phospholipase d/breast neoplasms

Lyen an sove nan clipboard la

AtikEsè klinikPatant

Chwazi kalite sòt

Paj 1 soti nan 62 rezilta yo

Inhibition of phorbol ester-stimulated phospholipase D activity by chronic tamoxifen treatment in breast cancer cells.

Se sèlman itilizatè ki anrejistre yo ki ka tradwi atik yo

We have shown that in an estrogen receptor-negative multidrug-resistant subline of MCF-7 human breast carcinoma cells longer-term (24 h), but not shorter-term (30 min), treatments with clinically relevant (2-5 microM) concentrations of tamoxifen (TAM) inhibited phorbol ester-stimulated phospholipase

Survival signals generated by estrogen and phospholipase D in MCF-7 breast cancer cells are dependent on Myc.

Se sèlman itilizatè ki anrejistre yo ki ka tradwi atik yo

Estrogens, which have been strongly implicated in the development of breast cancer, enhance proliferation of mammary epithelial cells and, importantly, estrogen receptor (ER)-positive breast cancer cells. In the absence of serum growth factors, the ER-positive MCF-7 breast cancer cell line undergoes

Selective estrogen receptor (ER) modulators differentially regulate phospholipase D catalytic activity in ER-negative breast cancer cells.

Se sèlman itilizatè ki anrejistre yo ki ka tradwi atik yo

Recent successes in the pharmacotherapeutic treatment of breast cancer are associated with the use of selective estrogen receptor modulators. Two commonly prescribed pharmaceuticals in this class, tamoxifen and raloxifene, have been shown to have effects through estrogen receptor (ER)-independent

Phospholipase D prevents apoptosis in v-Src-transformed rat fibroblasts and MDA-MB-231 breast cancer cells.

Se sèlman itilizatè ki anrejistre yo ki ka tradwi atik yo

Phospholipase D (PLD) activity is elevated in response to mitogenic and oncogenic signals. PLD also cooperates with overexpressed tyrosine kinases to transform rat fibroblasts. 3Y1 rat fibroblasts overexpressing the tyrosine kinase c-Src undergo apoptosis in response to serum withdrawal. We report

Phospholipase D inhibitor enhances radiosensitivity of breast cancer cells.

Se sèlman itilizatè ki anrejistre yo ki ka tradwi atik yo

Radiation and drug resistance remain the major challenges and causes of mortality in the treatment of locally advanced, recurrent and metastatic breast cancer. Dysregulation of phospholipase D (PLD) has been found in several human cancers and is associated with resistance to anticancer drugs. In the

Role of phospholipase D in migration and invasion induced by linoleic acid in breast cancer cells.

Se sèlman itilizatè ki anrejistre yo ki ka tradwi atik yo

Linoleic acid (LA) is an essential and omega-6 polyunsaturated fatty acid that mediates a variety of biological processes, including migration and invasion in breast cancer cells. Phospholipase D (PLD) catalyses the hydrolysis of phosphatidylcholine to produce phosphatidic acid and choline.

Triptolide-induced suppression of phospholipase D expression inhibits proliferation of MDA-MB-231 breast cancer cells.

Se sèlman itilizatè ki anrejistre yo ki ka tradwi atik yo

In spite of the importance of phospholipase D (PLD) in cell proliferation and tumorigenesis, little is known about the molecules regulating PLD expression. Thus, identification of small molecules inhibiting PLD expression would be an important advance for PLD- mediated physiology. We examined one

Increased phospholipase D activity in human breast cancer.

Se sèlman itilizatè ki anrejistre yo ki ka tradwi atik yo

Phospholipase D is believed to play an important role in cell proliferation and tumorigenesis. One of its major functions is to cause a sustained activation of protein kinase C through the primary production of phosphatidic acid from phosphatidylcholine by the enzyme, followed by dephosphorylation

Myc stabilization in response to estrogen and phospholipase D in MCF-7 breast cancer cells.

Se sèlman itilizatè ki anrejistre yo ki ka tradwi atik yo

Estrogen, which has been strongly implicated in breast cancer, suppresses apoptosis in estrogen receptor (ER) positive MCF-7 breast cancer cells. Phospholipase D (PLD), which is commonly elevated in ER negative breast cancer cells, also suppresses apoptosis. Survival signals generated by both

A new signaling pathway (JAK-Fes-phospholipase D) that is enhanced in highly proliferative breast cancer cells.

Se sèlman itilizatè ki anrejistre yo ki ka tradwi atik yo

The products of the oncogene Fes and JAK3 are tyrosine kinases, whose expressions are elevated in tumor growth, angiogenesis, and metastasis. Phosphatidic acid, as synthesized by phospholipase D (PLD), enhances cancer cell survival. We report a new signaling pathway that integrates the two kinases

Phospholipase D (PLD) drives cell invasion, tumor growth and metastasis in a human breast cancer xenograph model.

Se sèlman itilizatè ki anrejistre yo ki ka tradwi atik yo

Breast cancer is one of the most common malignancies in human females in the world. One protein that has elevated enzymatic lipase activity in breast cancers in vitro is phospholipase D (PLD), which is also involved in cell migration. We demonstrate that the PLD2 isoform, which was analyzed directly

Phospholipase D confers rapamycin resistance in human breast cancer cells.

Se sèlman itilizatè ki anrejistre yo ki ka tradwi atik yo

mTOR (mammalian target of rapamycin) is a protein kinase that regulates cell cycle progression and cell growth. Rapamycin is a highly specific inhibitor of mTOR in clinical trials for the treatment of breast and other cancers. mTOR signaling was reported to require phosphatidic acid (PA), the

Alternative phospholipase D/mTOR survival signal in human breast cancer cells.

Se sèlman itilizatè ki anrejistre yo ki ka tradwi atik yo

Cancer cells generate survival signals to suppress default apoptotic programs that protect from cancer. Phosphatidylinositol-3-kinase (PI3K) generates a survival signal that is frequently dysregulated in human cancers. Phospholipase D (PLD) has also been implicated in signals that promote survival.

mTOR-dependent suppression of protein phosphatase 2A is critical for phospholipase D survival signals in human breast cancer cells.

Se sèlman itilizatè ki anrejistre yo ki ka tradwi atik yo

A critical aspect of tumor progression is the generation of survival signals that overcome default apoptotic programs. Recent studies have revealed that elevated phospholipase D activity generates survival signals in breast and perhaps other human cancers. We report here that the elevated

Autoregulation of phospholipase D activity is coupled to selective induction of phospholipase D1 expression to promote invasion of breast cancer cells.

Se sèlman itilizatè ki anrejistre yo ki ka tradwi atik yo

Phospholipase D (PLD) is an important signaling enzyme implicated in the control of many biological processes, including cell proliferation and survival. Despite the importance of the duration and amplitude of PLD signaling in carcinogenesis, mechanisms that regulate PLD expression remain poorly

Antre nan paj
facebook nou an

Herbal & Natural Medicine

Baz done ki pi konplè remèd fèy medsin te apiye nan syans

Travay nan 55 lang
Geri èrbal te apiye nan syans
Remèd fèy rekonesans pa imaj
Kat entèaktif GPS - tag zèb sou kote (vini byento)
Li piblikasyon syantifik ki gen rapò ak rechèch ou an
Search remèd fèy medsin pa efè yo
Izeganize enterè ou yo ak rete kanpe fè dat ak rechèch la nouvèl, esè klinik ak rive

Tape yon sentòm oswa yon maladi epi li sou remèd fèy ki ta ka ede, tape yon zèb ak wè maladi ak sentòm li itilize kont.
* Tout enfòmasyon baze sou rechèch syantifik pibliye