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Inhibition of cytoplasmic EZH2 induces antitumor activity through stabilization of the DLC1 tumor suppressor protein

Nature communications, 2021-12, Vol.12 (1), p.6941-15, Article 6941

2021

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Targeting the SHP2 phosphatase promotes vascular damage and inhibition of tumor growth

EMBO molecular medicine, 2021-07, Vol.13 (7), p.e14089-n/a

2021

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Tumor-Infiltrating Myeloid Cells Activate DII4/Notch/TGF-β Signaling to Drive Malignant Progression

Cancer research (Chicago, Ill.), 2014-04, Vol.74 (7), p.2038-2049

2014

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The tumor suppressor activity of DLC1 requires the interaction of its START domain with Phosphatidylserine, PLCD1, and Caveolin-1

Molecular cancer, 2021-11, Vol.20 (1), p.141-141, Article 141

2021

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Function and clinical relevance of RHAMM isoforms in pancreatic tumor progression

Molecular cancer, 2019-05, Vol.18 (1), p.92-92, Article 92

2019

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Receptor tyrosine kinase activation of RhoA is mediated by AKT phosphorylation of DLC1

The Journal of cell biology, 2017-12, Vol.216 (12), p.4255-4270

2017

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CDK5 is a major regulator of the tumor suppressor DLC1

The Journal of cell biology, 2014-12, Vol.207 (5), p.627-642

2014

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The expression of glyceraldehyde-3-phosphate dehydrogenase associated cell cycle (GACC) genes correlates with cancer stage and poor survival in patients with solid tumors

PloS one, 2013-04, Vol.8 (4), p.e61262-e61262

2013

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DLC1 is the principal biologically-relevant down-regulated DLC family member in several cancers

Oncotarget, 2016-07, Vol.7 (29), p.45144-45157

2016

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Identification of Eph receptor signaling as a regulator of autophagy and a therapeutic target in colorectal carcinoma

Molecular oncology, 2019-11, Vol.13 (11), p.2441-2459

2019

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Abstract 2367: High expression of GAPDH is relevant to lung adenocarcinoma with low expression of the tumor suppressor gene Deleted in Liver Cancer-1 ( DLC1 )

Cancer research (Chicago, Ill.), 2014-10, Vol.74 (19_Supplement), p.2367-2367

2014

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Inactivation of the Dlc1 Gene Cooperates with Downregulation of p15INK4b and p16Ink4a, Leading to Neoplastic Transformation and Poor Prognosis in Human Cancer

Cancer research (Chicago, Ill.), 2012-11, Vol.72 (22), p.5900-5911

2012

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DLC1 deficiency and YAP signaling drive endothelial cell contact inhibition of growth and tumorigenesis

Oncogene, 2019-11, Vol.38 (45), p.7046-7059

2019

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Cancer-Associated Point Mutations in the DLC1 Tumor Suppressor and Other Rho-GAPs Occur Frequently and Are Associated with Decreased Function

Cancer research (Chicago, Ill.), 2020-09, Vol.80 (17), p.3568-3579

2020

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Abstract 2137: A high proportion of protein phosphorylation sites identified in CPTAC breast cancer and lung adenocarcinoma may result from direct phosphorylation by CDK1

Cancer research (Chicago, Ill.), 2020-08, Vol.80 (16_Supplement), p.2137-2137

2020

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High levels of truncated RHAMM cooperate with dysfunctional p53 to accelerate the progression of pancreatic cancer

Cancer letters, 2021-08, Vol.514, p.79-89

2021

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Abstract 1762: The START domain of the DLC1 tumor suppressor binds phosphatidylserine and two proteins, PLCD1 and Caveolin-1

Cancer research (Chicago, Ill.), 2019-07, Vol.79 (13_Supplement), p.1762-1762

2019

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Abstract 4235: Phosphorylation of Serine 861 in the ECT2 guanine nucleotide exchange factor activates Rho family GTPases and is a biomarker for several tumor types

Cancer research (Chicago, Ill.), 2019-07, Vol.79 (13_Supplement), p.4235-4235

2019

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Abstract PO-060: N-terminal RHAMM cooperates with dysfunctional p53 to accelerate the progression of pancreatic cancer

Cancer research (Chicago, Ill.), 2021-11, Vol.81 (22_Supplement), p.PO-060-PO-060

2021

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Abstract 2508: Targeting mutant KRAS tumors by inhibiting cytoplasmic EZH2, which directly methylates and destabilizes the DLC1 tumor suppressor protein

Cancer research (Chicago, Ill.), 2021-07, Vol.81 (13_Supplement), p.2508-2508

2021

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Bcl-xL is translocated to the nucleus via CtBP2 to epigenetically promote metastasis

Cancer letters, 2024-11, Vol.604, p.217240, Article 217240

2024

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Abstract 4359: Several cancer types are associated with increased expression and activity of the ECT2 RhoGEF and decreased expression and activity of the DLC1 RhoGAP, leading to increased RhoA activity

Cancer research (Chicago, Ill.), 2018-07, Vol.78 (13_Supplement), p.4359-4359

2018

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Abstract 5522: Cancer-associated point mutant in the START domain of DLC1 encodes a protein attenuated for tumor suppressor activity and for binding both Caveolin-1 and PLCD1 but not for Rho-GAP activity

Cancer research (Chicago, Ill.), 2018-07, Vol.78 (13_Supplement), p.5522-5522

2018

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Effects of DLC1 Deficiency on Endothelial Cell Contact Growth Inhibition and Angiosarcoma Progression

JNCI : Journal of the National Cancer Institute, 2018-04, Vol.110 (4), p.390-399

2018

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Abstract 2586: Identification of cancer-associated RhoA mutants and analogous K-Ras mutants that induce gain-of function despite low GTP binding

Cancer research (Chicago, Ill.), 2020-08, Vol.80 (16_Supplement), p.2586-2586

2020

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Inhibition of cytoplasmic EZH2 induces antitumor activity through stabilization of the DLC1 tumor suppressor protein

Targeting the SHP2 phosphatase promotes vascular damage and inhibition of tumor growth

Tumor-Infiltrating Myeloid Cells Activate DII4/Notch/TGF-β Signaling to Drive Malignant Progression

The tumor suppressor activity of DLC1 requires the interaction of its START domain with Phosphatidylserine, PLCD1, and Caveolin-1

Function and clinical relevance of RHAMM isoforms in pancreatic tumor progression

Receptor tyrosine kinase activation of RhoA is mediated by AKT phosphorylation of DLC1

CDK5 is a major regulator of the tumor suppressor DLC1

The expression of glyceraldehyde-3-phosphate dehydrogenase associated cell cycle (GACC) genes correlates with cancer stage and poor survival in patients with solid tumors

DLC1 is the principal biologically-relevant down-regulated DLC family member in several cancers

Identification of Eph receptor signaling as a regulator of autophagy and a therapeutic target in colorectal carcinoma

Abstract 2367: High expression of GAPDH is relevant to lung adenocarcinoma with low expression of the tumor suppressor gene Deleted in Liver Cancer-1 ( DLC1 )

Inactivation of the Dlc1 Gene Cooperates with Downregulation of p15INK4b and p16Ink4a, Leading to Neoplastic Transformation and Poor Prognosis in Human Cancer

DLC1 deficiency and YAP signaling drive endothelial cell contact inhibition of growth and tumorigenesis

Cancer-Associated Point Mutations in the DLC1 Tumor Suppressor and Other Rho-GAPs Occur Frequently and Are Associated with Decreased Function

Abstract 2137: A high proportion of protein phosphorylation sites identified in CPTAC breast cancer and lung adenocarcinoma may result from direct phosphorylation by CDK1

High levels of truncated RHAMM cooperate with dysfunctional p53 to accelerate the progression of pancreatic cancer

Abstract 1762: The START domain of the DLC1 tumor suppressor binds phosphatidylserine and two proteins, PLCD1 and Caveolin-1

Abstract 4235: Phosphorylation of Serine 861 in the ECT2 guanine nucleotide exchange factor activates Rho family GTPases and is a biomarker for several tumor types

Abstract PO-060: N-terminal RHAMM cooperates with dysfunctional p53 to accelerate the progression of pancreatic cancer

Abstract 2508: Targeting mutant KRAS tumors by inhibiting cytoplasmic EZH2, which directly methylates and destabilizes the DLC1 tumor suppressor protein

Bcl-xL is translocated to the nucleus via CtBP2 to epigenetically promote metastasis

Abstract 4359: Several cancer types are associated with increased expression and activity of the ECT2 RhoGEF and decreased expression and activity of the DLC1 RhoGAP, leading to increased RhoA activity

Abstract 5522: Cancer-associated point mutant in the START domain of DLC1 encodes a protein attenuated for tumor suppressor activity and for binding both Caveolin-1 and PLCD1 but not for Rho-GAP activity

Effects of DLC1 Deficiency on Endothelial Cell Contact Growth Inhibition and Angiosarcoma Progression

Abstract 2586: Identification of cancer-associated RhoA mutants and analogous K-Ras mutants that induce gain-of function despite low GTP binding

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