Yiwei Li

Karmanos Cancer Institute, Detroit, Michigan, United States

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Publications (156)698.39 Total impact

  • Yiwei Li · Fazlul H Sarkar ·
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    ABSTRACT: Castration-resistant prostate cancer (CRPC) progression after androgen deprivation therapy shows upregulated expression of androgen receptor (AR) splice variants, induced epithelial-to-mesenchymal transition phenotypes and enhanced stem cell characteristics, all of which are associated with resistance to enzalutamide. Since there is no curative treatment for CRPC, innovative treatments are urgently needed. In our recent study, we found that resistance to enzalutamide was partly due to deregulated expression of microRNAs such as miR-34a, miR-124, miR-27b, miR-320 and let-7, which play important roles in regulating AR and stem cell marker gene expression that appears to be linked with resistance to enzalutamide. Importantly, we found that BioResponse 3,3'-diindolylmethane (BR-DIM) treatment in vitro and in vivo caused downregulation in the expression of wild-type AR. The AR splice variants, Lin28B and EZH2, appear to be deregulated through the re-expression of let-7, miR-27b, miR-320 and miR-34a in human prostate cancer (PCa). BR-DIM administered in clinical trials was well tolerated, and 93% of patients had detectable prostatic DIM levels. The inhibitory effects of BR-DIM on AR and AR target gene such as prostate-specific antigen were also observed in the clinical trial. Our preclinical and clinical studies provide the scientific basis for a 'proof-of-concept' clinical trial in CRPC patients treated with enzalutamide in combination with BR-DIM. This strategy could be expanded in future clinical trials in patients with PCa to determine whether or not they could achieve a better treatment outcome which could be partly mediated by delaying or preventing the development of CRPC.
    Medical Principles and Practice 10/2015; DOI:10.1159/000439307 · 1.34 Impact Factor
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    ABSTRACT: The Raf kinase inhibitory protein (RKIP) has been demonstrated to modulate different intracellular signaling pathways in cancers. Studies have shown that RKIP is frequently downregulated in cancers; therefore, attempts have been made to upregulate the expression of RKIP using natural and synthetic agents for the treatment of human malignancies. Moreover, various regulators such as specific proteins and microRNAs (miRNAs) that are involved in the regulation of RKIP expression have also been identified. RKIP mechanistically modulates the apoptotic regulators of tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) signaling. Because of its critical role in human cancers, RKIP has drawn much research attention, and our understanding is expanding rapidly. Here, we summarize some of the biological complexities of RKIP regulation. However, we restrict our discussion to selected tumors by focusing on TRAIL, miRNAs and natural agents. Emerging evidence suggests a role for natural agents in RKIP regulation in cancer cells; therefore, naturally occurring agents may serve as cancer-targeting agents for cancer treatment. Although the literature suggests some advancement in our knowledge of RKIP biology, it is incomplete with regard to its preclinical and clinical efficacy; thus, further research is warranted. Furthermore, the mechanism by which chemotherapeutic drugs and novel compounds modulate RKIP and how nanotechnologically delivered RKIP can be therapeutically exploited remain to be determined.
    Experimental and Molecular Medicine 07/2015; 47(9). DOI:10.1038/emm.2015.70 · 3.45 Impact Factor
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    ABSTRACT: BACKGROUND The mechanism(s) by which androgen receptor (AR) splice variants contribute to castration-resistant prostate cancer (CRPC) is still lacking.METHODS Expressions of epithelial-to-mesenchymal transition (EMT) and stem cell markers were molecularly tested using prostate cancer (PCa) cells transfected with AR and AR3 (also known as AR-V7) plasmids or siRNA, and also cultured cells under androgen deprivation therapy (ADT) condition. Cell migration, clonogenicity, sphere-forming capacity was assessed using PCa cells under all experimental conditions and 3,3′-diindolylmethane (DIM; BR-DIM) treatment. Human PCa samples from BR-DIM untreated or treated patients were also used for assessing the expression of AR3 and stem cell markers.RESULTSOverexpression of AR led to the induction of EMT phenotype, while overexpression of AR3 not only induced EMT but also led to the expression of stem cell signature genes. More importantly, ADT enhanced the expression of AR and AR3 concomitant with up-regulated expression of EMT and stem cell marker genes. Dihydrotestosterone (DHT) treatment decreased the expression of AR and AR3, and reversed the expression of these EMT and stem cell marker genes. BR-DIM administered to PCa patients prior to radical prostatectomy inhibited the expression of cancer stem cell markers consistent with inhibition of self-renewal of PCa cells after BR-DIM treatment.CONCLUSIONAR variants could contribute to PCa progression through induction of EMT and acquisition of stem cell characteristics, which could be attenuated by BR-DIM, suggesting that BR-DIM could become a promising agent for the prevention of CRPC and/or for the treatment of PCa. Prostate © 2014 Wiley Periodicals, Inc.
    The Prostate 02/2015; 75(2). DOI:10.1002/pros.22901 · 3.57 Impact Factor
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    Yiwei Li · Fazlul H. Sarkar ·
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    ABSTRACT: In recent years, the epigenetic alterations, especially the regulation of microRNA (miRNA), have received much attention in the context of tumor development and progression. High level of oncogenic miRNAs and low expression of tumor-suppressive miRNAs are commonly observed in cancer cells. These aberrant expressions of miRNAs are intimately associated with tumor development and progression. The expression level of miRNAs could be controlled by epigenetic regulations. The hypermethylation at the promoter region of a tumor-suppressive miRNA could cause decreased expression of miRNA via the blockade of transcriptional elements. The histone modification could also indirectly cause reduced expression of tumor-suppressive miRNAs, resulting in the high expression of oncogenes. Interestingly, emerging evidences have demonstrated that several non-toxic natural agents known as nutraceuticals including isoflavone, curcumin, resveratrol, and 3,3′-diindolylmethane could significantly decrease the level of DNA hypermethylation in the promoter of miRNAs or modulate histone, leading to the alteration of miRNA expression which is believed to be associated with inhibition of tumor development and progression. Therefore, administration of these nutraceuticals combined with conventional chemotherapeutics could be a promising therapeutic strategy for fighting the war against cancers.
    02/2015; 1(1):1-10. DOI:10.1007/s40495-015-0016-z
  • Yiwei Li · Vay Liang W Go · Fazlul H Sarkar ·
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    ABSTRACT: Pancreatic cancer is one of the most aggressive malignancies in US adults. Experimental studies have found that antioxidant nutrients could reduce oxidative DNA damage, suggesting that these antioxidants may protect against pancreatic carcinogenesis. Several epidemiologic studies showed that dietary intake of antioxidants was inversely associated with the risk for pancreatic cancer, demonstrating the inhibitory effects of antioxidants on pancreatic carcinogenesis. Moreover, nutraceuticals, the anticancer agents from diet or natural plants, have been found to inhibit the development and progression of pancreatic cancer through the regulation of cellular signaling pathways. Importantly, nutraceuticals also up-regulate the expression of tumor-suppressive microRNAs (miRNAs) and down-regulate the expression of oncogenic miRNAs, leading to the inhibition of pancreatic cancer cell growth and pancreatic cancer stem cell self-renewal through modulation of cellular signaling network. Furthermore, nutraceuticals also regulate epigenetically deregulated DNAs and miRNAs, leading to the normalization of altered cellular signaling in pancreatic cancer cells. Therefore, nutraceuticals could have much broader use in the prevention and/or treatment of pancreatic cancer in combination with conventional chemotherapeutics. However, more in vitro mechanistic experiments, in vivo animal studies, and clinical trials are needed to realize the true value of nutraceuticals in the prevention and/or treatment of pancreatic cancer.
    Pancreas 01/2015; 44(1):1-10. DOI:10.1097/MPA.0000000000000257 · 2.96 Impact Factor
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    ABSTRACT: The relevance of naturopathy (defined as the practice of medicine for the treatment of human diseases with natural agents) in human cancer is beginning to be appreciated, as documented by renewed interest in nutraceutical research, the natural anticancer agents of dietary origin. Because of their pleiotropic effects and the ability to modulate multiple signaling pathways, which is a good attribute of natural agents, nutraceuticals have frequently been demonstrated to re-sensitize drug-resistant cancers. The effectiveness of nutraceuticals can be further enhanced if the tools for the relative assessment of their molecular targets are readily available. Such information can be critical for determining their most effective uses. Here, we discuss the anticancer potential of nutraceuticals and the associated challenges that have interfered with their translational potential as a naturopathic approach for the management of cancers. In the years to come, an efficient screening and assessment of molecular targets will be the key to make rapid progress in the area of drug design and discovery, especially focusing on evidence-based development of naturopathy for the treatment of human malignancies.
    Nutrients 01/2015; 7(1):321-334. DOI:10.3390/nu7010321 · 3.27 Impact Factor
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    ABSTRACT: microRNAs, or miRNAs, play critical roles in cell differentiation and organogenesis by regulating stem cell self-renewal and differentiation. They are important regulators of cancer stem cell formation, survival, and growth, and their aberrant expression may increase drug resistance and promote invasion and metastasis. miRNAs regulate TGF-β, Wnt, notch, and hedgehog signal transductions, which are critical in stem cell development and differentiation. Targeted miRNA regulation by synthetic oligonucleotides, novel agents, or nutraceuticals that inhibit cancer stem cell development and differentiation, in combination with conventional chemotherapeutics, promises better treatment outcomes.
    MicroRNA in Regenerative Medicine, 01/2015: pages 137-161; , ISBN: 9780124055445

  • Cancer Research 10/2014; 74(19 Supplement):5589-5589. DOI:10.1158/1538-7445.AM2014-5589 · 9.33 Impact Factor
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    10/2014; 3(5):S5–S6. DOI:10.1016/j.jasc.2014.09.012
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    ABSTRACT: Pancreatic cancer (PC) is one of the most deadly cancers. The higher mortality is in part due to treatment resistance and early onset of metastasis. The existence of cancer stem like cells (CSLCs) has been widely accepted to be responsible for tumor aggressiveness in PC. Emerging evidence suggests that CSLCs have the capacity for increased cell growth, cell migration/invasion, metastasis, and treatment resistance, which leads to poor clinical outcome. However, the molecular role of CSLCs in tumor development and progression is poorly understood. Therefore, mechanistic understanding, and targeted killing of CSLCs may provide a newer therapeutic strategy for the treatment of PC. It has been well accepted that microRNAs (miRNAs) play critical roles during tumor development and progression through deregulation of multiple genes. Moreover, deregulated expression of miRNAs may also play a key role in the regulation of CSLCs characteristics and functions. Here we show that isolated CD44+/CD133+/EpCAM+ cells (triple-positive cells) from human PC cell lines, MiaPaCa-2 and L3.6pl cells display aggressive characteristics such as increased cell growth, clonogenicity, cell migration, and self-renewal capacity, which is consistent with over-expression of CSLC signatures/markers. We also found deregulated expression of over 400 miRNAs including let-7, miR-30, miR-125b, and miR-335 in CSLCs. As a proof-of-concept, knockdown of miR-125b resulted in the inhibition of tumor cell aggressiveness of CSLCs (triple-positive cells), consistent with the down-regulation of CD44, EpCAM, EZH2, and snail. These results clearly suggest the importance of miRNAs in the regulation of CSLCs characteristics, and may serve as novel targets for therapy.
    Stem cells and development 04/2014; 23(16). DOI:10.1089/scd.2013.0551 · 3.73 Impact Factor
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    ABSTRACT: Sub-populations of cancer stem cells (CSCs) or cancer stem-like cells (CSLCs) have been identified from most tumors including pancreatic cancer (PC), and the existence of these cells is clinically relevant. Emerging evidence suggests that CSLCs participate in cell growth/proliferation, migration/invasion, metastasis, and chemo-radio-therapy resistance, ultimately contributing to poor clinical outcome. However, the pathogenesis and biological significance of CSLCs in PC has not been well characterized. In the present study, we found that isolated triple-marker positive (CD44+/CD133+/EpCAM+) cells of human PC MiaPaCa-2 and L3.6pl cells behave as CSLCs. These CSLCs exhibit aggressive behavior such as increased cell growth, migration, clonogenicity, and self-renewal capacity. The mRNA expression profiling analysis showed that CSLCs (CD44+/CD133+/EpCAM+) exhibit differential expression of more than 1600 mRNAs including FoxQ1, compared to the triple-marker negative (CD44-/CD133-/EpCAM-) cells. The knock-down of FoxQ1 by its siRNA in CSLCs resulted in the inhibition of aggressive behavior, consistent with the inhibition of EpCAM and snail expression. Mouse xenograft tumor studies showed that CSLCs have a 100-fold higher potential for tumor formation and rapid tumor growth, consistent with over-expression of CSC-associated markers/mediators including FoxQ1, compared to its parental MiaPaCa-2 cells. The inhibition of FoxQ1 attenuated tumor formation and growth, and expression of CSC markers in the xenograft tumor derived from CSLCs of MiaPaCa-2 cells. These data clearly suggesting the role of differentially expressed genes in the regulation of CSLC characteristics, further suggesting that targeting some of these genes could be important for the development of novel therapies for achieving better treatment outcome of PC.
    Journal of Biological Chemistry 04/2014; 289(21). DOI:10.1074/jbc.M113.532887 · 4.57 Impact Factor
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    ABSTRACT: Since the first report on cancer stem cells (CSC) in 1997, significant advances have been made in the field of experimental research on CSCs in hematopoietic and solid tumors. Growing evidence from these studies has demonstrated that CSCs are present in the malignancies and are responsible for the tumorigenesis and recurrence of malignancies. Importantly, CSCs have been found to cause drug resistance and promote cancer progression. Therefore, targeting CSCs could be a novel and efficient therapeutic strategy for the treatment of various cancers. However, the complexities of CSC markers in various cancers and the low sensitivity of these cells to existing therapeutics are challenging for designing novel therapeutic strategy. In this chapter, we will review the current knowledge about the markers of CSCs, the roles of CSCs in drug resistance and cancer progression, and the application of novel therapeutic strategies targeting CSCs for achieving better treatment outcome of patients diagnosed with cancers.
    Cancer Stem Cells, 01/2014: pages 461-471; , ISBN: 9781118356166
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    ABSTRACT: Nutraceuticals, the bioactive food components represented by many naturally occurring dietary compounds, have been investigated for a few decades for their numerous beneficial effects, including their anticancer properties. The initial interest in the cancer-preventing/therapeutic ability of these agents was based on their ability to affect multiple signaling pathways that are deregulated in cancer cells. With a shift in the focus of cancer research to the emerging areas such as epigenetic regulation, microRNAs (miRNAs) and the cancer stem cells (CSCs), nutraceuticals initially appeared out of place. However, research investigations over the last several years have slowly but firmly presented evidence that supports a relevance of these agents in modern day research. While nutraceuticals are increasingly being realized to alter miRNA/CSCs expression and function, the molecular mechanism(s) are not very clearly understood. Epigenetic regulation is one mechanism by which these agents exert their anticancer effects. In this focused mini review, we summarize our current understanding of epigenetic regulation of miRNAs and CSCs by nutraceuticals. We discuss both direct and indirect evidences that support such an activity of these compounds.
    Molecular Nutrition & Food Research 01/2014; 58(1). DOI:10.1002/mnfr.201300528 · 4.60 Impact Factor
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    ABSTRACT: The concept of cancer stem cells (CSCs) has great clinical implications because small sub-populations of CSCs have been identified in many different tumors that are associated with poor clinical outcome. Sufficient evidence supports central functions of CSCs in tumorigenesis, due to its distinct high potentials of self-renewal, pluripotent differentiation and apoptosis-resistance, contributing to tumor aggressiveness. Therefore, inhibiting/eliminating CSCs will provide a new effective therapeutic approach for the treatment of aggressive tumors. However, the mechanistic roles of CSCs in tumorigenesis are not well understood. MicroRNAs (miRNAs) have been discovered to act as key regulators of gene expression in tumorigenesis. Aberrant expression of miRNAs has been discovered to be related to worse clinical outcome of many different tumors. Evidence shows that these tumor-related miRNAs have key functions in the regulation of cell cycle/proliferation, migration/invasion, chemo-radiation resistance, and metastasis. Moreover, miRNAs may also exert important functions in modulating CSC characteristics; however, its detailed mechanism(s) has not been fully elucidated. Here, we will summarize the potential role of CSC-related miRNAs in CSC function, and will further define the role of genistein in targeting these CSC-related miRNAs.
    MicroRNAs: Key Regulators of Oncogenesis, 01/2014: pages 295-320; , ISBN: 978-3-319-03724-0
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    ABSTRACT: Recently, nutraceuticals have received increasing attention as the agents for cancer prevention and supplement with conventional therapy. Prostate cancer (PCa) is the most frequently diagnosed cancer and second leading cause of cancer-related death in men in the US. Growing evidences from epidemiological studies, in vitro experimental studies, animal studies, and clinical trials have shown that nutraceuticals could be very useful for the prevention and treatment of PCa. Several nutraceuticals including isoflavone, indole-3-carbinol, 3,3'-diindolylmethane, lycopene, (-)-epigallocatechin-3-gallate, and curcumin are known to downregulate the signal transductions in AR, Akt, NF-κB, and other signal transduction pathways which are vital for the development of PCa and the progression of PCa from androgen-sensitive to castrate-resistant PCa. Therefore, nutraceutical treatment in combination with conventional therapeutics could achieve better treatment outcome in prostate cancer therapy. Interestingly, some nutraceuticals could regulate the function of cancer stem cell (CSC)-related miRNAs and associated molecules, leading to the inhibition of prostatic CSCs which are responsible for drug resistance, tumor progression, and recurrence of PCa. Hence, nutraceuticals may serve as powerful agents for the prevention of PCa progression and they could also be useful in combination with chemotherapeutics or radiotherapy. Such strategy could become a promising newer approach for the treatment of metastatic PCa with better treatment outcome by improving overall survival.
    CANCER AND METASTASIS REVIEW 12/2013; 33(2-3). DOI:10.1007/s10555-013-9478-9 · 7.23 Impact Factor
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    ABSTRACT: Pancreatic cancer is the fourth leading cause of cancer related death in the US and exhibits aggressive features with short survival rate and high mortality. Therefore, it is important to understand the molecular mechanism(s) involved in the aggressive growth of pancreatic cancers, and further design novel targeted therapies for its treatment with better treatment outcome. In the present study, we found that the expression of miR-221 was significantly up-regulated in pancreatic cancer cell lines and tumor tissues compared to normal pancreatic duct epithelial cells and normal pancreas tissues. Moreover, we found that the pancreatic cancer patients with high miR-221 expression had a relatively shorter survival compared to those with lower expression, suggesting that miR-221 could be an oncogenic miRNA and a prognostic factor for poor survival of patients. Interestingly, transfection of miR-221 inhibitor suppressed the proliferative capacity of pancreatic cancer cells with concomitant up-regulation of PTEN, p27(kip1), p57(kip2), and PUMA, which are the tumor suppressors and the predicted targets of miR-221. Most importantly, we found that the treatment of pancreatic cancer cells with isoflavone mixture (G2535), formulated 3,3'-diindolylmethane (BR-DIM), or synthetic curcumin analogue (CDF) could down-regulate the expression of miR-221 and consequently up-regulate the expression of PTEN, p27(kip1), p57(kip2), and PUMA, leading to the inhibition of cell proliferation and migration of MiaPaCa-2 and Panc-1 cells. These results provide experimental evidence in support of the oncogenic role of miR-221 and also demonstrate the role of isoflavone, BR-DIM, and CDF as potential non-toxic agents that are capable of down-regulation of miR-221. Therefore, these agents combined with conventional chemotherapeutics could be useful in designing novel targeted therapeutic strategy for the treatment of pancreatic cancer for which there is no curative therapy.
    American Journal of Cancer Research 11/2013; 3(5):465-77. · 4.17 Impact Factor
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    ABSTRACT: Epidermal growth factor receptor- tyrosine kinase inhibitors (EGFR-TKIs) benefit Non-small cell lung cancer (NSCLC) patients, and an EGFR-TKIi erlotinib, is approved for patients with recurrent NSCLC. However, resistance to erlotinib is a major clinical problem. Earlier we have demonstrated the role of Hedgehog (Hh) signaling in Epithelial-to-Mesenchymal transition (EMT) of NSCLC cells, leading to increased proliferation and invasion. Here, we investigated the role of Hh signaling in erlotinib resistance of TGF-ß1-induced NSCLC cells that are reminiscent of EMT cells. Hh signaling was inhibited by specific siRNA and by GDC-0449, a small molecule antagonist of G protein coupled receptor smoothened in the Hh pathway. Not all NSCLC patients are likely to benefit from EGFR-TKIs and, therefore, cisplatin was used to further demonstrate a role of inhibition of Hh signaling in sensitization of resistant EMT cells. Specific pre- and anti-miRNA preparations were used to study the mechanistic involvement of miRNAs in drug resistance mechanism. siRNA-mediated inhibition as well as pharmacological inhibition of Hh signaling abrogated resistance of NSCLC cells to erlotinib and cisplatin. It also resulted in re-sensitization of TGF-ß1-induced A549 (A549M) cells as well the mesenchymal phenotypic H1299 cells to erlotinib and cisplatin treatment with concomitant up-regulation of cancer stem cell (CSC) markers (Sox2, Nanog and EpCAM) and down-regulation of miR-200 and let-7 family miRNAs. Ectopic up-regulation of miRNAs, especially miR-200b and let-7c, significantly diminished the erlotinib resistance of A549M cells. Inhibition of Hh signaling by GDC-0449 in EMT cells resulted in the attenuation of CSC markers and up-regulation of miR-200b and let-7c, leading to sensitization of EMT cells to drug treatment, thus, confirming a connection between Hh signaling, miRNAs and drug resistance. We demonstrate that Hh pathway, through EMT-induction, leads to reduced sensitivity to EGFR-TKIs in NSCLCs. Therefore, targeting Hh pathway may lead to the reversal of EMT phenotype and improve the therapeutic efficacy of EGFR-TKIs in NSCLC patients.
    Journal of Hematology & Oncology 10/2013; 6(1):77. DOI:10.1186/1756-8722-6-77 · 4.81 Impact Factor
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    ABSTRACT: Reactive oxygen species (ROS) have been widely considered as critical cellular signaling molecules involving in various biological processes such as cell growth, differentiation, proliferation, apoptosis, and angiogenesis. The homeostasis of ROS is critical to maintain normal biological processes. Increased production of ROS, namely oxidative stress, due to either endogenous or exogenous sources causes irreversible damage of bio-molecules such as DNA, proteins, lipids, and sugars, leading to genomic instability, genetic mutation, and altered gene expression, eventually contributing to tumorigenesis. A great amount of experimental studies in vitro and in vivo have produced solid evidence supporting that oxidative stress is strongly associated with increased tumor cell growth, treatment resistance, and metastasis, and all of which contribute to tumor aggressiveness. More recently, the data have indicated that altered production of ROS is also associated with cancer stem cells (CSCs), epithelial-to-mesenchymal transition (EMT), and hypoxia, the most common features or phenomena in tumorigenesis and tumor progression. However, the exact mechanism by which ROS is involved in the regulation of CSC and EMT characteristics as well as hypoxia- and, especially, HIF-mediated pathways is not well known. Emerging evidence suggests the role of miRNAs in tumorigenesis and progression of human tumors. Recently, the data have indicated that altered productions of ROS are associated with deregulated expression of miRNAs, suggesting their potential roles in the regulation of ROS production. Therefore, targeting ROS mediated through the deregulation of miRNAs by novel approaches or by naturally occurring anti-oxidant agents such as genistein could provide a new therapeutic approach for the prevention and/or treatment of human malignancies.
    Current Stem Cell Research & Therapy 08/2013; 9(1). DOI:10.2174/1574888X113089990053 · 2.21 Impact Factor

  • Cancer Research 08/2013; 73(8 Supplement):3296-3296. DOI:10.1158/1538-7445.AM2013-3296 · 9.33 Impact Factor

  • Medical Principles and Practice 08/2013; 22(5). DOI:10.1159/000353562 · 1.34 Impact Factor

Publication Stats

10k Citations
698.39 Total Impact Points


  • 1999-2015
    • Karmanos Cancer Institute
      • Division of Hematology and Oncology
      Detroit, Michigan, United States
    • Wayne State University
      • Department of Pathology
      Detroit, Michigan, United States
  • 2005
    • Oxford Biomedical Research, Rochester Hills
      Rochester Hills, Michigan, United States