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ONCOLOGY / CLINICAL RESEARCH
LncRNA KTN1-AS1 drives tumor progression in non-small cell lung cancer through the microRNA-153-3p/KLF5 axis
1
Department of Medical Oncology, Shaoxing People’s Hospital, Zhejiang, China
2
Alberta Institute, Wenzhou Medical University, Zhejiang, China
Submission date: 2023-09-20
Final revision date: 2024-01-24
Acceptance date: 2024-04-14
Online publication date: 2024-04-28
Corresponding author
KEYWORDS
KTN1-AS1 drove proliferationmigrationand invasion of NSCLC cells by regulating the microRNA-153-3p/KLF5 axis
TOPICS
ABSTRACT
Introduction:
The most typical kind of lung cancer is non-small cell lung cancer (NSCLC). Surgery, targeted therapy, chemotherapy, and immunotherapy are all options for the treatment of NSCLC. LncRNA KTN1-AS1 is significantly elevated in NSCLC, and it modulates the expression of microRNAs and downstream genes, promoting NSCLC progression.
Material and methods:
TCGA was employed to predict lncRNA KTN1-AS1 expression in NSCLC. The starBase database was utilized to predict downstream microRNAs of KTN1-AS1. The RNA22 database was employed to predict corresponding binding sites. Subcellular localization of KTN1-AS1 was forecasted using the lncLocator database, and the results were validated by FISH. qRT-PCR was used to test KTN1-AS1, microRNA-153-3p, and KLF5 expression. CCK-8, flow cytometry, and Transwell assay were used to determine cell viability, proliferation, migration, and invasion. Western blot was used to test KLF5 and Ki67 protein levels, and dual-luciferase assay was used to assess binding of KTN1-AS1 with microRNA-153-3p, and KLF5 with microRNA-153-3p.
Results:
KTN1-AS1 was significantly upregulated in NSCLC cells. Silencing KTN1-AS1 significantly repressed the proliferation, migration, and invasion of NSCLC cells. KTN1-AS1 bound to microRNA-153-3p, and KLF5 was a direct target of microRNA-153-3p. Inhibition of microRNA-153-3p or overexpression of KLF5 restored the stimulatory impact of KTN1-AS1 knockdown on NSCLC cell proliferation and migration.
Conclusions:
KTN1-AS1 drove proliferation, migration, and invasion of NSCLC cells by regulating the microRNA-153-3p/KLF5 axis.
The most typical kind of lung cancer is non-small cell lung cancer (NSCLC). Surgery, targeted therapy, chemotherapy, and immunotherapy are all options for the treatment of NSCLC. LncRNA KTN1-AS1 is significantly elevated in NSCLC, and it modulates the expression of microRNAs and downstream genes, promoting NSCLC progression.
Material and methods:
TCGA was employed to predict lncRNA KTN1-AS1 expression in NSCLC. The starBase database was utilized to predict downstream microRNAs of KTN1-AS1. The RNA22 database was employed to predict corresponding binding sites. Subcellular localization of KTN1-AS1 was forecasted using the lncLocator database, and the results were validated by FISH. qRT-PCR was used to test KTN1-AS1, microRNA-153-3p, and KLF5 expression. CCK-8, flow cytometry, and Transwell assay were used to determine cell viability, proliferation, migration, and invasion. Western blot was used to test KLF5 and Ki67 protein levels, and dual-luciferase assay was used to assess binding of KTN1-AS1 with microRNA-153-3p, and KLF5 with microRNA-153-3p.
Results:
KTN1-AS1 was significantly upregulated in NSCLC cells. Silencing KTN1-AS1 significantly repressed the proliferation, migration, and invasion of NSCLC cells. KTN1-AS1 bound to microRNA-153-3p, and KLF5 was a direct target of microRNA-153-3p. Inhibition of microRNA-153-3p or overexpression of KLF5 restored the stimulatory impact of KTN1-AS1 knockdown on NSCLC cell proliferation and migration.
Conclusions:
KTN1-AS1 drove proliferation, migration, and invasion of NSCLC cells by regulating the microRNA-153-3p/KLF5 axis.
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| eISSN: | 1896-9151 |
| ISSN: | 1734-1922 |
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