Upregulation of miRNA3195 and miRNA374b Mediates the Anti-Angiogenic Properties of Melatonin in Hypoxic PC-3 Prostate Cancer Cells

Sohn, Eun Jung; Won, Gunho; Lee, Ji‐Hyun; Lee, Sang Yoon; Kim, Sung Hoon

doi:10.7150/jca.9591

Cited by 98 publications

(83 citation statements)

References 42 publications

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“…In relation to this point, an investigation of the anti-angiogenic effects of melatonin on hypoxic PCa PC3 cells identified a melatonindependent increase in the expression of miR-374b. Subsequent studies confirmed that miR-374b mediated the anti-angiogenic effects of melatonin by inhibiting VEGF expression (Sohn et al 2015).…”

Section: Post-transcriptional Regulation Of Vegf Signaling In Pcamentioning

confidence: 59%

Regulation of vascular endothelial growth factor in prostate cancer

Brot¹,

Ntekim²,

Cardenas³

et al. 2015

Endocrine-Related Cancer

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Prostate cancer (PCa) is the most common malignancy affecting men in the western world. Although radical prostatectomy and radiation therapy can successfully treat PCa in the majority of patients, up to w30% will experience local recurrence or metastatic disease. Prostate carcinogenesis and progression is typically an androgen-dependent process. For this reason, therapies for recurrent PCa target androgen biosynthesis and androgen receptor function. Such androgen deprivation therapies (ADT) are effective initially, but the duration of response is typically %24 months. Although ADT and taxane-based chemotherapy have delivered survival benefits, metastatic PCa remains incurable. Therefore, it is essential to establish the cellular and molecular mechanisms that enable localized PCas to invade and disseminate. It has long been accepted that metastases require angiogenesis. In the present review, we examine the essential role for angiogenesis in PCa metastases, and we focus in particular on the current understanding of the regulation of vascular endothelial growth factor (VEGF) in localized and metastatic PCa. We highlight recent advances in understanding the role of VEGF in regulating the interaction of cancer cells with tumor-associated immune cells during the metastatic process of PCa. We summarize the established mechanisms of transcriptional and post-transcriptional regulation of VEGF in PCa cells and outline the molecular insights obtained from preclinical animal models of PCa. Finally, we summarize the current state of anti-angiogenesis therapies for PCa and consider how existing therapies impact VEGF signaling.

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Section: Post-transcriptional Regulation Of Vegf Signaling In Pcamentioning

confidence: 59%

Regulation of vascular endothelial growth factor in prostate cancer

Brot¹,

Ntekim²,

Cardenas³

et al. 2015

Endocrine-Related Cancer

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“…Melatonin inhibition of HIF1α signaling and reactive oxygen species generation has also been established (Cho, et al 2011; Park et al 2009; Paroni, et al 2014). Several microRNA (miRNA)s including miR3195 and miR374b were significantly up-regulated while other miRNAs were down-regulated in melatonin-treated cells under hypoxia compared to untreated control (Sohn, et al 2015). In addition to hypoxia and androgen deprivation, melatonin also seems to sensitize CaP cell lines to cell death under hypoglycemic conditions (Gobbo, et al 2015; Kabasakal, et al 2011).…”

Section: Melatonin Regulation Of Prostate Carcinogenesismentioning

confidence: 99%

WOMEN IN CANCER THEMATIC REVIEW: Circadian rhythmicity and the influence of ‘clock’ genes on prostate cancer

Kiss

Ghosh

2016

Endocrine-Related Cancer

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The androgen receptor (AR) plays a key role in the development and progression of prostate cancer (CaP). Since the mid-1990s, reports in the literature pointed out higher incidences of CaP in some select groups, such as airline pilots and night shift workers in comparison to those working regular hours. The common finding in these “high-risk” groups was that they all experienced a deregulation of the body’s internal circadian rhythm. Here we discuss how the circadian rhythm affects androgen levels and modulates CaP development and progression. Circadian rhythmicity of androgen production is lost in CaP patients, with the clock genes Per1 and Per2 decreasing, and Bmal1 increasing, in these individuals. Periodic expression of the clock genes was restored upon administration of the neurohormone melatonin, thereby suppressing CaP progression. Activation of the melatonin receptors and the AR antagonized each other, and therefore the tumor suppressive effects of melatonin and the clock genes were most clearly observed in the absence of androgens, that is, in conjunction with androgen deprivation therapy (ADT). In addition, a large-scale study found that high-dose radiation was more effective in CaP patients when it was delivered before 5PM, compared to those delivered after 5PM, suggesting that the therapy was more effective when delivered in synchrony with the patient’s circadian clock. As CaP patients are shown to become easily resistant to new therapies, perhaps circadian delivery of these therapeutic agents or delivery in conjunction with melatonin and its novel analogs should be tested to see if they prevent this resistance.

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“…However, the mechanisms of melatonin's antiangiogenic in any tumor including NSCLC are still unclear. Numerous studies have documented that melatonin exhibits antiangiogenic actions, in part, by downregulating VEGF and HIF-1α in several cancers via different mechanisms; the cancer types included breast [16, 149], prostate [150–152], colon [153, 154], liver [155], and pancreatic cancer [156, 157]. These studies may provide reference for the future work in the NSCLC research field.…”

Section: Potential Directionsmentioning

confidence: 99%

Melatonin as a potential anticarcinogen for non-small-cell lung cancer

Yang

Fan

et al. 2016

Oncotarget

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Non-small-cell lung cancer (NSCLC) is a leading cause of death from cancer worldwide. Melatonin, an indoleamine discovered in the pineal gland, exerts pleiotropic anticancer effects against a variety of cancer types. In particular, melatonin may be an important anticancer drug in the treatment of NSCLC. Herein, we review the correlation between the disruption of the melatonin rhythm and NSCLC incidence; we also evaluate the evidence related to the effects of melatonin in inhibiting lung carcinogenesis. Special focus is placed on the oncostatic effects of melatonin, including anti-proliferation, induction of apoptosis, inhibition of invasion and metastasis, and enhancement of immunomodulation. We suggest the drug synergy of melatonin with radio- or chemotherapy for NSCLC could prove to be useful. Taken together, the information complied herein may serve as a comprehensive reference for the anticancer mechanisms of melatonin against NSCLC, and may be helpful for the design of future experimental research and for advancing melatonin as a therapeutic agent for NSCLC.

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Upregulation of miRNA3195 and miRNA374b Mediates the Anti-Angiogenic Properties of Melatonin in Hypoxic PC-3 Prostate Cancer Cells

Cited by 98 publications

References 42 publications

Regulation of vascular endothelial growth factor in prostate cancer

Regulation of vascular endothelial growth factor in prostate cancer

WOMEN IN CANCER THEMATIC REVIEW: Circadian rhythmicity and the influence of ‘clock’ genes on prostate cancer

Melatonin as a potential anticarcinogen for non-small-cell lung cancer

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