“Thymineless” death in androgen-independent prostatic cancer cells

Kyprianou, Natasha; Isaacs, John T.

doi:10.1016/0006-291x(89)91035-8

Cited by 86 publications

(38 citation statements)

References 21 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…In this regard, several important publications have revealed the fact that, despite offering resistance to several apoptotic stimuli such as androgen withdrawal, serum starvation or phorbol ester treatment, androgen-insensitive prostate cancer cells do in fact maintain the basic and apparently functional apoptotic machinery which could be activated under certain circumstances. 40,41 So, a central aim of this study has been to test the hypothesis that the apoptotic machinery of the prostate cancer cells may be activated despite the presence of apoptosis suppressor proteins such as bcl-2 and bcl-X L for tumoricidal purposes and that the unwanted hormone refractory prostate cancer cells can be forced to commit to apoptosis. Hence, a down-regulation of proteins such a bcl-2 and bcl-X L will have signi®cant therapeutic bene®ts in a major fraction of prostate cancer patients who over-express these proteins.…”

Section: Discussionmentioning

confidence: 99%

Therapeutic potential of curcumin in human prostate cancer—I. curcumin induces apoptosis in both androgen-dependent and androgen-independent prostate cancer cells

Dorai

Gehani

Katz

2000

Prostate Cancer Prostatic Dis

108

View full text Add to dashboard Cite

In an effort to ®nd an alternative nontoxic means of inducing the apoptosis potential in both androgen-dependent and hormone refractory prostate cancer cells, attention was focused on curcumin (turmeric), traditionally used in medicine and cuisine in India and other south-east Asian countries. The results indicate that curcumin is a novel and potent inducer of apoptosis in both androgen-dependent and androgen-independent prostate cancer cells. This was accomplished by down-regulating apoptosis suppressor proteins and other crucial proteins such as the androgen receptor. It is concluded that curcumin may provide an alternative, nontoxic modality by which the clinician may prevent the progression of prostate cancer to its hormone refractory state or to treat advanced prostate cancer by forcing them to undergo apoptosis. Prostate Cancer and Prostatic Diseases (2000) 3, 84±93.

show abstract

Section: Discussionmentioning

confidence: 99%

Therapeutic potential of curcumin in human prostate cancer—I. curcumin induces apoptosis in both androgen-dependent and androgen-independent prostate cancer cells

Dorai

Gehani

Katz

2000

Prostate Cancer Prostatic Dis

108

View full text Add to dashboard Cite

show abstract

“…Besides inactivation of key androgen-dependent genes (for example, prostate-specific antigen), androgen withdrawal leads to the activation of specific genes involved in programmed cell death. 8,9 In addition to these direct effects many growth factors and their receptors are regulated by androgens. Thus, the action of testosterone and DHT in the prostate is mediated indirectly through autocrine and paracrine pathways.…”

Section: Etiology Of Bphmentioning

confidence: 99%

Pathology of benign prostatic hyperplasia

2008

View full text Add to dashboard Cite

The epidemiology of benign prostatic hyperplasia (BPH) is complex and not fully understood. The androgenic hormones testosterones and dihydrotestosterone play at least a permissive and important role. Growth factors and other hormones including estrogens may also play a role. BPH is a truely hyperplastic process resulting in growth of glandular-epithelial and stromal/muscle tissue in the prostate, leading to often measurable growth taking on different shapes and configurations which may impact symptoms and secondary outcomes. It is important to recognize that BPH is a histological conditions, which is one but not the only cause of lower urinary tract symptoms, and may or may not be associated with prostate enlargement and bladder outlet obstruction. Recognizing the different entities and determining their presence in individual patients may help with therapeutic decision making.

show abstract

“…There are a variety of agents that induce apoptotic death of normal and malignant cells through highly variable signaling pathways that do not produce an initial rise in [Ca 2+ ] i : the thymidylate synthase inhibitor, 5-FdUR; 25 the alkylating/ topoisomerase inhibitor, doxorubicin; 26 ionizing g-irradiation; 27,28 and growth factor TGFb-1. 29,30 We followed the kinetics of apoptosis for each of these agents (see Table 1 for concentrations) in a series of normal and malignant cell lines by measuring the loss of clonogenic survival and the DNA fragmentation at 0, 12, 24, 48, 72 and 96 h post-exposure to the inducing agent.…”

Section: Resultsmentioning

confidence: 99%

A supramicromolar elevation of intracellular free calcium ([Ca2+]i) is consistently required to induce the execution phase of apoptosis

Tombal

Denmeade²,

Gillis

et al. 2002

Cell Death Differ

View full text Add to dashboard Cite

Many agents, such as the endoplasmic reticulum Ca 2+ ATPase inhibitor, thapsigargin, or the ionophore, ionomycin, induce apoptosis by transiently elevating [Ca 2+ ] i . The role of [Ca 2+ ] i in apoptosis induced by agents that do not immediately increase [Ca 2+ ] i , such as 5-FdUr, TGFb-1, doxorubicin, or radiation, is far more controversial. In the present paper, [Ca 2+ ] i was measured continuously for 120 h. in prostate and bladder cancer cell lines exposed to these four agents: 5-FdUR, TGFb-1, doxorubicin, or radiation. Each of them consistently induced a delayed [Ca 2+ ] i rise associated with the morphological changes that characterize the execution phase of apoptosis (i.e. rounding, blebbing). This [Ca 2+ ] i rise occurred in two consecutive steps (410 mM and 410 mM) and resulted from a Ca 2+ influx from the extracellular medium. This delayed supramicromolar [Ca 2+ ] i rise was also observed previously in breast, prostate and bladder cancer cell lines exposed to thapsigargin. This influx regulated transcriptional reprogramming of Gadd153 and is required to activate cytochrome c release, caspase-3 activation, loss of clonal survival and DNA fragmentation. When cells were maintained in low extracellular Ca 2+ media, these phenomena were temporarily delayed but occurred on return to normal Ca 2+ medium. Similarly, apoptosis could be delayed by overexpressing the Ca 2+ -binding proteins, Calbindin-D 28K and parvalbumin. As this delayed 510 mM [Ca 2+ ] i elevation was observed in a number of cell lines exposed to a variety of different agents, we conclude that such elevation constitutes a key and general event of apoptosis in these malignant cells.

show abstract

“Thymineless” death in androgen-independent prostatic cancer cells

Cited by 86 publications

References 21 publications

Therapeutic potential of curcumin in human prostate cancer—I. curcumin induces apoptosis in both androgen-dependent and androgen-independent prostate cancer cells

Therapeutic potential of curcumin in human prostate cancer—I. curcumin induces apoptosis in both androgen-dependent and androgen-independent prostate cancer cells

Pathology of benign prostatic hyperplasia

A supramicromolar elevation of intracellular free calcium ([Ca2+]i) is consistently required to induce the execution phase of apoptosis

Contact Info

Product

Resources

About