microRNA-100 functions as a tumor suppressor in non-small cell lung cancer via regulating epithelial-mesenchymal transition and Wnt/β-catenin by targeting HOXA1.
Adenocarcinoma of Lung
/ genetics
Animals
Apoptosis
Biomarkers, Tumor
/ genetics
Carcinoma, Non-Small-Cell Lung
/ genetics
Carcinoma, Squamous Cell
/ genetics
Cell Movement
Cell Proliferation
Epithelial-Mesenchymal Transition
Female
Gene Expression Regulation, Neoplastic
Homeodomain Proteins
/ genetics
Humans
Lung Neoplasms
/ genetics
Lymphatic Metastasis
Male
Mice
Mice, Nude
MicroRNAs
/ genetics
Middle Aged
Prognosis
Survival Rate
Transcription Factors
/ genetics
Tumor Cells, Cultured
Tumor Suppressor Proteins
/ genetics
Wnt1 Protein
/ genetics
Xenograft Model Antitumor Assays
beta Catenin
/ genetics
Epithelial-mesenchymal transition
HOXA1
Wnt/β-catenin
miR-100
non-small cell lung cancer
Journal
Thoracic cancer
ISSN: 1759-7714
Titre abrégé: Thorac Cancer
Pays: Singapore
ID NLM: 101531441
Informations de publication
Date de publication:
06 2020
06 2020
Historique:
received:
24
02
2020
revised:
09
04
2020
accepted:
10
04
2020
pubmed:
5
5
2020
medline:
16
3
2021
entrez:
5
5
2020
Statut:
ppublish
Résumé
Non-small cell lung cancer (NSCLC) is a leading subtype in lung cancer, with high morbidities and mortalities worldwide. microRNA (miRNA) has appeared to play indispensable roles in a variety of solid carcinomas. The current study focused on the functions of miR-100 in NSCLC. qRT-PCR was performed to detect miR-100 and HOXA1 expressions in NSCLC tissues and cells. MTT and transwell assays were used to determine the functions of miR-100 in NSCLC cell proliferation, invasion and migration abilities. Western blot was used to measure related protein expressions. qRT-PCR results showed that miR-100 expressions were dramatically decreased in NSCLC tissues. MTT assays indicated that miR-100 restoration inhibited NSCLC cell proliferation. Furthermore, transwell assay was performed to determine the impacts of miR-100 on NSCLC invasion and migration abilities. As expected, the invasion and migration capacities were significantly repressed. Direct interactions between HOXA1 and miR-100 were also verified via dual-luciferase reporter assays. Western blot analysis demonstrated that miR-100 exerted suppressive functions via regulating EMT and Wnt/β-catenin in NSCLC cells. Our results showed that miR-100 served antitumor roles in NSCLC, providing new evidence of miR-100 as a promising therapeutic biomarker in NSCLC.
Sections du résumé
BACKGROUND
Non-small cell lung cancer (NSCLC) is a leading subtype in lung cancer, with high morbidities and mortalities worldwide. microRNA (miRNA) has appeared to play indispensable roles in a variety of solid carcinomas. The current study focused on the functions of miR-100 in NSCLC.
METHODS
qRT-PCR was performed to detect miR-100 and HOXA1 expressions in NSCLC tissues and cells. MTT and transwell assays were used to determine the functions of miR-100 in NSCLC cell proliferation, invasion and migration abilities. Western blot was used to measure related protein expressions.
RESULTS
qRT-PCR results showed that miR-100 expressions were dramatically decreased in NSCLC tissues. MTT assays indicated that miR-100 restoration inhibited NSCLC cell proliferation. Furthermore, transwell assay was performed to determine the impacts of miR-100 on NSCLC invasion and migration abilities. As expected, the invasion and migration capacities were significantly repressed. Direct interactions between HOXA1 and miR-100 were also verified via dual-luciferase reporter assays. Western blot analysis demonstrated that miR-100 exerted suppressive functions via regulating EMT and Wnt/β-catenin in NSCLC cells.
CONCLUSIONS
Our results showed that miR-100 served antitumor roles in NSCLC, providing new evidence of miR-100 as a promising therapeutic biomarker in NSCLC.
Identifiants
pubmed: 32364673
doi: 10.1111/1759-7714.13459
pmc: PMC7262897
doi:
Substances chimiques
Biomarkers, Tumor
0
CTNNB1 protein, human
0
Homeodomain Proteins
0
MIRN100 microRNA, human
0
MicroRNAs
0
Transcription Factors
0
Tumor Suppressor Proteins
0
WNT1 protein, human
0
Wnt1 Protein
0
beta Catenin
0
homeobox A1 protein
0
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
1679-1688Informations de copyright
© 2020 The Authors. Thoracic Cancer published by China Lung Oncology Group and John Wiley & Sons Australia, Ltd.
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