Cancer
- Genetic and compound screens uncover factors modulating cancer cell response to indisulam
The authors identify that loss of SRPK1 sensitises cancer cells to indisulam treatment and loss of CAND1 confers resistance. Resistance is mediated through RBM39. Furthermore, pharmacological Bcl-xL inhibition prevents acquired resistance to indisulam.
- Rab40c regulates focal adhesions and PP6 activity by controlling ANKRD28 ubiquitylation
The role of novel Rab40c/CRL5 ubiquitylation complex in regulating PP6 activity and cell migration.
- Systematic identification of ALK substrates by integrated phosphoproteome and interactome analysis
Integrated analysis of the phosphoproteome and interactome of anaplastic lymphoma kinase (ALK)-overexpressing HEK 293 cells revealed 37 ALK substrate candidates, contributing to the improvement of kinase activity prediction.
- Exploring YAP1-centered networks linking dysfunctional CFTR to epithelial–mesenchymal transition
In this work, a systems biology approach identifies potentially dysregulated EMT signaling in CF (including the Hippo, Wnt, TGF-β, p53, and MYC pathways), integrated by YAP1 and TEAD4.
- Fluorescent tracking identifies key migratory dendritic cells in the lymph node after radiotherapy
Radiation therapy impacts all cells within the treatment field. Using novel technology, we track dendritic cells from the tumor to lymph nodes and demonstrate their importance in immune control of tumors.
- The miR-26 family regulates early B cell development and transformation
We show that the activity of the miR-26 family determines early B cell behavior: high miR-26 levels promote cell expansion and block the pre-B to immature B cell transition, whereas a miR-26 reduction limits expansion and enhances pre-B cell differentiation.
- Polycomb group ring finger protein 6 suppresses Myc-induced lymphomagenesis
Max dimerizes with Mga to form the repressive complex PRC1.6; another PRC1.6 subunit, Pcgf6, suppresses Myc-induced lymphomagenesis but, unexpectedly, does so in a Mga- and PRC1.6-independent manner.
- The hexosamine pathway and coat complex II promote malignant adaptation to nutrient scarcity
We present adaptive mechanisms of resistance of lung adenocarcinoma to their harsh microenvironment, which typically contains a lower glucose concentration compared with normal tissue.
- ESCRT-I fuels lysosomal degradation to restrict TFEB/TFE3 signaling via the Rag-mTORC1 pathway
ESCRT-I deficiency impairs lysosome membrane turnover and induces homeostatic responses to lysosomal nutrient starvation including activation of MiT-TFE signaling caused by inhibition of the substrate-specific mTORC1 pathway.
- TET2-mediated epigenetic reprogramming of breast cancer cells impairs lysosome biogenesis
TET2-mediated oxidation of 5-methylcytosine establishes an antiviral state and contributes to MYC-dependent down-regulation of genes involved in lysosome biogenesis and function in breast cancer cells.