a Department of Respiratory Medicine, Taizhou Central Hospital , Taizhou , Zhejiang , China.
b Department of ICU, The People's Hospital of Jiaozuo City , Jiaozuo , Hebei , China.
Artif Cells Nanomed Biotechnol. 2019 Dec;47(1):3172-3179. doi: 10.1080/21691401.2019.1642904.
We aimed to determine the roles and possible mechanism of long non-coding RNA SDPR-AS in the processes of non-small cell lung cancer (NSCLC). The expressions of SDPR-AS and SDPR in different subtypes of lung cancer (AC, SCC, LCC and SCLC) tissues and cells were determined. Three NSCLC cells were infused with pcDNA-SDPR-AS, pcDNA3.1, sh-SDPR-AS, sh-NC, si-SDPR and si-NC. The effects of SDPR-AS dysregulation on cell behaviors (including cell viability, colony forming ability, migration, invasion and apoptosis) were assessed. Moreover, the combined effects of SDPR-AS overexpression and SDPR-AS knockdown on H522 cell behaviors and the levels of p-p38 and p-ERK were investigated. SDPR-AS was lowly expressed in NSCLC tissues and cells, but had no changes in SCLC tissues and cells. Down-regulation of SDPR-AS enhanced the proliferation, migration and invasion and inhibited apoptosis of NSCLC cells (H522, H661 and H520). Overexpression of SDPR-AS exhibited opposite effects. Moreover, SDPR was positively regulated by SDPR-AS and effects of SDPR-AS on the cell biological processes of NSCLC cells were through regulation of SDPR. Besides, the levels of p-p38 and p-ERK were significantly decreased after SDPR-AS overexpression, which were dramatically changeover by SDPR knockdownsimultaneously. Our findings indicate that SDPR-AS was lowly expressed in NSCLC cells and down-regulation of SDPR-AS may promote the malignant behaviors of NSCLC cells possible through regulating SDPR expression and involving in p38 MAPK/ERK signaling pathway. SDPR-AS may serve as a prospective target for NSCLC diagnosis and therapy.
我们旨在确定长链非编码 RNA SDPR-AS 在非小细胞肺癌（NSCLC）过程中的作用和可能的机制。测定了不同亚型肺癌（AC、SCC、LCC 和 SCLC）组织和细胞中 SDPR-AS 和 SDPR 的表达。将 pcDNA-SDPR-AS、pcDNA3.1、sh-SDPR-AS、sh-NC、si-SDPR 和 si-NC 注入三种 NSCLC 细胞中。评估 SDPR-AS 失调对细胞行为（包括细胞活力、集落形成能力、迁移、侵袭和凋亡）的影响。此外，还研究了 SDPR-AS 过表达和 SDPR-AS 敲低对 H522 细胞行为和 p-p38 和 p-ERK 水平的综合影响。SDPR-AS 在 NSCLC 组织和细胞中低表达，但在 SCLC 组织和细胞中无变化。SDPR-AS 下调增强了 NSCLC 细胞（H522、H661 和 H520）的增殖、迁移和侵袭，抑制了凋亡。SDPR-AS 的过表达则表现出相反的效果。此外，SDPR 被 SDPR-AS 正向调节，SDPR-AS 对 NSCLC 细胞的细胞生物学过程的影响是通过调节 SDPR 实现的。此外，SDPR-AS 过表达后 p-p38 和 p-ERK 水平显著降低，同时 SDPR 敲低则明显改变。我们的研究结果表明，SDPR-AS 在 NSCLC 细胞中低表达，下调 SDPR-AS 可能通过调节 SDPR 表达促进 NSCLC 细胞的恶性行为，并涉及 p38 MAPK/ERK 信号通路。SDPR-AS 可能成为 NSCLC 诊断和治疗的有前途的靶点。
