ArticleCancer science2013
TIMELESS is overexpressed in lung cancer and its expression correlates with poor patient survival.
Article in Cancer science, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 36 papers.
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Who cites it
36 citing papers in PubMed, 74 citations in OpenAlex.
- TIPIN coordinates ATM-dependent checkpoint and NF-κB signaling to counteract DNA replication damage from topoisomerase inhibition.Communications biology · 2025Article
- TIMELESS as a prognostic biomarker and therapeutic target in gastric cancer.Journal, genetic engineering & biotechnology · 2025Article
- Article
- SP3-induced Timeless transcription contributes to cell growth of lung adenocarcinoma cells.PloS one · 2024Article
- Six-hour time-restricted feeding inhibits lung cancer progression and reshapes circadian metabolism.BMC medicine · 2023Article
- A nine-gene signature as prognostic biomarker in gastric cancer by bioinformatics analysis.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2023Article
- The role of circadian clocks in cancer: Mechanisms and clinical implications.Genes & diseases · 2023Review
- The TIMELESS effort for timely DNA replication and protection.Cellular and molecular life sciences : CMLS · 2023Review
- CRS: a circadian rhythm score model for predicting prognosis and treatment response in cancer patients.Journal of translational medicine · 2023Article
- Association of the Timeless Gene with Prognosis and Clinical Characteristics of Human Lung Cancer.Diagnostics (Basel, Switzerland) · 2022Article
- TIMELESS is a key gene mediating thrombogenesis in COVID-19 and antiphospholipid syndrome.Scientific reports · 2022Article
- Loss of circadian gene Timeless induces EMT and tumor progression in colorectal cancer via Zeb1-dependent mechanism.Cell death and differentiation · 2022Article
- Circadian Rhythm Dysregulation and Leukemia Development: The Role of Clock Genes as Promising Biomarkers.International journal of molecular sciences · 2022Review
- Identifying General Tumor and Specific Lung Cancer Biomarkers by Transcriptomic Analysis.Biology · 2022Article
- Identification of TIMELESS and RORA as key clock molecules of non-small cell lung cancer and the comprehensive analysis.BMC cancer · 2022Article
- High Expression of TIMELESS Predicts Poor Prognosis: A Potential Therapeutic Target for Skin Cutaneous Melanoma.Frontiers in surgery · 2022Article
- Identification of the key genes and pathways involved in B cells in primary Sjögren' s syndrome.Bioengineered · 2021Article
- Article
- Activation of the clock gene TIMELESS by H3k27 acetylation promotes colorectal cancer tumorigenesis by binding to Myosin-9.Journal of experimental & clinical cancer research : CR · 2021Article
- TIMELESS inhibits breast cancer cell invasion and metastasis by down-regulating the expression of MMP9.Cancer cell international · 2021Article
Corrections and comments
- Erratum issued
Authors and funding
13 authors at 3 institutions in 2 countries.
Funding
Abstract
TIMELESS (TIM) is a mammalian homolog of a Drosophila circadian rhythm gene, but its circadian properties in mammals have yet to be determined. TIM appears to be essential for replication protection and genomic stability. Recently, the involvement of TIM in human malignancies has been reported; therefore, we investigated the role of TIM in lung cancer. Microarray expression analysis of lung cancer cell lines showed that TIM expression was elevated 3.7-fold (P < 0.001) in non-small cell lung cancer cell lines (n = 116) compared to normal lung controls (n = 59). In addition, small cell lung cancer cell lines (n = 29) expressed TIM at levels 2.2-fold (P < 0.001) higher than non-small cell lung cancer. Western blot analysis of 22 lung cancer cell lines revealed that all of them expressed TIM protein and that 20 cell lines (91%) expressed TIM protein at higher levels than a normal control line. Remarkably, immunohistochemistry of 30 surgically resected lung cancer specimens showed that all lung cancer specimens but no matched normal lung tissues were positive for TIM expression. Moreover, immunohistochemistry of surgically resected specimens from 88 consecutive patients showed that high TIM protein levels correlated with poor overall survival (P = 0.013). Mutation analysis for TIM in 23 lung cancer cell lines revealed no mutation. TIM knockdown suppressed proliferation and clonogenic growth, and induced apoptosis in H157 and H460 cells. Taken together, our findings suggest that TIM could be useful as a diagnostic and prognostic marker for lung cancer and targeting it would be of high therapeutic value for this disease.
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