. The downregulation of LIFR-AS1 in PTC tissues and cell lines was predicted by bioinformatics analysis and verified by qRT-PCR. After overexpressing or silencing LIFR-AS1, the regulatory role of LIFR-AS1 in PTC was examined by performing MTT, colony formation, wound healing, Transwell, ELISA, tube formation and xenograft tumor experiment. MiR-31-5p and SID1 transmembrane family member 2 (SIDT2) expressions in PTC tissues or cell lines were detected by qRT-PCR, Western blot, or in situ hybridization. The relationship between miR-31-5p and LIFR-AS1/SIDT2 was predicted by LncBase, TargetScan or Pearson correlation test and then verified by Dual-Luciferase Reporter assay, RNA pull-down assay and qRT-PCR. The regulatory effect of LIFR-AS1/miR-31-5p/SIDT2 axis on the biological behaviors of PTC cells was confirmed by functional experiments and rescue experiments mentioned above. The tumor size and lymphatic metastasis were correlated with LIFR-AS1 overexpression. Overexpressed LIFR-AS1 suppressed tumorigenesis . LIFR-AS1 and SIDT2 expressions were suppressed in PTC tissues, while that of miR-31-5p was elevated in PTC tissues. LIFR-AS1 was negatively correlated with miR-31-5p. LIFR-AS1 sponged miR-31-5p to upregulate SIDT2, thereby inhibiting the viability, proliferation, migration, invasion, and the secretion of vascular endothelial growth factor (VEGF) of PTC cells and angiogenesis of human umbilical vein endothelial cells (HUVECs). This paper demonstrates that LIFR-AS1/miR-31-5p/SIDT2 axis modulated the development of PTC.
长链非编码 RNA LIFR-AS1 在许多癌症中低表达，但它在甲状腺乳头状癌 (PTC) 中的功能尚未确定，需要进一步研究。通过统计学分析，研究了 LIFR-AS1 表达与 PTC 患者临床病理特征之间的关系。通过生物信息学分析预测了 LIFR-AS1 在 PTC 组织和细胞系中的下调，并通过 qRT-PCR 进行了验证。通过过表达或沉默 LIFR-AS1，通过 MTT、集落形成、划痕愈合、Transwell、ELISA、管形成和异种移植肿瘤实验检测 LIFR-AS1 对 PTC 的调节作用。通过 qRT-PCR、Western blot 或原位杂交检测 PTC 组织或细胞系中 miR-31-5p 和 SID1 跨膜家族成员 2 (SIDT2) 的表达。通过 LncBase、TargetScan 或 Pearson 相关性检验预测 miR-31-5p 与 LIFR-AS1/SIDT2 的关系，然后通过双荧光素酶报告基因检测、RNA 下拉检测和 qRT-PCR 进行验证。通过上述功能实验和挽救实验证实了 LIFR-AS1/miR-31-5p/SIDT2 轴对 PTC 细胞生物学行为的调节作用。肿瘤大小和淋巴转移与 LIFR-AS1 的过表达相关。过表达的 LIFR-AS1 抑制肿瘤发生。LIFR-AS1 和 SIDT2 在 PTC 组织中表达下调，而 miR-31-5p 在 PTC 组织中表达上调。LIFR-AS1 与 miR-31-5p 呈负相关。LIFR-AS1 吸附 miR-31-5p 上调 SIDT2，从而抑制 PTC 细胞的活力、增殖、迁移、侵袭和血管内皮生长因子 (VEGF) 的分泌以及人脐静脉内皮细胞 (HUVECs) 的血管生成。本文证明 LIFR-AS1/miR-31-5p/SIDT2 轴调节 PTC 的发生发展。
