Clinical trials of note

Printz, Carrie

doi:10.1002/cncr.24673

Cited by 46 publications

(12 citation statements)

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“…Lapatinib and pazopanib were also demonstrated effective in preventing breast cancer metastasis [191, 192]. What is more is that sorafenib was suggested to be applied for preventing hepatocellular carcinoma recurrence after liver transplantation [193]. All these findings implied that Cav-1 phosphorylation inhibition might be a promising strategy for cancer prevention, and it is of great value to develop Cav-1-targeted TKI for cancer prevention.…”

Section: Therapeutic Implication Of Cav-1-targeted Treatment For Cmentioning

confidence: 99%

Caveolin-1: An Oxidative Stress-Related Target for Cancer Prevention

Wang

Zheng

et al. 2017

Oxidative Medicine and Cellular Longevity

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Aberrant oxidative metabolism is one of the hallmarks of cancer. Reactive species overproduction could promote carcinogenesis via inducing genetic mutations and activating oncogenic pathways, and thus, antioxidant therapy was considered as an important strategy for cancer prevention and treatment. Caveolin-1 (Cav-1), a constituent protein of caveolae, has been shown to mediate tumorigenesis and progression through oxidative stress modulation recently. Reactive species could modulate the expression, degradation, posttranslational modifications, and membrane trafficking of Cav-1, while Cav-1-targeted treatments could scavenge the reactive species. More importantly, emerging evidences have indicated that multiple antioxidants could exert antitumor activities in cancer cells and protective activities in normal cells by modulating the Cav-1 pathway. Altogether, these findings indicate that Cav-1 may be a promising oxidative stress-related target for cancer antioxidant prevention. Elucidating the underlying interaction mechanisms between oxidative stress and Cav-1 is helpful for enhancing the preventive effects of antioxidants on cancer, for improving clinical outcomes of antioxidant-related therapeutics in cancer patients, and for developing Cav-1 targeted drugs. Herein, we summarize the available evidence of the roles of Cav-1 and oxidative stress in tumorigenesis and development and shed novel light on designing strategies for cancer prevention or treatment by utilizing the interaction mode between Cav-1 and oxidative stress.

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Section: Therapeutic Implication Of Cav-1-targeted Treatment For Cmentioning

confidence: 99%

Caveolin-1: An Oxidative Stress-Related Target for Cancer Prevention

Wang

Zheng

et al. 2017

Oxidative Medicine and Cellular Longevity

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“…To date, several relatively large phase 3 trials have been conducted, which demonstrated limited efficacy and utility of the tested therapies [130–132]. Tertiary prevention targets recurrence of de novo second primary HCC after curative treatment of initial primary HCC, but available evidence is still scarce [149–151]. Theoretically, secondary and tertiary prevention could be achieved by anti-HCV therapies and/or non-etiology-specific therapies targeting inflammation, fibrogenesis, and/or carcinogenesis, which have been extensively studied in the past decades.…”

Section: Prevention Of Hcv-induced Hccmentioning

confidence: 99%

Pathogenesis and prevention of hepatitis C virus-induced hepatocellular carcinoma

Hoshida

Fuchs

Bardeesy

et al. 2014

Journal of Hepatology

185

173

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Summary Hepatitis C virus (HCV) is one of the major etiologic agents that causes hepatocellular carcinoma (HCC) by generating an inflammatory, fibrogenic, and carcinogenic tissue microenvironment in the liver. HCV-induced HCC is a rational target for cancer preventive intervention because of the clear-cut high-risk condition, cirrhosis, associated with high cancer incidence (1% to 7% per year). Studies have elucidated direct and indirect carcinogenic effects of HCV, which have in turn led to identification of candidate HCC chemoprevention targets. Selective molecular targeted agents may enable personalized strategies for HCC chemoprevention. In addition, multiple experimental and epidemiological studies suggest the potential value of generic drugs or dietary supplements targeting inflammation, oxidant stress, or metabolic derangements as possible HCC chemopreventive agents. While the successful use of highly effective direct-acting antiviral agents will make important inroads into reducing long term HCC risk, there will remain an important role for HCC chemoprevention even after viral cure, given the persistence of HCC risk in persons with advanced HCV fibrosis as shown in recent studies. The successful development of cancer preventive therapies will be more challenging compared to cancer therapeutics because of the requirement for larger and longer clinical trials and the need for a safer toxicity profile given its use as a preventive agent. Molecular biomarkers to selectively identify high-risk population could help mitigate these challenges. Genome-wide, unbiased molecular characterization, high-throughput drug/gene screening, experimental model-based functional analysis, and systems-level in silico modeling are expected to complement each other to facilitate discovery of new HCC chemoprevention targets and therapies.

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“…Nowadays, drug intervention with antineoplastic and laparoscopic surgery is widely utilized to treat HCC patients [3]. But their 5-year survival rate remains low because many patients are diagnosed at the late stage of HCC and due to a high incidence of recurrence [4]. An improved understanding of the pathogenesis of HCC development would facilitate the development of more effective outcomes for the diagnosis and treatment of HCC at earlier stages.…”

Section: Introductionmentioning

confidence: 99%

Down-regulated miR-28-5p in human hepatocellular carcinoma correlated with tumor proliferation and migration by targeting insulin-like growth factor-1 (IGF-1)

Shi

Teng

2015

Mol Cell Biochem

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Hepatocellular carcinoma (HCC) is a rapidly progressing, incurable cancer that frequently spreads to portal vein and lung. New insights are needed to identify therapeutic targets to prevent or retard HCC metastatic progression. Because microRNAs (miRNA) often act as tumor regulators, we investigated their role in preclinical models of HCC. Here we found miR-28-5p is a liver-relevant anti-proliferative miRNA whose expression, functions, and mechanisms were analyzed in human hepatoma cells, HepG2 and Huh7. Interestingly, when evaluating the specific targets of miR-28-5p, we found that ectopic miR-28-5p expression down-regulates insulin-like growth factor 1 (IGF1) protein and that the expression of miR-28-5p correlates negatively with IGF1 protein in HCC cells. Luciferase report in HCC cells expressing miR-28-5p suggests that miR-28-5p reduces luciferase activity by targeting the 3'-UTR of IGF1 mRNA. Additionally, we show that the selective inhibition of either the PI3K/AKT pathway prior to miR-28-5p stimulation prevents the expression of previously described tumor suppressor miRNAs that are family and cluster specific. Together, our results defined miR-28-5p as a critical regulator of IGF1 mRNA translation function, down-regulated miR-28-5p in HCC was associated with tumor growth through PI3K/AKT pathway by targeting IGF1. miR-28-5p-IGF1-PI3K/AKT pathway may play an important role in the development of HCC.

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Clinical trials of note

Cited by 46 publications

References 0 publications

Caveolin-1: An Oxidative Stress-Related Target for Cancer Prevention

Caveolin-1: An Oxidative Stress-Related Target for Cancer Prevention

Pathogenesis and prevention of hepatitis C virus-induced hepatocellular carcinoma

Down-regulated miR-28-5p in human hepatocellular carcinoma correlated with tumor proliferation and migration by targeting insulin-like growth factor-1 (IGF-1)

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