Activation of phospholipase D by growth factors and oncogenes in murine fibroblasts follow alternative but cross-talking pathways

Peso, Luis del; Lucas, Luisa; Esteve, Pilar; Lacal, Juan Carlos

doi:10.1042/bj3220519

Cited by 22 publications

(3 citation statements)

References 55 publications

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“…It is critically important to understand the molecular causes underlying these metabolic differences, because these may identify novel targets for anticancer therapy selective for cancer cells. The major molecular causes of the increased PC and tCho levels in cancer cells and tumors include an increased expression and activity of choline kinase α (CHK‐α) , a higher rate of choline transport and increased activities of phosphatidylcholine (PtdCho)‐specific phospholipase C (PtdCho‐PLC) and D (PtdCho‐PLD) , and several phospholipases A 2 . Other enzymes in the choline phospholipid metabolic pathways are in the process of investigation .…”

Section: Key Molecules Driving Altered Choline Metabolism In Cancermentioning

confidence: 99%

MRS and MRSI guidance in molecular medicine: targeting and monitoring of choline and glucose metabolism in cancer

et al. 2011

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Magnetic resonance spectroscopy (MRS) and spectroscopic imaging (MRSI) are valuable tools to detect metabolic changes in tumors. The currently emerging era of molecular medicine, which is shaped by molecularly targeted anticancer therapies combined with molecular imaging of the effects of such therapies, requires powerful imaging technologies that are able to detect molecular information. MRS and MRSI (MRS/I) are such technologies that are able to detect metabolites arising from glucose and choline metabolism in noninvasive in vivo settings and at higher resolution in tissue samples. The roles that MRS/I plays in diagnosing different types of cancer as well as in early monitoring of tumor response to traditional chemotherapies are reviewed. Emerging roles of MRS/I in the development and detection of novel targeted anticancer therapies that target oncogenic signaling pathways or targets in choline or glucose metabolism are discussed.

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Section: Key Molecules Driving Altered Choline Metabolism In Cancermentioning

confidence: 99%

MRS and MRSI guidance in molecular medicine: targeting and monitoring of choline and glucose metabolism in cancer

et al. 2011

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“…Transfections were carried out by the calcium phosphate method (Chen and Okayama, 1987) with minor modi®cations. The ras-and mettransformed cell lines have been described previously (Peso et al, 1996). The cell lines transformed by rac-1, dbl, ost and vav used in this study are mass cultures of NIH3T3 cells transfected with the corresponding activated genes and selected with 1 mg/ml of G418.…”

Section: Cell Culture and Reagentsmentioning

confidence: 99%

Rho proteins induce metastatic properties in vivo

Peso

Hernández-Alcoceba²,

Embade³

et al. 1997

Oncogene

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141

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Rho proteins have been implicated in the regulation of multiple signal transduction processes. Some of the members of this family, including the rho gene from Aplysia californica and the human genes (rhoA, rhoB and rac-1), are proto-oncogenes since when properly mutated they can induce cell transformation, and the generated rho-transformed cells are tumorigenic when inoculated into mice. In addition to their tumorigenic activity, there is evidence suggesting that Rho proteins may contribute to the metastatic phenotype. However, all the experiments implicating Rho proteins or Rhoregulating proteins in the induction of metastatic potential are either indirect or have been performed in vitro. In this study we investigated whether cells transformed by rho oncogenes do have metastatic potential in vivo. We present evidence that cells transformed by the Aplysia californica rho gene, when injected directly into the blood stream are able to eciently colonize lungs and secondary organs, consistent with the acquisition of the metastatic potential. Moreover, tumors derived from subcutaneous injections of these rho-transformed cells are also able to metastasize in distant organs, a strong support to the hypothesis that Rho proteins play a role in the metastatic phenotype. Finally, cells transformed by the human oncogenes dbl, vav and ost, three well-known guanine exchange factors for members of the Rho family, or cells transformed by the activated human rac-1 or rhoA genes do also have metastatic potential when injected into the blood stream. These results demonstrate that signaling pathways regulated by Rho proteins play an important role in the acquisition of the metastatic phenotype in vivo.

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“…In addition to the activation of the effectors mentioned above, phospholipid-derived second messengers are also components of the Ras response. As such, Ras activates phosphatidylcholine-specific PLD (PC-PLD), and PLD activation by protein kinase C is greatly enhanced in Ras-transformed cells [69,70].…”

Section: Ral-gds and The Ral Gtpase Pathwaymentioning

confidence: 99%

Ras proteins in the control of the cell cycle and cell differentiation

Crespo¹,

León²

2000

CMLS, Cell. Mol. Life Sci.

166

135

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The Ras family of small GTPases includes three closely related proteins: H-, K-, and N-Ras. Ras proteins are involved in the transduction of signals elicited by activated surface receptors, acting as key components by relaying signals downstream through diverse pathways. Mutant, constitutively activated forms of Ras proteins are frequently found in cancer. While constitutive Ras activation induces oncogenic-like transformation in immortalized fibroblasts, it causes growth arrest in primary vertebrate cells. Induction of p53 and cyclin-dependent kinase inhibitors such as p15INK4b, p16INK4a, p19ARF, and p21WAF1 accounts for this response. Interestingly, while ras has usually been regarded as a transforming oncogene, the analysis of Ras function in most of the cellular systems studied so far indicates that the promotion of differentiation is the most prominent effect of Ras. While in some cell types, particularly muscle, Ras inhibits differentiation, in others such as neuronal, adipocytic, or myeloid cells, Ras induces differentiation, in some cases accompanied by growth arrest. Several possible mechanisms for the pleiotropic effects' of Ras in animal cells are discussed.

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Activation of phospholipase D by growth factors and oncogenes in murine fibroblasts follow alternative but cross-talking pathways

Cited by 22 publications

References 55 publications

MRS and MRSI guidance in molecular medicine: targeting and monitoring of choline and glucose metabolism in cancer

MRS and MRSI guidance in molecular medicine: targeting and monitoring of choline and glucose metabolism in cancer

Rho proteins induce metastatic properties in vivo

Ras proteins in the control of the cell cycle and cell differentiation

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