Metallothioneins and resistance to cisplatin and radiation in prostate cancer

Smith, David J.; Jaggi, Meena; Zhang, Wenguang; Galich, Anton; Du, Cheng; Sterrett, Samuel P.; Smith, Lynette M.; Balaji, K.C.

doi:10.1016/j.urology.2005.12.032

Cited by 37 publications

(31 citation statements)

References 14 publications

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“…Prostate cancer cells treated with Zn showed induction of MT expression in association with resistance to cisplatin [91]. Moreover, double knockout mice bearing MT-I/II deletions exhibited elevated sensitivities to cisplatin-induced hepatocellular carcinoma [92].…”

Section: Metallothioneinsmentioning

confidence: 99%

The roles of copper transporters in cisplatin resistance

Kuo

Chen

Song

et al. 2007

Cancer Metastasis Rev

252

222

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Platinum-based antitumor agents have been effective in the treatments of many human malignancies but the ultimate success of these agents is often compromised by development of drug resistance. One mechanism associated with resistance to platinum drugs is reduced intracellular accumulation owing to impaired drug intake, enhanced outward transport, or both. Mechanisms for transporting platinum drugs were not known until recent demonstrations that import and export transporters involved in maintenance copper homeostasis are also involved in the transport of these drugs. Ctr1, the major copper influx transporter, has been convincingly demonstrated to transport cisplatin and its analogues, carboplatin, and oxaliplatin. Evidence also suggests that the two copper efflux transporters ATP7A and ATP7B regulate the efflux of cisplatin. These observations are intriguing, because conventional thinking of the inorganic physiologic chemistry of cisplatin and copper is quite different. Hence, understanding the underlying mechanistic aspects of these transporters is critically important. While the mechanisms by which hCtr1, ATP7A and ATP7B transport copper ions have been studied extensively, very little is known about the mechanisms by which these transporters shuffle platinum-based antitumor agents. This review discusses the identification of copper transporters as platinum drug transporters, the structural-functional and mechanistic aspects of these transporters, the mechanisms that regulate their expression, and future research directions that may eventually lead to improved efficacy of platinum-based-based drugs in cancer chemotherapy through modulation of their transporters' activities.

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Section: Metallothioneinsmentioning

confidence: 99%

The roles of copper transporters in cisplatin resistance

Kuo

Chen

Song

et al. 2007

Cancer Metastasis Rev

252

222

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“…The metal ion-binding metallothionein (MT) superfamily has also been implicated in treatment-resistant prostate cancer. As there are unusually high levels of zinc in the prostate compared to the rest of the body [166], it is possible that this tissue already has high basal MT levels [167].…”

Section: / 19mentioning

confidence: 99%

Therapy escape mechanisms in the malignant prostate

Santer

Erb

McNeill

2015

Seminars in Cancer Biology

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Androgen receptor (AR) is the main target for prostate cancer therapy. Clinical approaches for AR inactivation include chemical castration, inhibition of androgen synthesis and AR antagonists (anti-androgens). However, treatment resistance occurs for which an important number of therapy escape mechanisms have been identified. Herein, we summarise the current knowledge of molecular mechanisms underlying therapy resistance in prostate cancer. Moreover, the tumour escape mechanisms are arranged into the concepts of target modification, bypass signalling, histologic transformation, cancer stem cells and miscellaneous mechanisms. This may help researchers to compare and understand same or similar concepts of therapy resistance in prostate cancer and other cancer types.

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“…Studies with overexpression or knockdown cell line models of PKD1 showed that PKD1 negatively modulates the function of AR (37) through the modulation of Hsp27-mediated AR functions (38). Additionally, PKD1 was found to be involved in the invasion of prostate cancer cells via modulation of matrix metalloproteinase (MMP)-2 and MMP-9 (66) or metallothionin 2A, a protein that is involved in cell proliferation and chemoresistance of cancer cells (67, 68). A recent study revealed that PKD1 plays a vital role in epithelial-mesenchymal transition (EMT) by modulating the function of transcription factor snail, a central regulator of EMT (65).…”

Section: Pkd1 In Cancermentioning

confidence: 99%

Emerging Roles of Protein Kinase D1 in Cancer

Sundram

Chauhan

Jaggi

2011

Molecular Cancer Research

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Protein kinase D1 (PKD1) is a serine-threonine kinase that regulates various functions within the cell, including cell proliferation, apoptosis, adhesion, and cell motility. In normal cells, this protein plays key roles in multiple signaling pathways by relaying information from the extracellular environment and/or upstream kinases and converting them into a regulated intracellular response. The aberrant expression of PKD1 is associated with enhanced cancer phenotypes, such as deregulated cell proliferation, survival, motility, and epithelial mesenchymal transition. In this review, we summarize the structural and functional aspects of PKD1 and highlight the pathobiological roles of this kinase in cancer.

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Metallothioneins and resistance to cisplatin and radiation in prostate cancer

Cited by 37 publications

References 14 publications

The roles of copper transporters in cisplatin resistance

The roles of copper transporters in cisplatin resistance

Therapy escape mechanisms in the malignant prostate

Emerging Roles of Protein Kinase D1 in Cancer

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