Dormancy has evolved in plants to restrict germination to favourable growth seasons. Seeds from most crop plants have low dormancy levels due to selection for immediate germination during domestication. Seed dormancy is usually not completely lost and low levels are required to maintain sufficient seed quality. Brassica napus cultivars show low levels of primary seed dormancy. However, B. napus seeds are prone to the induction of secondary dormancy, which can lead to the occurrence of volunteers in the field in subsequent years after cultivation. The DELAY OF GERMINATION 1 (DOG1) gene has been identified as a major dormancy gene in the model plant Arabidopsis thaliana. DOG1 is a conserved gene and has been shown to be required for seed dormancy in various monocot and dicot plant species. We have identified three B. napus genes with high homology to AtDOG1, which we named BnaA. DOG1.a, BnaC.DOG1.a and BnaC.DOG1.b. The transcripts of these genes could only be detected in seeds and showed a similar expression pattern during seed maturation as AtDOG1. In addition, the Bna-DOG1 genes showed enhanced transcript levels after the induction of secondary dormancy. These results suggest a role for DOG1 in the induction of secondary dormancy in B. napus.

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Epigenetic modifications are known to regulate cell phenotype during cancer progression, including breast cancer. Unlike genetic alterations, changes in the epigenome are reversible, thus potentially reversed by epi-drugs. Breast cancer, the most common cause of cancer death worldwide in women, encompasses multiple histopathological and molecular subtypes. Several lines of evidence demonstrated distortion of the epigenetic landscape in breast cancer. Interestingly, mammary cells isolated from breast cancer patients and cultured ex vivo maintained the tumorigenic phenotype and exhibited aberrant epigenetic modifications. Recent studies indicated that the therapeutic efficiency for breast cancer regimens has increased over time, resulting in reduced mortality. Future medical treatment for breast cancer patients, however, will likely depend upon a better understanding of epigenetic modifications. The present review aims to outline different epigenetic mechanisms including DNA methylation, histone modifications, and ncRNAs with their impact on breast cancer, as well as to discuss studies highlighting the central role of epigenetic mechanisms in breast cancer pathogenesis. We propose new research areas that may facilitate locus-specific epigenome editing as breast cancer therapeutics.

As a pathologically heterogeneous disease, cancer is one of the leading causes of global morbidity. According to the World Health Organization, approximately one in six deaths are caused by cancer. Fortunately, many cancers can be cured if diagnosed at early stages and treated efficiently. Despite the benefits of conventional cancer treatments such as surgery, chemotherapy, hormone therapy, and radiation therapy, they have several drawbacks, including cytotoxicity, inaccurate targeting of tumor cells, and multi-drug resistance, which underscore the importance of developing novel and effective strategies to improve diagnosis, prognosis, therapy, and patient survival. Recently, the advancement of nanotechnology has opened new horizons for cancer treatment thanks to the discovery of nanoparticles (NPs) and the small-sized molecules that revolutionized the drug delivery methods in cancerous tissues. The specific characteristics of NPs, such as reduced toxicity, improved permeability, and accurate targeting of tumor cells, provide a great advantage in cancer treatment and help to overcome the limitations and challenges of conventional cancer treatment methods. Besides, the role of NPs in immunotherapy has created a novel concept for cancer treatment. This review gives a brief overview regarding the importance of NPs and their targeting mechanism, as well as the challenges and limitations associated with their use in cancer treatment.