LINC02418 promotes malignant behaviors in lung adenocarcinoma cells by sponging miR-4677-3p to upregulate KNL1 expression

Abstract Background Lung adenocarcinoma (LAD) is a prevalent type of bronchogenic malignant tumor and one of the most critical factors related to human death. Long noncoding RNAs (lncRNAs) are involved in many complex biological processes and have been emerged as extremely important regulators of va...

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Main Authors: Tao Wang, Ruiren Zhai, Xiuhua Lv, Ke Wang, Junqing Xu
Format: Article
Language:English
Published: BMC 2020-08-01
Series:BMC Pulmonary Medicine
Subjects:
Online Access:http://link.springer.com/article/10.1186/s12890-020-01229-0
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author Tao Wang
Ruiren Zhai
Xiuhua Lv
Ke Wang
Junqing Xu
author_facet Tao Wang
Ruiren Zhai
Xiuhua Lv
Ke Wang
Junqing Xu
author_sort Tao Wang
collection DOAJ
description Abstract Background Lung adenocarcinoma (LAD) is a prevalent type of bronchogenic malignant tumor and one of the most critical factors related to human death. Long noncoding RNAs (lncRNAs) are involved in many complex biological processes and have been emerged as extremely important regulators of various cancers. LINC02418, a novel lncRNA, hasn’t been mentioned in previous studies on cancer development. Therefore, it’s important to define the potential function of LINC02418 in LAD. Methods Gene expression was examined by RT-qPCR or western blot. CCK-8, colony formation, TUNEL, and transwell assays were utilized to study the role of LINC02418 in LAD. The interaction of miR-4677-3p with LINC02418 (or KNL1) was verified through luciferase reporter, RIP and RNA pull-down assays. Results High expression of LINC02418 was observed in LAD specimens and cells. Downregulation of LINC02418 obstructed the proliferation and motility of LAD cells. Moreover, LINC02418 negatively modulated miR-4677-3p expression and miR-4677-3p overexpression could repress cell proliferation and migration. Moreover, kinetochore scaffold 1 (KNL1) expression was negatively modulated by miR-4677-3p but positively regulated by LINC02418. Furthermore, miR-4677-3p could bind with LINC02418 (or KNL1). Finally, KNL1 overexpression reversed the inhibitory function of LINC02418 deficiency in the malignant behaviors of LAD cells. Conclusions LINC02418 contributes to the malignancy in LAD via miR-4677-3p/KNL1 signaling, providing a probable therapeutic direction for LAD.
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spelling doaj.art-70d72879ccfe4905897bb06b742aec702022-12-22T01:06:35ZengBMCBMC Pulmonary Medicine1471-24662020-08-0120111010.1186/s12890-020-01229-0LINC02418 promotes malignant behaviors in lung adenocarcinoma cells by sponging miR-4677-3p to upregulate KNL1 expressionTao Wang0Ruiren Zhai1Xiuhua Lv2Ke Wang3Junqing Xu4Department of Thoracic Surgery, The Second Affiliated Hospital of Air Force Medical UniversityDepartment of Tumor Center, Sunshine Union HospitalDepartment of Radiology, Xijing Hospital, Fourth Military Medical UniversityDepartment of Radiology, Xijing Hospital, Fourth Military Medical UniversityDepartment of Radiology, Shenzhen University General Hospital, Shenzhen University Clinical Medical AcademyAbstract Background Lung adenocarcinoma (LAD) is a prevalent type of bronchogenic malignant tumor and one of the most critical factors related to human death. Long noncoding RNAs (lncRNAs) are involved in many complex biological processes and have been emerged as extremely important regulators of various cancers. LINC02418, a novel lncRNA, hasn’t been mentioned in previous studies on cancer development. Therefore, it’s important to define the potential function of LINC02418 in LAD. Methods Gene expression was examined by RT-qPCR or western blot. CCK-8, colony formation, TUNEL, and transwell assays were utilized to study the role of LINC02418 in LAD. The interaction of miR-4677-3p with LINC02418 (or KNL1) was verified through luciferase reporter, RIP and RNA pull-down assays. Results High expression of LINC02418 was observed in LAD specimens and cells. Downregulation of LINC02418 obstructed the proliferation and motility of LAD cells. Moreover, LINC02418 negatively modulated miR-4677-3p expression and miR-4677-3p overexpression could repress cell proliferation and migration. Moreover, kinetochore scaffold 1 (KNL1) expression was negatively modulated by miR-4677-3p but positively regulated by LINC02418. Furthermore, miR-4677-3p could bind with LINC02418 (or KNL1). Finally, KNL1 overexpression reversed the inhibitory function of LINC02418 deficiency in the malignant behaviors of LAD cells. Conclusions LINC02418 contributes to the malignancy in LAD via miR-4677-3p/KNL1 signaling, providing a probable therapeutic direction for LAD.http://link.springer.com/article/10.1186/s12890-020-01229-0LINC02418miR-4677-3pKNL1LAD
spellingShingle Tao Wang
Ruiren Zhai
Xiuhua Lv
Ke Wang
Junqing Xu
LINC02418 promotes malignant behaviors in lung adenocarcinoma cells by sponging miR-4677-3p to upregulate KNL1 expression
BMC Pulmonary Medicine
LINC02418
miR-4677-3p
KNL1
LAD
title LINC02418 promotes malignant behaviors in lung adenocarcinoma cells by sponging miR-4677-3p to upregulate KNL1 expression
title_full LINC02418 promotes malignant behaviors in lung adenocarcinoma cells by sponging miR-4677-3p to upregulate KNL1 expression
title_fullStr LINC02418 promotes malignant behaviors in lung adenocarcinoma cells by sponging miR-4677-3p to upregulate KNL1 expression
title_full_unstemmed LINC02418 promotes malignant behaviors in lung adenocarcinoma cells by sponging miR-4677-3p to upregulate KNL1 expression
title_short LINC02418 promotes malignant behaviors in lung adenocarcinoma cells by sponging miR-4677-3p to upregulate KNL1 expression
title_sort linc02418 promotes malignant behaviors in lung adenocarcinoma cells by sponging mir 4677 3p to upregulate knl1 expression
topic LINC02418
miR-4677-3p
KNL1
LAD
url http://link.springer.com/article/10.1186/s12890-020-01229-0
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