Experts and Doctors on hct116 cells in Boston, Massachusetts, United States


Locale: Boston, Massachusetts, United States
Topic: hct116 cells

Top Publications

  1. Raina D, Ahmad R, Chen D, Kumar S, Kharbanda S, Kufe D. MUC1 oncoprotein suppresses activation of the ARF-MDM2-p53 pathway. Cancer Biol Ther. 2008;7:1959-67 pubmed
    ..We also show that the MUC1(Y60F) mutant functions as dominant negative inhibitor of tumorigenicity. These findings indicate that the oncogenic function of MUC1 is conferred by suppressing activation of the ARF-MDM2-p53 pathway. ..
  2. Kulshreshtha R, Ferracin M, Wojcik S, Garzon R, Alder H, Agosto Perez F, et al. A microRNA signature of hypoxia. Mol Cell Biol. 2007;27:1859-67 pubmed
    ..Interestingly, the vast majority of hypoxia-induced microRNAs are also overexpressed in a variety of human tumors. ..
  3. Zhang W, Wu K, Sartori M, Kamadurai H, Ordureau A, Jiang C, et al. System-Wide Modulation of HECT E3 Ligases with Selective Ubiquitin Variant Probes. Mol Cell. 2016;62:121-36 pubmed publisher
  4. Tan M, Lim H, Bennett E, Shi Y, Harper J. Parallel SCF adaptor capture proteomics reveals a role for SCFFBXL17 in NRF2 activation via BACH1 repressor turnover. Mol Cell. 2013;52:9-24 pubmed publisher
    ..This work identifies a role for SCF(FBXL17) in controlling the threshold for NRF2-dependent gene activation and provides a framework for elucidating the functions of CRL adaptor proteins. ..
  5. Winter G, Mayer A, Buckley D, Erb M, Roderick J, Vittori S, et al. BET Bromodomain Proteins Function as Master Transcription Elongation Factors Independent of CDK9 Recruitment. Mol Cell. 2017;67:5-18.e19 pubmed publisher
    ..These studies, performed in translational models of T cell leukemia, establish a mechanism-based rationale for the development of BET bromodomain degradation as cancer therapy. ..
  6. Ren B, Song K, Parangi S, Jin T, Ye M, Humphreys R, et al. A double hit to kill tumor and endothelial cells by TRAIL and antiangiogenic 3TSR. Cancer Res. 2009;69:3856-65 pubmed publisher
  7. Rodriguez Bravo V, Maciejowski J, Corona J, Buch H, Collin P, Kanemaki M, et al. Nuclear pores protect genome integrity by assembling a premitotic and Mad1-dependent anaphase inhibitor. Cell. 2014;156:1017-31 pubmed publisher
    ..A heterologous Mad1-NPC tether restored Cdc20 inhibitor production and normal M phase control. We conclude that nuclear pores and kinetochores both emit "wait anaphase" signals that preserve genome integrity. ..
  8. Fung H, Weinstock D. Repair at single targeted DNA double-strand breaks in pluripotent and differentiated human cells. PLoS ONE. 2011;6:e20514 pubmed publisher
    ..Our approach to single DSB analysis has broad utility for defining the effects of genetic and environmental modifications on repair precision in pluripotent cells and their differentiated progeny. ..
  9. Kim W, Bennett E, Huttlin E, Guo A, Li J, Possemato A, et al. Systematic and quantitative assessment of the ubiquitin-modified proteome. Mol Cell. 2011;44:325-40 pubmed publisher
    ..Interrogation of the ubiquitinome allows for not only a quantitative assessment of alterations in protein homeostasis fidelity, but also identification of substrates for individual ubiquitin pathway enzymes. ..

More Information


  1. Zhao Y, Alonso C, Ballester I, Song J, Chang S, Guleng B, et al. Control of NOD2 and Rip2-dependent innate immune activation by GEF-H1. Inflamm Bowel Dis. 2012;18:603-12 pubmed publisher
    ..GEF-H1 connects tyrosine kinase function to NOD-like receptor signaling and is fundamental to the regulation of microbial recognition by ubiquitous innate immune mechanisms mediated by Rip2 kinase. ..
  2. Sun Y, Li X. The canonical wnt signal restricts the glycogen synthase kinase 3/fbw7-dependent ubiquitination and degradation of eya1 phosphatase. Mol Cell Biol. 2014;34:2409-17 pubmed publisher
    ..Together, these findings reveal that the canonical Wnt and PI3K/Akt signal pathways restrain the GSK3/Fbw7-dependent Eya1 ubiquitination, and they further suggest that dysregulation of this novel axis contributes to tumorigenesis. ..
  3. Lu C, Chen J, Xu H, Zhou X, He Q, Li Y, et al. MIR106B and MIR93 prevent removal of bacteria from epithelial cells by disrupting ATG16L1-mediated autophagy. Gastroenterology. 2014;146:188-99 pubmed publisher
    ..In human cell lines, MIR106B and MIR93 reduce levels of ATG16L1 and autophagy and prevent autophagy-dependent eradication of intracellular bacteria. This process also appears to be altered in colon tissues from patients with active CD. ..
  4. Coffee E, Faber A, Roper J, Sinnamon M, Goel G, Keung L, et al. Concomitant BRAF and PI3K/mTOR blockade is required for effective treatment of BRAF(V600E) colorectal cancer. Clin Cancer Res. 2013;19:2688-98 pubmed publisher
    ..We have established a novel GEMM to interrogate BRAF(V600E) CRC biology and identify more efficacious treatment strategies. Combination BRAF and PI3K/mTOR inhibitor treatment should be explored in clinical trials. ..
  5. Lal A, Thomas M, Altschuler G, Navarro F, O Day E, Li X, et al. Capture of microRNA-bound mRNAs identifies the tumor suppressor miR-34a as a regulator of growth factor signaling. PLoS Genet. 2011;7:e1002363 pubmed publisher
    ..Thus miR-34a tempers the proliferative and pro-survival effect of growth factor stimulation by interfering with growth factor signal transduction and downstream pathways required for cell division. ..
  6. Roper J, Richardson M, Wang W, Richard L, Chen W, Coffee E, et al. The dual PI3K/mTOR inhibitor NVP-BEZ235 induces tumor regression in a genetically engineered mouse model of PIK3CA wild-type colorectal cancer. PLoS ONE. 2011;6:e25132 pubmed publisher
    ..013). These studies provide the preclinical rationale for studies examining the efficacy of the dual PI3K/mTOR inhibitor NVP-BEZ235 in treatment of PIK3CA wild-type CRC. ..
  7. Yin L, Huang L, Kufe D. MUC1 oncoprotein activates the FOXO3a transcription factor in a survival response to oxidative stress. J Biol Chem. 2004;279:45721-7 pubmed
    ..These findings indicate that MUC1 regulates the FOXO3a signaling pathway in a survival response to oxidative stress. ..
  8. Du W, Wu J, Walsh E, Zhang Y, Chen C, Xiao Z. Nutlin-3 affects expression and function of retinoblastoma protein: role of retinoblastoma protein in cellular response to nutlin-3. J Biol Chem. 2009;284:26315-21 pubmed publisher
    ..Taken together, these results suggest that Rb plays a critical role in influencing cellular response to activation of p53 pathway by nutlin-3. ..
  9. Zhan Y, Ginanni N, Tota M, Wu M, Bays N, Richon V, et al. Control of cell growth and survival by enzymes of the fatty acid synthesis pathway in HCT-116 colon cancer cells. Clin Cancer Res. 2008;14:5735-42 pubmed publisher
    ..The experimental approach described here may be extended to other targets or disease-relevant pathways to identify steps suitable for therapeutic intervention. ..
  10. Teer J, Machida Y, Labit H, Novac O, Hyrien O, Marheineke K, et al. Proliferating human cells hypomorphic for origin recognition complex 2 and pre-replicative complex formation have a defect in p53 activation and Cdk2 kinase activation. J Biol Chem. 2006;281:6253-60 pubmed
    ..The results suggest that hypomorphic mutations in initiation factor genes may be particularly deleterious in cancers with mutant p53 or increased activity of Cyclin E/Cdk2. ..
  11. Papageorgis P, Cheng K, Ozturk S, Gong Y, Lambert A, Abdolmaleky H, et al. Smad4 inactivation promotes malignancy and drug resistance of colon cancer. Cancer Res. 2011;71:998-1008 pubmed publisher
    ..These findings are also consistent with targeting TGF?-induced auxiliary pathways, such as MEK-ERK, and p38-MAPK and the glycolytic cascade, in SMAD4-deficient tumors as attractive strategies for therapeutic intervention. ..
  12. Zhou X, Munger K. Clld7, a candidate tumor suppressor on chromosome 13q14, regulates pathways of DNA damage/repair and apoptosis. Cancer Res. 2010;70:9434-43 pubmed publisher
    ..Furthermore, depletion of Clld7 in normal human epithelial cells conferred resistance to apoptosis triggered by DNA damage. Taken together, the biological actions of Clld7 are consistent with those of a tumor suppressor. ..
  13. Guarani V, Paulo J, Zhai B, Huttlin E, Gygi S, Harper J. TIMMDC1/C3orf1 functions as a membrane-embedded mitochondrial complex I assembly factor through association with the MCIA complex. Mol Cell Biol. 2014;34:847-61 pubmed publisher
    ..This study defines a new membrane-embedded CI assembly factor and provides a resource for further analysis of CI biology. ..
  14. Kalabis J, Rosenberg I, Podolsky D. Vangl1 protein acts as a downstream effector of intestinal trefoil factor (ITF)/TFF3 signaling and regulates wound healing of intestinal epithelium. J Biol Chem. 2006;281:6434-41 pubmed
    ..Vangl1 protein may serve as an effector mediating the ITF healing response of the intestinal mucosa. ..