ArticleOncology letters2021
lncRNA FOXD3-AS1 promotes the progression of non-small cell lung cancer by regulating the miR-135a-5p/CDK6 axis.
Article in Oncology letters, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 17 citations in OpenAlex.
- Long noncoding RNAs at the crossroads of smoking, oxidative stress, inflammation, and lung disease.Archives of toxicology · 2026Review
- Knockdown of FOXD3-AS1 inhibits the progression of prostate cancer by targeting miR-491-5p/PEG10.Journal of cancer research and clinical oncology · 2025Article
- Circular RNA CCT3 is a unique molecular marker in bladder cancer.BMC cancer · 2023Article
- Prognostic and predictive value of a lncRNA signature in patients with stage II colon cancer.Scientific reports · 2023Article
- Cell Cycle-Related lncRNAs as Innovative Targets to Advance Cancer Management.Cancer management and research · 2023Review
- Evaluation of lncRNA FOXD3-AS1 as a Biomarker for Early-Stage Lung Cancer Diagnosis and Subtype Identification.Evidence-based complementary and alternative medicine : eCAM · 2022Article
- Emerging Roles and Mechanisms of lncRNA FOXD3-AS1 in Human Diseases.Frontiers in oncology · 2022Review
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Long non-coding RNA (lncRNA) is essential to the development and progression of malignant human cancer. Growing evidence suggests that the lncRNA forkhead box D3 antisense 1 (FOXD3-AS1) is a crucial regulatory effector for multiple cancer types and is closely associated with poor prognosis. However, in most cases, the molecular mechanism underlying the role of FOXD3-AS1 in cancer development has not yet been fully elucidated. The present study focused on non-small cell lung cancer (NSCLC) in order to gain insight into how FOXD3-AS1 drives cancer progression. First, FOXD3-AS1 expression in NSCLC tissue samples was detected using reverse transcription-quantitative (RT-qPCR). Moreover, cell proliferation and apoptosis were determined using Cell Counting Kit-8 assays and flow cytometry, respectively. A luciferase reporter assay was then performed to determine whether there was a direct binding association between FOXD3-AS1 and microRNA (miR)-135a-5p. Lastly, a tumor subcutaneous xenograft model was established to examine the role of FOXD3-AS1 in tumor growth. FOXD3-AS1 was significantly overexpressed in NSCLC tissue samples and cell lines compared with normal tissue samples and cells. FOXD3-AS1 silencing expression significantly inhibited A549 and H1229 cell proliferation while inducing apoptosis compared with sh-NC group. The luciferase reporter assay demonstrated the direct binding interaction between FOXD3-AS1 and miR-135a-5p. Moreover, FOXD3-AS1 silencing led to the upregulation of miR-135a-5p in A549 and H1229 cells compared with sh-NC group. It was also demonstrated that miR-135a-5p could bind to the 3' untranslated region of cyclin-dependent kinase 6 (CDK6) and negatively modulate its transcription. miR-135a-5p knockdown or CDK6 overexpression reversed the inhibition on cell proliferation and apoptosis following FOXD3-AS1 knockdown. Altogether, the present study suggests that FOXD3-AS1 sponges miR-135a-5p to promote cell proliferation and concomitantly inhibit apoptosis by regulating CDK6 expression in NSCLC cells.
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