Targeting molecular resistance in castration-resistant prostate cancer

Chandrasekar, Thenappan; Yang, Joy C.; Gao, Allen C.; Evans, Christopher P.

doi:10.1186/s12916-015-0457-6

Cited by 268 publications

(389 citation statements)

References 118 publications

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“…7) AR controlled signalling pathway can be triggered in castration-resistant prostate cancer (CRPC). 8) Therefore, therapeutic strategy focusing on inhibiting AR signalling pathway continues being a trend of research and clinical treatment.…”

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confidence: 99%

<i>Artesunate</i> Suppresses the Growth of Prostatic Cancer Cells through Inhibiting Androgen Receptor

Wang¹,

Wang²,

et al. 2017

Biological & Pharmaceutical Bulletin

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Prostatic cancer (PCa) is a leading cause of cancer related death in males and is often regarded as a kind of androgen-sensitive cancer. Artesunate (ART), a semi-synthetic derivative of the Chinese herb Artemisia annua, is such an anti-cancer agent. However, the effects and mechanism of ART on PCa cells remains unclear. The study aims to elaborate the mechanism of the involvement of androgen receptor (AR) in antiprostatic cancer (PCa) of artesunate (ART). PCa cells 22rvl were used in vivo and in vitro, and the viability and apoptosis were conducted using 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2H-tetrazolium bromide (MTT) and terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate nick-end labeling (TUNEL) assay, respectively. Ectopic expressions of AR and DNA methyltransferase (DNMT) were detected in cells in overexpression or interference of AR or DNMT3b. ART dose-dependently suppressed tumor growth, inhibited cell viability, enhanced apoptosis, decreased AR expression, and increased the expression and the catalytic activity of DNMT3b in 22rv1 cells either in transplanted mice or in vitro. Furthermore, AR downregulated DNMT3b expression, and overexpression of AR or interference of DNMT3b could reverse ART-induced cytotoxicity and apoptosis in 22rvl cells, whereas overexpression of DNMT3b could not change the effect profiles of ART on the cells. The results indicated that ART suppressed tumor growth of prostatic cancer cells through AR-DNMT3b pathway, underlying ART will allow for the utilization of this Chinese therapeutic agent for the potential treatment of prostate cancer.Key words artesunate; prostatic cancer; androgen receptor; DNA methyltransferase; apoptosis Prostatic cancer (PCa) is the most common cause of cancerrelated death in males. Morbidity and mortality of PCa underscore the need for novel treatment options. Although improved therapies have been recently developed to treat and prevent PCa, prostate cancer still remains refractory disease. Lately, herbs and phytochemicals 1) have been attractive as therapeutic agents for tumorigenesis suppression. Understanding how the production of these Chinese herbs is regulated during cancer progression would help develop new cancer therapeutic strategy.Artesunate (ART) is a semi-synthetic derivative of artemisinin, the active principle of the Chinese herb Artemisia annua. ART has been revealed remarkable activity against otherwise multidrug-resistant Plasmodium falciparum and P. vivax malaria. With the recognition of ART, it has now been analyzed for its anti-cancer activity in various tissues-specificity. For example, Tran et al. found that enhancement of ART activity could effectively induce the apoptosis of breast cancer cells. 2)Moreover, ART was proved to be as a novel therapeutic agent for metastatic renal cell carcinoma due to its attenuation action on tumor growth, metastasis.3) Recently, Michaelsen et al. clinically treated PCa patients with long-term Artemisia annua capsules via oral administration combined with shortterm ART inj...

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confidence: 99%

<i>Artesunate</i> Suppresses the Growth of Prostatic Cancer Cells through Inhibiting Androgen Receptor

Wang¹,

Wang²,

et al. 2017

Biological & Pharmaceutical Bulletin

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“…The current regimen requires administration of high doses of DTX, which induces toxic reactions; thus, combination of DTX with other agents is difficult. Acquired resistance to DTX-based therapy has also been observed [3]. To improve the survival and quality of life of patients with CRPC, it is necessary to modify classical chemotherapies and develop new combination therapies, as well as develop novel therapeutic strategies targeting the molecular basis of CRPC.…”

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confidence: 99%

Combined Effects of Fe3O4 Nanoparticles and Chemotherapeutic Agents on Prostate Cancer Cells In Vitro

et al. 2018

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Abstract:Patients with metastatic castration-resistant prostate cancer (mCRPC) have poor outcomes. Docetaxel (DTX)-based therapy is a current standard treatment for patients with mCRPC. Approaches combining conventional chemotherapeutic agents and nanoparticles (NPs), particularly iron oxide NPs, may overcome the serious side effects and drug resistance, resulting in the establishment of new therapeutic strategies. We previously reported the combined effects of

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“…The majority of cases with PCa responds to initial therapy and achieve a long-term remission; however, development of advanced castrationresistant PCa (CRPC) is inevitable [3,4]. Several drugs with different therapeutic mechanisms of action have been shown to prolong overall survival (OS) in patients with CRPC.…”

Section: Introductionmentioning

confidence: 99%

DNA Mismatch Repair in Advanced Metastatic Prostate Carcinoma: Clinical Perspective

Soni¹,

Bansal²

2017

JCPCR

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Prostate carcinoma (PCa) is among the most frequently diagnosed cancer in men worldwide. Men with metastatic PCa receive primary androgen deprivation therapy (ADT). However, nearly all men will develop resistance to primary ADT, a state known as castration-resistant prostate carcinoma a (CRPC). Several therapeutic drugs with different mechanisms of action have been approved for CRPC including systemic chemotherapeutics (docetaxel and cabazitaxel) and drugs targeting the resistance pathways leading to CRPC, including enzalutamide and abiraterone. Despite significant survival benefit, resistance to these therapies develops rapidly. Thus, deciphering the mechanisms of resistance and pathways leading to progression is the most critical objectives in PCa research. Some proofof-concept clinical trials have identified that personalized therapies with PARP inhibition, platinum chemotherapy, and immunotherapy may be beneficial to a subset of PCa and CRCP with underlying DNA repair defects. This review aims to address the potential therapeutic implication of Mismatch repair (MMR) pathways in advanced PCa and CRPC.

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Targeting molecular resistance in castration-resistant prostate cancer

Cited by 268 publications

References 118 publications

<i>Artesunate</i> Suppresses the Growth of Prostatic Cancer Cells through Inhibiting Androgen Receptor

<i>Artesunate</i> Suppresses the Growth of Prostatic Cancer Cells through Inhibiting Androgen Receptor

Combined Effects of Fe3O4 Nanoparticles and Chemotherapeutic Agents on Prostate Cancer Cells In Vitro

DNA Mismatch Repair in Advanced Metastatic Prostate Carcinoma: Clinical Perspective

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