ArticleInternational journal of clinical and experimental pathology2018
Period 3, a tumor suppressor in non-small cell lung cancer, is silenced by hypermethylation.
Article in International journal of clinical and experimental pathology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 16 citations in OpenAlex.
- Role of the circadian rhythm in squamous cell carcinoma: From molecular mechanism to therapy (Review).Molecular medicine reports · 2026Review
- Article
- PER3 suppresses tumor metastasis of oral squamous cell carcinoma by promoting HIF-1α degradation.Translational oncology · 2025Article
- The Common Hallmarks and Interconnected Pathways of Aging, Circadian Rhythms, and Cancer: Implications for Therapeutic Strategies.Research (Washington, D.C.) · 2025Review
- PER3 promoter hypermethylation correlates to the progression of pan-cancer.Clinical epigenetics · 2024Article
- Sex differences in the tumor promoting effects of tobacco smoke in a cRaf transgenic lung cancer disease model.Archives of toxicology · 2024Article
- The role of circadian clocks in cancer: Mechanisms and clinical implications.Genes & diseases · 2023Review
- Circadian clock-based therapeutics in chronic pulmonary diseases.Trends in pharmacological sciences · 2022Review
- Co-alterations of circadian clock gene transcripts in human placenta in preeclampsia.Scientific reports · 2022Article
- An IDH-independent mechanism of DNA hypermethylation upon VHL inactivation in cancer.Epigenetics · 2022Article
- RUNX3-regulated circRNA METTL3 inhibits colorectal cancer proliferation and metastasis via miR-107/PER3 axis.Cell death & disease · 2022Article
- Advances in the Study of Circadian Genes in Non-Small Cell Lung Cancer.Integrative cancer therapiesArticle
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Lung cancer is one of the most preventable forms of cancer, which is the second leading cause of cancer-related death. Emerging evidence has suggested a possible link between the endogenous circadian clock and cell growth, and even cancer development. However, the role of important clock gene period 3 (PER3) in lung cancer remains fully understand, especially its regulatory mechanism. In this study, we investigated the biological role of PER3 in non-small cell lung cancer (NSCLC), and also demonstrated the possible mechanism that induces dysfunction of PER3 in lung cancer. QPCR was performed to measure the expression of PER3 in NSCLC tissues and cell lines. Bisulfite genomic sequencing PCR (BSP) and methylation specific PCR (MSP) were used to determine the methylation status of PER3. And a battery of cell biology assays was used to measure the effects of PER3 on cell proliferation, apoptosis, migration and invasion. We found that PER3 was downregulated in NSCLC tissues and cell lines compared with the adjacent or normal cells control. The promoter of PER3 was hypermethylated, which could be restored by demethylation drug 5-Aza. And overexpression of PER3 suppressed NSCLC cell proliferation, induced apoptosis and inhibited the ability of migration and invasion. These findings reveal that PER3 is a tumor suppressor in NSCLC and provide a promising target and a novel strategy to control cancer progression.
Indexed as
Identifiers
31938093PMC6957972W3028469014What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.