Molecular and cellular biology of prostate cancer—the role of apoptosis as a target for therapy

Costa-Pereira, Ana P.; Cotter, Thomas G.

doi:10.1038/sj.pcan.4500305

Cited by 9 publications

(4 citation statements)

References 127 publications

(161 reference statements)

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“…Endogenous cannaboids play an important role in the neuronal control of the digestive tract [98], and Izzo and Coutts have suggested that the pharmacological administration of cannaboids, which, in part, act through TRPV1 channels could be used to treat colon cancer [98].As discussed above, TRPM8 is expressed in prostate cancer cells, its expression decreases as the cancer progresses to a more metastatic state, and hence TRPM8 is considered potentially useful for both the diagnosis of prostate cancer and as a target for cancer therapy. The treatment of prostate cancer would be greatly enhanced by better prediction of the course of the disease, including the likelihood of the development of androgen insensitivity and metastases, and by new strategies to kill androgen-insensitive prostate cancer cells which, as mentioned above, are resistant to apoptosis[78][79][80].…”

mentioning

confidence: 99%

TRP channels in cancer

Prevarskaya

Zhang²,

Barritt

2007

Biochimica et Biophysica Acta (BBA) - Molecular Basis of Diseas

282

201

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The progression of cells from a normal differentiated state in which rates of proliferation and apoptosis are balanced to a tumorigenic and metastatic state involves the accumulation of mutations in multiple key signalling proteins and the evolution and clonal selection of more aggressive cell phenotypes. These events are associated with changes in the expression of numerous other proteins. This process of tumorigenesis involves the altered expression of one or more TRP proteins, depending on the nature of the cancer. The most clearly described changes are those involving TRPM8, TRPV6 and TRPM1. Expression of TRPM8 is substantially increased in androgen-dependent prostate cancer cells, but is decreased in androgen independent and metastatic prostate cancer. TRPM8 expression is regulated, in part, by androgens, most likely through androgen response elements in the TRPM8 promoter region. TRPM8 channels are involved in the regulation of cell proliferation and apoptosis. Expression of TRPV6 is also increased in prostate cancer and in a number of other cancers. In contrast to TRPM8, expression of TRPV6 is not directly regulated by androgens. TRPM1 is highly expressed in early stage melanomas but its expression declines with increases in the degree of aggressiveness of the melanoma. The expression of TRPV1, TRPC1, TRPC6, TRPM4, and TRPM5 is also increased in some cancers. The level of expression of TRPM8 and TRPV6 in prostate cancer, and of TRPM1 in melanomas, potentially provides a good prognostic marker for predicting the course of the cancer in individuals. The Drosophila melanogaster, TRPL, and the TRPV1 and TRPM8 proteins, have been used to try to develop strategies to selectively kill cancer cells by activating Ca(2+) and Na(+) entry, producing a sustained increase in the cytoplasmic concentration of these ions, and subsequent cell death by apoptosis and necrosis. TRPV1 is expressed in neurones involved in sensing cancer pain, and is a potential target for pharmacological inhibition of cancer pain in bone metastases, pancreatic cancer and most likely in other cancers. Further studies are required to assess which other TRP proteins are associated with the development and progression of cancer, what roles TRP proteins play in this process, and to develop further knowledge of TRP proteins as targets for pharmaceutical intervention and targeting in cancer.

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mentioning

confidence: 99%

TRP channels in cancer

Prevarskaya

Zhang²,

Barritt

2007

Biochimica et Biophysica Acta (BBA) - Molecular Basis of Diseas

282

201

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“…The onset and progression of cancer is characterized by cell cycle dysregulation, leading to enhanced cell growth, concomitant with suppression of mechanisms responsible for cell death (1)(2)(3)(4). Notably, dysregulated homeostasis of intracellular Ca 2+ is involved in cancer.…”

Section: Introductionmentioning

confidence: 99%

“…For example, ligand binding to several membrane receptors triggers a series of events, leading to the activation of phospholipase C (PLC) and synthesis of inositol-1,4,5-trisphosphate (Ins(1,4,5)P3). Ins (1,4,5)P3 opens the Ins (1,4,5)P3 receptor (IP3R), which is an intracellular ion channel and expressed mostly in the endoplasmic reticulum, resulting in the release of Ca 2+ from the endoplasmic reticulum (7,8). Ca 2+ signals in the form of spikes, oscillations or waves are spatially and temporally tightly regulated (9) to avoid prolonged intracellular elevation of Ca 2+ that is toxic and lethal for cells (10).…”

Section: Introductionmentioning

confidence: 99%

Emerging role of transient receptor potential (TRP) channels in cancer progression

Yang

Kim

2020

BMB Rep.

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Transient receptor potential (TRP) channels comprise a diverse family of ion channels, the majority of which are calcium permeable and show sophisticated regulatory patterns in response to various environmental cues. Early studies led to the recognition of TRP channels as environmental and chemical sensors. Later studies revealed that TRP channels mediated the regulation of intracellular calcium. Mutations in TRP channel genes result in abnormal regulation of TRP channel function or expression, and interfere with normal spatial and temporal patterns of intracellular local Ca 2+ distribution. The resulting dysregulation of multiple downstream effectors, depending on Ca 2+ homeostasis, is associated with hallmarks of cancer pathophysiology, including enhanced proliferation, survival and invasion of cancer cells. These findings indicate that TRP channels affect multiple events that control cellular fate and play a key role in cancer progression. This review discusses the accumulating evidence supporting the role of TRP channels in tumorigenesis, with emphasis on prostate cancer. [BMB Reports 2020; 53(3): 125-132]

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“…Contradictions as to the direct role of TP53 in prostate cancer abound in the literature, but TP53 mutations appear to be more common in high-grade, metastatic and androgen-independent human prostate cancer (Bookstein et al, 1993; Chi et al, 1994; Costa-Pereira and Cotter, 1999; Gumerlock et al, 1997; Meyers et al, 1998). …”

Section: Introductionmentioning

confidence: 99%

Simultaneous haploinsufficiency of Pten and Trp53 tumor suppressor genes accelerates tumorigenesis in a mouse model of prostate cancer

et al. 2009

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Tumor suppressor gene PTEN is important in the initiation and progression of human prostate carcinoma, whereas the role of TP53 remains controversial. Since Pten/Trp53 double conditional knockout mice show earlier onset and fast progression of prostate cancer when compared to Pten knockout mice, we asked whether heterozygosity of these two tumor suppressor genes was sufficient to accelerate prostatic tumorigenesis. To answer this question we examined prostatic lesion progression of Pten/Trp53 double heterozygous mice and a series of controls such as Pten heterozygous, Pten conditional knockout, Trp53 heterozygous and Trp53 knockout mice. Tissue recombination of adult prostatic epithelium coupled with embryonic rat seminal vesicle mesenchyme was used as a tool to stimulate prostatic epithelial proliferation. In our study, high-grade prostatic intraepithelial neoplasia (PIN) was found with high frequency at 8 weeks post-tissue recombination transplantation. PIN lesions in Pten/Trp53 double heterozygous mice were more severe than those seen in Pten heterozygous alone. Furthermore, morphologic features attributable to Pten or Trp53 loss appeared to be enhanced in double heterozygous tissues. LOH analysis of Pten and Trp53 in genomic DNA collected from high-grade PIN lesions in Pten heterozygous and Pten/Trp53 double heterozygous mice showed an intact wild-type allele for both genes in all samples examined. In conclusion, simultaneous heterozygosity of Pten and Trp53 accelerates prostatic tumorigenesis in this mouse model of prostate cancer independently of loss of heterozygosity of either gene.

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Molecular and cellular biology of prostate cancer—the role of apoptosis as a target for therapy

Cited by 9 publications

References 127 publications

TRP channels in cancer

TRP channels in cancer

Emerging role of transient receptor potential (TRP) channels in cancer progression

Simultaneous haploinsufficiency of Pten and Trp53 tumor suppressor genes accelerates tumorigenesis in a mouse model of prostate cancer

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