PTHrP on MCF-7 breast cancer cells: a growth factor or an antimitogenic peptide?

Maioli, Emanuela; Fortino, Vittoria

doi:10.1038/sj.bjc.6601689

Cited by 10 publications

(14 citation statements)

References 14 publications

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“…As Fig. 4b shown, the treatment of PTHrP (1-40) inhibits cell proliferation in MCF-7 cells, which is coincident with the previous findings (Maioli and Fortino 2004). The similar effect was observed in the group treated with dbcAMP.…”

Section: Pthrp Inhibits Bmp-6 Transcription Through the Pka Signalingsupporting

confidence: 92%

“…PTHrP inhibits endothelial cell migration in vitro and angiogenesis in vivo by activating protein kinase A (Bakre et al 2002). Maioli and Fortino (2004) found that PTHrP inhibits breast cancer cell proliferation through the combined action of the adenylylcyclase (AC)/PKA and phospholipase C (PLC)/PKC pathways. In our experiment, we have observed the same function of PTHrP/PKA.…”

Section: Discussionmentioning

confidence: 99%

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PTHrP inhibits BMP-6 expression through the PKA signaling pathway in breast cancer cells

Zhang

Yan

et al. 2010

J Cancer Res Clin Oncol

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Section: Pthrp Inhibits Bmp-6 Transcription Through the Pka Signalingsupporting

confidence: 92%

Section: Discussionmentioning

confidence: 99%

PTHrP inhibits BMP-6 expression through the PKA signaling pathway in breast cancer cells

Zhang

Yan

et al. 2010

J Cancer Res Clin Oncol

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“…In addition, overexpression of PTHrP specifically in the mammary gland shortened tumor latency and increased tumor incidence following exposure to the chemical carcinogen dimethylbenzanthracene [75]. In this case, visceral metastasis was not accompanied by bone metastasis [76]. On the other hand, when mice inoculated with PTHrP secreting MDA-MB-231, bone metastases was significantly attenuated by neutralizing antibody against PTHrP-(1-34) [77].…”

Section: Car and Breast Cancermentioning

confidence: 91%

Calcium-sensing receptor in cancer: good cop or bad cop?

Chakravarti

Dwivedi

Mithal

et al. 2008

Endocr

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The extracellular calcium-sensing receptor (CaR) is a versatile 'sensor' for di- and polycationic molecules in the body. CaR plays a key role in the defense against hypercalcemia by "sensing" extracellular calcium levels in the parathyroid and kidney, the key organs maintaining systemic calcium homeostasis. Although mutation of CaR gene has so far not been associated with any malignancy, aberrant functions of CaR have implications in malignant progression. One situation is loss of CaR expression, resulting in loss of growth suppressing effects of elevated extracellular Ca(2+) by CaR, reported in parathyroid adenoma and in colon carcinoma. Another situation is activation of CaR, resulting in increased production of parathyroid hormone-related peptide (PTHrP), a primary causal factor in hypercalcemia of malignancy and a contributor to metastatic processes involving bone. CaR signaling and effects have been studied in several cancers including ovarian cancers, gastrinomas, and gliomas in addition to comparatively detailed studies in breast, prostate, and colon cancers. Studies on H-500 rat Leydig cells, a xenotransplantable model of humoral hypercalcemia of malignancy has shed much light on the mechanisms of CaR-induced cancer cell growth and survival. Pharmacological agonists and antagonists of CaR hold therapeutic promise depending on whether activation of CaR is required such as in case of colon cancer or inactivating the receptor is required as in the case of breast- and prostate tumors.

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“…As far as the action of cAMP/PKA on cell growth is concerned, a stimulatory effect has been described, for example, in PC12 cells [6] and in rat enterocytes [11], whereas growth arrest is evoked in skin fibroblasts [4] and in MCF-7 breast cancer cells [12].…”

Section: The Pka/raf-1/ras-mek-erk Cascadementioning

confidence: 99%

Functional interactions of protein kinase A and C in signalling networks: a recapitulation

Maioli

Torricelli

Fortino

2006

Cell. Mol. Life Sci.

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On the basis of evidence collected from the literature, we propose a general model by which protein kinase (PK) A and the different PKC isoforms can inversely affect cell growth. Molecular switches, which are able to direct the signal towards antiproliferative or mitogenic pathways, are the different isoforms of Raf and PKC. Conflicting data are also reported and discussed in an attempt to reconcile them.

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PTHrP on MCF-7 breast cancer cells: a growth factor or an antimitogenic peptide?

Cited by 10 publications

References 14 publications

PTHrP inhibits BMP-6 expression through the PKA signaling pathway in breast cancer cells

PTHrP inhibits BMP-6 expression through the PKA signaling pathway in breast cancer cells

Calcium-sensing receptor in cancer: good cop or bad cop?

Functional interactions of protein kinase A and C in signalling networks: a recapitulation

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