Thank you for visiting nature.com. You are using a browser version with limited support for CSS. To obtain
the best experience, we recommend you use a more up to date browser (or turn off compatibility mode in
Internet Explorer). In the meantime, to ensure continued support, we are displaying the site without styles
and JavaScript.
In this Progress article, Wu, Jusiak and Lu discuss how synthetic biology-based design principles can be applied to living cells to overcome key challenges in current cancer therapy and generate more robust, specific and effective gene circuit therapies.
The CRISPR–Cas9 (clustered regularly interspaced short palindromic repeats–CRISPR-associated 9) system provides many avenues for improving how we generate models of cancer. This system has numerous uses, including providing a means to understand the importance of genetic alterations as a tumour evolves, and CRISPR–Cas9 may potentially constitute a therapeutic strategy in the future.
YAP and TAZ are the major downstream effectors of the Hippo pathway. This Progress article summarizes the latest findings regarding the biological functions of YAP and TAZ, and their role in connecting the Hippo pathway with other relevant pathways in cancer.
The cohesin complex is involved in sister chromatid cohesion, as well as other processes, such as transcriptional regulation. Mutations in genes encoding cohesin subunits and cohesin regulators have recently been identified in several tumour types. This Progress article discusses the roles of the cohesin complex and how its mutation might contribute to cancer progression.
The vast majority of the research into cancer metabolism has been limited to a handful of metabolic pathways, with other pathways being sidelined. This Progress article brings to light the potential contribution of fatty acid oxidation to cancer cell function.
BAP1 is a deubiquitylase that is associated with multiprotein complexes that regulate key cellular pathways. Recent findings have indicated that germlineBAP1mutations might cause a novel cancer syndrome. Michele Carbone and colleagues discuss the evidence for this.
Pioneer factors are a special class of transcription factor that can associate with compacted chromatin to facilitate the binding of additional transcription factors. This Progress article discusses the importance of pioneer factors in breast cancer and prostate cancer.
The primary role for small nucleolar RNAs (snoRNAs) has typically been considered to be the guiding of the post-transcriptional modifications of particular RNAs. This Progress article discusses the intriguing recent findings that various snoRNAs, and the host genes that encode them, could have previously unsuspected and varied roles in cancer.
Desmosomes are adhesion complexes that are related to adherens junctions, and recent studies using mouse genetic approaches have uncovered a role for desmosomes in tumour suppression.
The function of the deacetylase SIRT1 in cancer is complex and controversial. This article discusses the recent progress that has been made in mouse models to address the role of SIRT1 in tumour development.
Can combining oncogenic kinase inhibitors with direct activators of the apoptosis machinery, such as the BH3 mimetic ABT-737, produce durable clinical responses in patients with cancer?
Increased RNA polymerase III activity in cancer has been observed for over 30 years but how this occurs and affects cellular transformation is only beginning to be understood. Lynne Marshall and Robert J. White discuss recent progress made in this emerging field.
The recent determination of the structure of the class I phosphoinositide 3-kinase PI3Kα has identified important structural differences between the class 1 PI3Ks. How can this information be used to improve cancer therapy?
CDC37 is oncogenic because it stabilizes the structures of mutated or overexpressed oncogenic kinases. Targeting this chaperone activity, on which many tumours depend, is therefore an attractive option for broad-based therapy.
Several recent papers have shown that the miR-34 family of microRNAs is directly involved in mediating the effects of p53, indicating that non-coding RNAs have an important role in tumorigenesis. This Progress article discusses these papers and their implications.
Glioblastoma stem cells might be dependent on cues from aberrant vascular niches that mimic the normal neural stem cell niche. What are the implications of these findings for treatment of this disease?
Three major tumour-suppressor proteins have recently been shown to undergo monoubiquitylation-mediated nuclear–cytoplasmic shuttling. Can our increasing knowledge of this mechanism be used to treat cancer?
Several recent papers have shown that the Delta-like ligand 4 (Dll4)-Notch system restrains angiogenesis but, paradoxically, Dll4 inhibition decreases tumour growth. Is too much angiogenesis actually a good thing?
