hsa_circ_0005963 downregulation suppresses NSCLC malignant progression by miR-506-3p/SOX9-mediated stemness regulation

PURPOSE: This study investigated the role and regulatory mechanisms underlying hsa_circ_0005963 in NSCLC. METHODS: FISH and RT-qPCR were used to assess hsa_circ_0005963 expression in NSCLC cells and tissues. Dual-luciferase reporter assay was employed to characterize hsa_circ_0005963 downstream targets. Transwell migration and EdU incorporation were performed to detect NSCLC cell proliferation and migration. A mouse tumor xenograft model was constructed to assess hsa_circ_0005963 functions in NSCLC metastasis and progressions. RESULTS: hsa_circ_0005963 expression was upregulated in NSCLC tissues and cells. High hsa_circ_0005963 expression indicates poor prognosis, including overall survival. hsa_circ_0005963 silencing inhibited NSCLC proliferation and migration. Experiments confirmed that hsa_circ_0005963 downregulation suppresses A549 tumor invasions. A dual-luciferase reporter assay identified SOX9 and microRNA as hsa_circ_0005963 downstream targets, which was validated by RT-qPCR. SOX9 overexpression or miR-506-3p downregulation reversed the hsa_circ_0005963 silencing inhibitory effects upon proliferation and migrations. SOX9 overexpression reversed miR-506-3p effects to inhibit proliferation and migration in both cell lines. CONCLUSION: hsa_circ_0005963 promotes NSCLC development by sponging miR-506-3p to enhance SOX9 expression.

Authors

Institutions

Publication Details

Journal
Epigenomics
Published
2026-05-21
DOI
https://doi.org/10.1080/17501911.2026.2654577
Primary Topic
Circular RNAs in diseases
Type
article
Field-Weighted Citation Impact
0.00
Controls
|||
ALL TIME
JAN
FEB
MAR
APR
MAY
JUN
JUL
AUG
SEP
OCT
article

hsa_circ_0005963 downregulation suppresses NSCLC malignant progression by miR-506-3p/SOX9-mediated stemness regulation

Huaiyin Ding, Yu Yao, Xuechao Zhou
Epigenomics
Circular RNAs in diseases
article

hsa_circ_0005963 downregulation suppresses NSCLC malignant progression by miR-506-3p/SOX9-mediated stemness regulation

Huaiyin Ding, Yu Yao, Xuechao Zhou
article en

Abstract

PURPOSE: This study investigated the role and regulatory mechanisms underlying hsa_circ_0005963 in NSCLC. METHODS: FISH and RT-qPCR were used to assess hsa_circ_0005963 expression in NSCLC cells and tissues. Dual-luciferase reporter assay was employed to characterize hsa_circ_0005963 downstream targets. Transwell migration and EdU incorporation were performed to detect NSCLC cell proliferation and migration. A mouse tumor xenograft model was constructed to assess hsa_circ_0005963 functions in NSCLC metastasis and progressions. RESULTS: hsa_circ_0005963 expression was upregulated in NSCLC tissues and cells. High hsa_circ_0005963 expression indicates poor prognosis, including overall survival. hsa_circ_0005963 silencing inhibited NSCLC proliferation and migration. Experiments confirmed that hsa_circ_0005963 downregulation suppresses A549 tumor invasions. A dual-luciferase reporter assay identified SOX9 and microRNA as hsa_circ_0005963 downstream targets, which was validated by RT-qPCR. SOX9 overexpression or miR-506-3p downregulation reversed the hsa_circ_0005963 silencing inhibitory effects upon proliferation and migrations. SOX9 overexpression reversed miR-506-3p effects to inhibit proliferation and migration in both cell lines. CONCLUSION: hsa_circ_0005963 promotes NSCLC development by sponging miR-506-3p to enhance SOX9 expression.

Epigenomics
Nanjing University of Chinese Medicine (CN)
Openalex Percentile: Top 9%
Circular RNAs in diseases
AI Navigator

Ask Laika to Summarize, Analyze, and Connect papers live on the map.

Summarize Papers & Methodologies

Extract key findings, datasets, and comparative methods across publications.

Benchmark Rankings & Visual Analytics

Rank top research institutions, authors, funders, topics, and journals by Field-Weighted Citation Impact (FWCI) and paper volume with instant charts.

Connect Distant Disciplines

Bridge topological clusters on the map to find hidden collaborative intersections.