Abstract：
Non-small cell lung cancer (NSCLC) is associated with high morbidity and mortality. Dysregulation of lncRNAs leads to NSCLC progression.
This study aims to explore the regulatory mechanism of lncRNA LINC01234 in NSCLC.
LINC01234 expression in NSCLC cells was determined. Cell proliferation was detected using CCK-8, colony formation, and EDU assays after transfection of siRNA LINC01234 into H1299 cells and transfection of pcDNA3.1-LINC01234 into H1975 cells. Subcellular localization of LINC01234 was predicted and the binding relations between LINC01234 and miR-433-3p as well as miR-433-3p and GRB2 were verified. The expression levels of miR-433-3p and GRB2 in NSCLC cells were determined. Joint experiments of miR-433-3p inhibitor + si- LINC01234-1 or oe-GRB2 + si-LINC01234-1 were conducted to verify the role of miR-433-3p and GRB2 in NSCLC cell malignant proliferation.
LINC01234 was abundantly expressed in NSCLC cells. LINC01234 silencing reduced NSCLC cell proliferation while LINC01234 overexpression enhanced cell proliferation. LINC01234 competitively bound to miR-433-3p and miR-433-3p directly targeted GRB2. miR- 433-3p knockdown or GRB2 overexpression counteracted the repressive effect of LINC01234 silencing on NSCLC cell malignant proliferation.
LINC01234 competitively bound to miR-433-3p and promoted GRB2 transcription to augment NSCLC cell malignant proliferation.
This study aims to explore the regulatory mechanism of lncRNA LINC01234 in NSCLC.
LINC01234 expression in NSCLC cells was determined. Cell proliferation was detected using CCK-8, colony formation, and EDU assays after transfection of siRNA LINC01234 into H1299 cells and transfection of pcDNA3.1-LINC01234 into H1975 cells. Subcellular localization of LINC01234 was predicted and the binding relations between LINC01234 and miR-433-3p as well as miR-433-3p and GRB2 were verified. The expression levels of miR-433-3p and GRB2 in NSCLC cells were determined. Joint experiments of miR-433-3p inhibitor + si- LINC01234-1 or oe-GRB2 + si-LINC01234-1 were conducted to verify the role of miR-433-3p and GRB2 in NSCLC cell malignant proliferation.
LINC01234 was abundantly expressed in NSCLC cells. LINC01234 silencing reduced NSCLC cell proliferation while LINC01234 overexpression enhanced cell proliferation. LINC01234 competitively bound to miR-433-3p and miR-433-3p directly targeted GRB2. miR- 433-3p knockdown or GRB2 overexpression counteracted the repressive effect of LINC01234 silencing on NSCLC cell malignant proliferation.
LINC01234 competitively bound to miR-433-3p and promoted GRB2 transcription to augment NSCLC cell malignant proliferation.
摘要：
背景：非小细胞肺癌（NSCLC）与高发病率和高死亡率相关。lncRNAs的失调导致NSCLC进展。
目的：本研究旨在探讨lncRNALINC01234在非小细胞肺癌中的调控机制。
方法：测定LINC01234在NSCLC细胞中的表达。使用CCK-8检测细胞增殖，集落形成，在将siRNALINC01234转染到H1299细胞中并将pcDNA3.1-LINC01234转染到H1975细胞中之后进行EDU测定。预测了LINC01234的亚细胞定位，并验证了LINC01234与miR-433-3p以及miR-433-3p与GRB2的结合关系。测定miR-433-3p和GRB2在NSCLC细胞中的表达水平。miR-433-3p抑制剂+si-LINC01234-1或oe-GRB2+si-LINC01234-1联合实验验证miR-433-3p和GRB2在NSCLC细胞恶性增殖中的作用。
结果：LINC01234在NSCLC细胞中大量表达。LINC01234沉默降低NSCLC细胞增殖,而LINC01234过表达增强细胞增殖。LINC01234竞争性结合miR-433-3p和miR-433-3p直接靶向GRB2。miR-433-3p敲低或GRB2过表达抵消了LINC01234沉默对NSCLC细胞恶性增殖的抑制作用。
结论：LINC01234竞争性结合miR-433-3p并促进GRB2转录以增强NSCLC细胞恶性增殖。
目的：本研究旨在探讨lncRNALINC01234在非小细胞肺癌中的调控机制。
方法：测定LINC01234在NSCLC细胞中的表达。使用CCK-8检测细胞增殖，集落形成，在将siRNALINC01234转染到H1299细胞中并将pcDNA3.1-LINC01234转染到H1975细胞中之后进行EDU测定。预测了LINC01234的亚细胞定位，并验证了LINC01234与miR-433-3p以及miR-433-3p与GRB2的结合关系。测定miR-433-3p和GRB2在NSCLC细胞中的表达水平。miR-433-3p抑制剂+si-LINC01234-1或oe-GRB2+si-LINC01234-1联合实验验证miR-433-3p和GRB2在NSCLC细胞恶性增殖中的作用。
结果：LINC01234在NSCLC细胞中大量表达。LINC01234沉默降低NSCLC细胞增殖,而LINC01234过表达增强细胞增殖。LINC01234竞争性结合miR-433-3p和miR-433-3p直接靶向GRB2。miR-433-3p敲低或GRB2过表达抵消了LINC01234沉默对NSCLC细胞恶性增殖的抑制作用。
结论：LINC01234竞争性结合miR-433-3p并促进GRB2转录以增强NSCLC细胞恶性增殖。
