ArticleBreast cancer research : BCR2017
TIMELESS contributes to the progression of breast cancer through activation of MYC.
Article in Breast cancer research : BCR, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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Who cites it
30 citing papers in PubMed, 48 citations in OpenAlex.
- Two fork protection complexes at the replication fork play distinct roles in fork progression and stress response.Research square · 2026Article
- A new model for coordinating the functions of TIMELESS at the replication fork.bioRxiv : the preprint server for biology · 2025Article
- Circadian genes and non-coding RNAs: interactions and implications in cancer.Animal cells and systems · 2025Review
- The YTH domain-containing protein family: Emerging players in immunomodulation and tumour immunotherapy targets.Clinical and translational medicine · 2024Review
- Article
- TIMELESS upregulates PD-L1 expression and exerts an immunosuppressive role in breast cancer.Journal of translational medicine · 2023Article
- The TIMELESS effort for timely DNA replication and protection.Cellular and molecular life sciences : CMLS · 2023Review
- Article
- Association of the Timeless Gene with Prognosis and Clinical Characteristics of Human Lung Cancer.Diagnostics (Basel, Switzerland) · 2022Article
- Loss of circadian gene Timeless induces EMT and tumor progression in colorectal cancer via Zeb1-dependent mechanism.Cell death and differentiation · 2022Article
- MEX3A promotes the malignant progression of ovarian cancer by regulating intron retention in TIMELESS.Cell death & disease · 2022Article
- [TIM-3 gene is highly expressed in ephithelial ovarian cancer to promote proliferation and migration of ovarian cancer cells].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2022Article
- A circadian rhythm-related gene signature for prognosis, invasion and immune microenvironment of breast cancer.Frontiers in genetics · 2022Article
- 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
- Genetic co-expression networks contribute to creating predictive model and exploring novel biomarkers for the prognosis of breast cancer.Scientific reports · 2021Article
- Circadian clock genes promote glioma progression by affecting tumour immune infiltration and tumour cell proliferation.Cell proliferation · 2021Article
- ARNTL2 is a Prognostic Biomarker and Correlates with Immune Cell Infiltration in Triple-Negative Breast Cancer.Pharmacogenomics and personalized medicine · 2021Article
- Article
- TIMELESS Promotes Tumor Progression by Enhancing Macrophages Recruitment in Ovarian Cancer.Frontiers in oncology · 2021Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundBreast cancer is the most common malignancy and the leading cause of cancer death among women. TIMELESS (TIM), a circadian rhythm regulator, has been recently implicated in the progression of human cancer. However, the role of TIM in the progression of breast cancer has not been well-characterized.
methodsImmunohistochemistry (IHC) staining was used to examine TIM levels in breast cancer specimens. Mammosphere formation analysis and side population analysis were used to examine the effect of TIM on the self-renewal of breast cancer stem cells. A wound healing assay and a Transwell assay were used to determine the role of TIM in breast cancer cell migration and invasion. A soft agar growth assay in vitro and tumorigenicity in vivo were used to determine the role of TIM in tumorigenicity.
resultsTIM levels in both breast cancer cell lines and tissues were significantly upregulated. Patients with high TIM had poorer prognosis than patients with low TIM. Overexpression of TIM dramatically enhanced, while knockdown of TIM suppressed the self-renewal of cancer stem cells (CSCs), cell invasion and migration abilities of breast cancer cells in vitro. Moreover, overexpression of TIM significantly augmented, while knockdown of TIM reduced the tumorigenicity of breast cancer cells in vivo. Mechanism studies revealed that TIM upregulated the expression and the trans-activity of the well-known oncogene MYC. Inhibition of MYC significantly blocked the effects of TIM on CSC population, cell invasion and anchor-independent cell growth.
conclusionTIM plays an important role in promoting breast cancer progression and may represent a novel therapeutic target for breast cancer.
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