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Dengfeng Gao - One of the best experts on this subject based on the ideXlab platform.

  • the antagonistic effects and mechanisms of microRNA 26a action in hypertensive vascular remodelling
    British Journal of Pharmacology, 2021
    Co-Authors: Wenqian Zhang, Qiaozhu Wang, Lijun Yang, Xiaolin Niu, Xin Xing, Chunhui Cao, Rong Wang, Dengfeng Gao
    Abstract:

    BACKGROUND AND PURPOSE Hypertensive vascular remodelling is responsible for end-organ damage and is the result of increased extracellular matrix accumulation and excessive vascular smooth muscle cell (VSMC) proliferation. microRNA-26a (miR-26a), a non-coding small RNA, is involved in several cardiovascular diseases. We aimed to validate the effect and mechanisms of miR-26a in hypertensive vascular remodelling. EXPERIMENTAL APPROACH Male spontaneously hypertensive rats (SHRs) were injected intravenously with recombinant adeno-associated virus-miR-26a. Samples of thoracic aorta were examined histologically with H&E staining. In vitro, angiotensin II (AngII)-induced VSMCs cultured from thoracic aortae of female Sprague-Dawley rats, were transfected with miR-26a mimic or inhibitor. Western blots, qRT-PCR and immunohistological methods were used, along with chromatin-immunoprecipitation and luciferase reporter assays. Specific siRNAs were used to silence Smad production in VSMCs KEY RESULTS: Levels of miR-26a were lower in the thoracic aorta and plasma of SHRs than in WKY rats. Overexpression of miR-26a inhibited extracellular matrix deposition by targeting connective tissue growth factor (CTGF) and decreased VSMC proliferation by regulating the enhancer of zeste homologue 2 (EZH2)/p21 pathway both in vitro and in vivo. AngII-mediated Smad3 activation suppressed miR-26a expression, which in turn promoted Smad3 activation via targeted regulation of Smad4, leading to further down-regulation of miR-26a. CONCLUSION AND IMPLICATIONS Our data show that AngII stimulated a Smads/miR-26a positive feedback loop, which further reduced expression of miR-26a, leading to collagen production and VSMC proliferation and consequently vascular remodelling. MiR-26a has an antagonistic effect on hypertensive vascular remodelling and can be a strategy for treating hypertensive vascular remodelling.

  • The antagonistic effects and mechanisms of microRNA‐26a action in hypertensive vascular remodelling
    British journal of pharmacology, 2021
    Co-Authors: Wenqian Zhang, Qiaozhu Wang, Lijun Yang, Xiaolin Niu, Xin Xing, Chunhui Cao, Rong Wang, Dengfeng Gao
    Abstract:

    BACKGROUND AND PURPOSE Hypertensive vascular remodelling is responsible for end-organ damage and is the result of increased extracellular matrix accumulation and excessive vascular smooth muscle cell (VSMC) proliferation. microRNA-26a (miR-26a), a non-coding small RNA, is involved in several cardiovascular diseases. We aimed to validate the effect and mechanisms of miR-26a in hypertensive vascular remodelling. EXPERIMENTAL APPROACH Male spontaneously hypertensive rats (SHRs) were injected intravenously with recombinant adeno-associated virus-miR-26a. Samples of thoracic aorta were examined histologically with H&E staining. In vitro, angiotensin II (AngII)-induced VSMCs cultured from thoracic aortae of female Sprague-Dawley rats, were transfected with miR-26a mimic or inhibitor. Western blots, qRT-PCR and immunohistological methods were used, along with chromatin-immunoprecipitation and luciferase reporter assays. Specific siRNAs were used to silence Smad production in VSMCs KEY RESULTS: Levels of miR-26a were lower in the thoracic aorta and plasma of SHRs than in WKY rats. Overexpression of miR-26a inhibited extracellular matrix deposition by targeting connective tissue growth factor (CTGF) and decreased VSMC proliferation by regulating the enhancer of zeste homologue 2 (EZH2)/p21 pathway both in vitro and in vivo. AngII-mediated Smad3 activation suppressed miR-26a expression, which in turn promoted Smad3 activation via targeted regulation of Smad4, leading to further down-regulation of miR-26a. CONCLUSION AND IMPLICATIONS Our data show that AngII stimulated a Smads/miR-26a positive feedback loop, which further reduced expression of miR-26a, leading to collagen production and VSMC proliferation and consequently vascular remodelling. MiR-26a has an antagonistic effect on hypertensive vascular remodelling and can be a strategy for treating hypertensive vascular remodelling.

  • microRNA-26a Protects the Heart Against Hypertension-Induced Myocardial Fibrosis.
    Journal of the American Heart Association, 2020
    Co-Authors: Wenqian Zhang, Qiaozhu Wang, Yanjing Feng, Xuegui Chen, Lijun Yang, Xiaofang Wang, Xiaolin Niu, Dengfeng Gao
    Abstract:

    Background Hypertensive myocardial fibrosis (MF) is characterized by excessive deposition of extracellular matrix and cardiac fibroblast proliferation, which can lead to heart failure, malignant arrhythmia, and sudden death. In recent years, with the deepening of research, microRNAs have been found to have an important role in blood pressure control and maintaining normal ventricular structure and function. Methods and Results In this study, we first documented the downregulation of microRNA-26a (miR-26a) in the plasma and myocardium of spontaneously hypertensive rats; more importantly, miR-26a-deficient mice showed MF, whereas overexpression of miR-26a significantly prevented elevated blood pressure and inhibited MF in vivo and angiotensin II-induced fibrogenesis in cardiac fibroblasts by directly targeting connective tissue growth factor and Smad4. miR-26a inhibited cardiac fibroblast proliferation by the enhancer of zeste homolog 2/p21 pathway. Conclusions Our study identified a novel role for miR-26a in blood pressure control and hypertensive MF and provides a possible treatment strategy for miR-26a to alleviate and reverse hypertensive MF.

  • The antagonistic effects and mechanisms of microRNA-26a action in hypertensive vascular remodeling
    2020
    Co-Authors: Wenqian Zhang, Qiaozhu Wang, Lijun Yang, Xiaolin Niu, Xin Xing, Chunhui Cao, Rong Wang, Dengfeng Gao
    Abstract:

    Background and Purpose: Hypertensive vascular remodeling (VR) is responsible for end-organ damage and is the result of increased extracellular matrix accumulation and excessive vascular smooth muscle cell (VSMC) proliferation. microRNA-26a (miR-26a), a non-coding small RNA, is involved in multiple cardiovascular diseases. We aimed to validate the effect and mechanisms of miR-26a in hypertensive VR. Experimental Approach: Spontaneously hypertensive rats (SHRs) were injected intravenously with recombinant adeno-associated virus-miR-26a. In vitro experiments, angiotensin II (AngII)-induced VSMCs were transfected with miR-26a mimic or inhibitor. Key Results: We found miR-26a downregulated in the thoracic aorta and plasma of SHRs. Overexpression of miR-26a inhibited extracellular matrix deposition by targeting connective tissue growth factor (CTGF) and mitigated VSMC proliferation by regulating the enhancer of zeste homolog 2 (EZH2)/p21 pathway both in vitro and in vivo. AngII-mediated Smad3 activation suppressed miR-26a expression, which in turn promoted Smad3 activation via targeted regulation of Smad4, leading to further downregulation of miR-26a. Conclusion and Implications: Our study reveals that AngII stimulates a Smads/miR-26a positive feedback loop, which further reduces miR-26a expression, leading to collagen production and VSMC proliferation and consequently, VR. MiR-26a has an antagonistic effect on hypertensive VR and can be a strategy for treating hypertensive VR.

Joshua M Spin - One of the best experts on this subject based on the ideXlab platform.

  • microRNA 26a is a novel regulator of vascular smooth muscle cell function
    Journal of Cellular Physiology, 2011
    Co-Authors: Nicholas J Leeper, Azad Raiesdana, Yoko Kojima, Hyung J Chun, Junya Azuma, Lars Maegdefessel, Ramendra K Kundu, Thomas Quertermous, Philip S Tsao, Joshua M Spin
    Abstract:

    Aberrant smooth muscle cell (SMC) plasticity has been implicated in a variety of vascular disorders including atherosclerosis, restenosis, and abdominal aortic aneurysm (AAA) formation. While the pathways governing this process remain unclear, epigenetic regulation by specific microRNAs (miRNAs) has been demonstrated in SMCs. We hypothesized that additional miRNAs might play an important role in determining vascular SMC phenotype. Microarray analysis of miRNAs was performed on human aortic SMCs undergoing phenotypic switching in response to serum withdrawal, and identified 31 significantly regulated entities. We chose the highly conserved candidate miRNA-26a for additional studies. Inhibition of miRNA-26a accelerated SMC differentiation, and also promoted apoptosis, while inhibiting proliferation and migration. Overexpression of miRNA-26a blunted differentiation. As a potential mechanism, we investigated whether miRNA-26a influences TGF-β-pathway signaling. Dual-luciferase reporter assays demonstrated enhanced SMAD signaling with miRNA-26a inhibition, and the opposite effect with miRNA-26a overexpression in transfected human cells. Furthermore, inhibition of miRNA-26a increased gene expression of SMAD-1 and SMAD-4, while overexpression inhibited SMAD-1. microRNA-26a was also found to be downregulated in two mouse models of AAA formation (2.5- to 3.8-fold decrease, P < 0.02) in which enhanced switching from contractile to synthetic phenotype occurs. In summary, miRNA-26a promotes vascular SMC proliferation while inhibiting cellular differentiation and apoptosis, and alters TGF-β pathway signaling. microRNA-26a represents an important new regulator of SMC biology and a potential therapeutic target in AAA disease.

  • microRNA-26a Is a Novel Regulator of Vascular Smooth Muscle Cell Function
    Journal of cellular physiology, 2011
    Co-Authors: Nicholas J Leeper, Azad Raiesdana, Yoko Kojima, Hyung J Chun, Junya Azuma, Lars Maegdefessel, Ramendra K Kundu, Thomas Quertermous, Philip S Tsao, Joshua M Spin
    Abstract:

    Aberrant smooth muscle cell (SMC) plasticity has been implicated in a variety of vascular disorders including atherosclerosis, restenosis, and abdominal aortic aneurysm (AAA) formation. While the pathways governing this process remain unclear, epigenetic regulation by specific microRNAs (miRNAs) has been demonstrated in SMCs. We hypothesized that additional miRNAs might play an important role in determining vascular SMC phenotype. Microarray analysis of miRNAs was performed on human aortic SMCs undergoing phenotypic switching in response to serum withdrawal, and identified 31 significantly regulated entities. We chose the highly conserved candidate miRNA-26a for additional studies. Inhibition of miRNA-26a accelerated SMC differentiation, and also promoted apoptosis, while inhibiting proliferation and migration. Overexpression of miRNA-26a blunted differentiation. As a potential mechanism, we investigated whether miRNA-26a influences TGF-β-pathway signaling. Dual-luciferase reporter assays demonstrated enhanced SMAD signaling with miRNA-26a inhibition, and the opposite effect with miRNA-26a overexpression in transfected human cells. Furthermore, inhibition of miRNA-26a increased gene expression of SMAD-1 and SMAD-4, while overexpression inhibited SMAD-1. microRNA-26a was also found to be downregulated in two mouse models of AAA formation (2.5- to 3.8-fold decrease, P 

Janaiah Kota - One of the best experts on this subject based on the ideXlab platform.

  • lower expression of tumor microRNA 26a is associated with higher recurrence in patients with hepatocellular carcinoma undergoing surgical treatment
    Journal of Surgical Oncology, 2018
    Co-Authors: Keaton R. Jones, Sarah C. Nabinger, Sangbin Lee, Smiti Snigdha Sahu, Sandra K. Althouse, Romil Saxena, Mathew S. Johnson, Naga Chalasani, Samer Gawrieh, Janaiah Kota
    Abstract:

    BACKGROUND AND OBJECTIVES Hepatocellular carcinoma (HCC) in patients with hepatitis B virus (HBV) exhibit lower tumor microRNA-26a (miR-26a) expression which is associated with worse outcomes. It is unknown if similar miR-26a loss occurs in HCC developed in other liver diseases. We examined tumor miR-26a expression and its impact on recurrence and mortality in a North American HCC cohort. METHODS MiR-26a levels from tumor and surrounding nontumor liver tissue in 186 subjects were collected. We defined lower tumor expression of miR-26a as <1-fold that of the adjacent nontumor liver tissue. RESULTS Viral hepatitis (42%; 40% hepatitis C and 2% HBV), alcohol (19%), and nonalcoholic fatty liver disease (NAFLD) (18%) were the most common causes of liver disease. The prevalence of lower tumor miR-26a expression was 68%, and it was evident in HCCs arising in all etiologies (viral hepatitis 60%, alcohol 61%, and NAFLD 76%). Subjects with lower tumor miR-26a expression had significantly higher tumor recurrence (hazard ratio [HR], 2.45; 95% confidence interval [CI], 1.18 to 5.1; P = 0.016) and higher mortality of borderline significance (HR, 1.51; 95% CI, 0.94 to 2.41; P = 0.086). CONCLUSION Reduced miR-26a expression is a common phenomenon in HCC arising in North American patients with different underlying liver diseases and may increase recurrence and mortality after surgery.

  • Lower expression of tumor microRNA‐26a is associated with higher recurrence in patients with hepatocellular carcinoma undergoing surgical treatment
    Journal of surgical oncology, 2018
    Co-Authors: Keaton R. Jones, Sarah C. Nabinger, Sangbin Lee, Smiti Snigdha Sahu, Sandra K. Althouse, Romil Saxena, Mathew S. Johnson, Naga Chalasani, Samer Gawrieh, Janaiah Kota
    Abstract:

    BACKGROUND AND OBJECTIVES Hepatocellular carcinoma (HCC) in patients with hepatitis B virus (HBV) exhibit lower tumor microRNA-26a (miR-26a) expression which is associated with worse outcomes. It is unknown if similar miR-26a loss occurs in HCC developed in other liver diseases. We examined tumor miR-26a expression and its impact on recurrence and mortality in a North American HCC cohort. METHODS MiR-26a levels from tumor and surrounding nontumor liver tissue in 186 subjects were collected. We defined lower tumor expression of miR-26a as

Wenqian Zhang - One of the best experts on this subject based on the ideXlab platform.

  • the antagonistic effects and mechanisms of microRNA 26a action in hypertensive vascular remodelling
    British Journal of Pharmacology, 2021
    Co-Authors: Wenqian Zhang, Qiaozhu Wang, Lijun Yang, Xiaolin Niu, Xin Xing, Chunhui Cao, Rong Wang, Dengfeng Gao
    Abstract:

    BACKGROUND AND PURPOSE Hypertensive vascular remodelling is responsible for end-organ damage and is the result of increased extracellular matrix accumulation and excessive vascular smooth muscle cell (VSMC) proliferation. microRNA-26a (miR-26a), a non-coding small RNA, is involved in several cardiovascular diseases. We aimed to validate the effect and mechanisms of miR-26a in hypertensive vascular remodelling. EXPERIMENTAL APPROACH Male spontaneously hypertensive rats (SHRs) were injected intravenously with recombinant adeno-associated virus-miR-26a. Samples of thoracic aorta were examined histologically with H&E staining. In vitro, angiotensin II (AngII)-induced VSMCs cultured from thoracic aortae of female Sprague-Dawley rats, were transfected with miR-26a mimic or inhibitor. Western blots, qRT-PCR and immunohistological methods were used, along with chromatin-immunoprecipitation and luciferase reporter assays. Specific siRNAs were used to silence Smad production in VSMCs KEY RESULTS: Levels of miR-26a were lower in the thoracic aorta and plasma of SHRs than in WKY rats. Overexpression of miR-26a inhibited extracellular matrix deposition by targeting connective tissue growth factor (CTGF) and decreased VSMC proliferation by regulating the enhancer of zeste homologue 2 (EZH2)/p21 pathway both in vitro and in vivo. AngII-mediated Smad3 activation suppressed miR-26a expression, which in turn promoted Smad3 activation via targeted regulation of Smad4, leading to further down-regulation of miR-26a. CONCLUSION AND IMPLICATIONS Our data show that AngII stimulated a Smads/miR-26a positive feedback loop, which further reduced expression of miR-26a, leading to collagen production and VSMC proliferation and consequently vascular remodelling. MiR-26a has an antagonistic effect on hypertensive vascular remodelling and can be a strategy for treating hypertensive vascular remodelling.

  • The antagonistic effects and mechanisms of microRNA‐26a action in hypertensive vascular remodelling
    British journal of pharmacology, 2021
    Co-Authors: Wenqian Zhang, Qiaozhu Wang, Lijun Yang, Xiaolin Niu, Xin Xing, Chunhui Cao, Rong Wang, Dengfeng Gao
    Abstract:

    BACKGROUND AND PURPOSE Hypertensive vascular remodelling is responsible for end-organ damage and is the result of increased extracellular matrix accumulation and excessive vascular smooth muscle cell (VSMC) proliferation. microRNA-26a (miR-26a), a non-coding small RNA, is involved in several cardiovascular diseases. We aimed to validate the effect and mechanisms of miR-26a in hypertensive vascular remodelling. EXPERIMENTAL APPROACH Male spontaneously hypertensive rats (SHRs) were injected intravenously with recombinant adeno-associated virus-miR-26a. Samples of thoracic aorta were examined histologically with H&E staining. In vitro, angiotensin II (AngII)-induced VSMCs cultured from thoracic aortae of female Sprague-Dawley rats, were transfected with miR-26a mimic or inhibitor. Western blots, qRT-PCR and immunohistological methods were used, along with chromatin-immunoprecipitation and luciferase reporter assays. Specific siRNAs were used to silence Smad production in VSMCs KEY RESULTS: Levels of miR-26a were lower in the thoracic aorta and plasma of SHRs than in WKY rats. Overexpression of miR-26a inhibited extracellular matrix deposition by targeting connective tissue growth factor (CTGF) and decreased VSMC proliferation by regulating the enhancer of zeste homologue 2 (EZH2)/p21 pathway both in vitro and in vivo. AngII-mediated Smad3 activation suppressed miR-26a expression, which in turn promoted Smad3 activation via targeted regulation of Smad4, leading to further down-regulation of miR-26a. CONCLUSION AND IMPLICATIONS Our data show that AngII stimulated a Smads/miR-26a positive feedback loop, which further reduced expression of miR-26a, leading to collagen production and VSMC proliferation and consequently vascular remodelling. MiR-26a has an antagonistic effect on hypertensive vascular remodelling and can be a strategy for treating hypertensive vascular remodelling.

  • microRNA-26a Protects the Heart Against Hypertension-Induced Myocardial Fibrosis.
    Journal of the American Heart Association, 2020
    Co-Authors: Wenqian Zhang, Qiaozhu Wang, Yanjing Feng, Xuegui Chen, Lijun Yang, Xiaofang Wang, Xiaolin Niu, Dengfeng Gao
    Abstract:

    Background Hypertensive myocardial fibrosis (MF) is characterized by excessive deposition of extracellular matrix and cardiac fibroblast proliferation, which can lead to heart failure, malignant arrhythmia, and sudden death. In recent years, with the deepening of research, microRNAs have been found to have an important role in blood pressure control and maintaining normal ventricular structure and function. Methods and Results In this study, we first documented the downregulation of microRNA-26a (miR-26a) in the plasma and myocardium of spontaneously hypertensive rats; more importantly, miR-26a-deficient mice showed MF, whereas overexpression of miR-26a significantly prevented elevated blood pressure and inhibited MF in vivo and angiotensin II-induced fibrogenesis in cardiac fibroblasts by directly targeting connective tissue growth factor and Smad4. miR-26a inhibited cardiac fibroblast proliferation by the enhancer of zeste homolog 2/p21 pathway. Conclusions Our study identified a novel role for miR-26a in blood pressure control and hypertensive MF and provides a possible treatment strategy for miR-26a to alleviate and reverse hypertensive MF.

  • The antagonistic effects and mechanisms of microRNA-26a action in hypertensive vascular remodeling
    2020
    Co-Authors: Wenqian Zhang, Qiaozhu Wang, Lijun Yang, Xiaolin Niu, Xin Xing, Chunhui Cao, Rong Wang, Dengfeng Gao
    Abstract:

    Background and Purpose: Hypertensive vascular remodeling (VR) is responsible for end-organ damage and is the result of increased extracellular matrix accumulation and excessive vascular smooth muscle cell (VSMC) proliferation. microRNA-26a (miR-26a), a non-coding small RNA, is involved in multiple cardiovascular diseases. We aimed to validate the effect and mechanisms of miR-26a in hypertensive VR. Experimental Approach: Spontaneously hypertensive rats (SHRs) were injected intravenously with recombinant adeno-associated virus-miR-26a. In vitro experiments, angiotensin II (AngII)-induced VSMCs were transfected with miR-26a mimic or inhibitor. Key Results: We found miR-26a downregulated in the thoracic aorta and plasma of SHRs. Overexpression of miR-26a inhibited extracellular matrix deposition by targeting connective tissue growth factor (CTGF) and mitigated VSMC proliferation by regulating the enhancer of zeste homolog 2 (EZH2)/p21 pathway both in vitro and in vivo. AngII-mediated Smad3 activation suppressed miR-26a expression, which in turn promoted Smad3 activation via targeted regulation of Smad4, leading to further downregulation of miR-26a. Conclusion and Implications: Our study reveals that AngII stimulates a Smads/miR-26a positive feedback loop, which further reduces miR-26a expression, leading to collagen production and VSMC proliferation and consequently, VR. MiR-26a has an antagonistic effect on hypertensive VR and can be a strategy for treating hypertensive VR.

Masayuki Nakagawa - One of the best experts on this subject based on the ideXlab platform.

  • microRNA 26a b directly regulate la related protein 1 and inhibit cancer cell invasion in prostate cancer
    International Journal of Oncology, 2015
    Co-Authors: Mayuko Kato, Ichiro Fukumoto, Yusuke Goto, Rika Nishikawa, Hideki Enokida, Masayuki Nakagawa, Ryosuke Matsushita, Akira Kurozumi, Shinichi Sakamoto, Tomohiko Ichikawa
    Abstract:

    Abstract Our past studies of microRNA (miRNA) expression signatures of cancers including prostate cancer (PCa) revealed that microRNA-26a and microRNA-26b (miR-26a and miR-26b) were significantly downregulated in cancer tissues. In the present study, we found that restoration of miR-26a or miR-26b significantly inhibited PCa cell invasion. Gene expression data and in silico analysis showed that the gene encoding La-related protein 1 (LARP1) was a putative candidate of miR-26a and miR-26b regulation. Moreover, luciferase reporter assays revealed that LARP1 was a direct target of both miR-26a and miR-26b. Overexpression of LARP1 was observed in PCa clinical specimens and knockdown of LARP1 inhibited cancer cell migration. Therefore, LARP1 acted as an oncogene in PCa cells. Moreover, 'ribosome', 'RNA transport' and 'mTOR signaling pathway' were identified as LARP1-regulated pathways. Our present data suggested that loss of tumor-suppressive miR-26a and miR-26b enhanced cancer cell invasion in PCa through direct regulation of oncogenic LARP1. Elucidation of the molecular networks regulated by tumor-suppressive miRNAs will provide insights into the molecular mechanisms of PCa oncogenesis and metastasis.

  • microRNA-26a/b directly regulate La-related protein 1 and inhibit cancer cell invasion in prostate cancer
    International journal of oncology, 2015
    Co-Authors: Mayuko Kato, Ichiro Fukumoto, Yusuke Goto, Rika Nishikawa, Hideki Enokida, Masayuki Nakagawa, Ryosuke Matsushita, Akira Kurozumi, Shinichi Sakamoto, Tomohiko Ichikawa
    Abstract:

    Abstract Our past studies of microRNA (miRNA) expression signatures of cancers including prostate cancer (PCa) revealed that microRNA-26a and microRNA-26b (miR-26a and miR-26b) were significantly downregulated in cancer tissues. In the present study, we found that restoration of miR-26a or miR-26b significantly inhibited PCa cell invasion. Gene expression data and in silico analysis showed that the gene encoding La-related protein 1 (LARP1) was a putative candidate of miR-26a and miR-26b regulation. Moreover, luciferase reporter assays revealed that LARP1 was a direct target of both miR-26a and miR-26b. Overexpression of LARP1 was observed in PCa clinical specimens and knockdown of LARP1 inhibited cancer cell migration. Therefore, LARP1 acted as an oncogene in PCa cells. Moreover, 'ribosome', 'RNA transport' and 'mTOR signaling pathway' were identified as LARP1-regulated pathways. Our present data suggested that loss of tumor-suppressive miR-26a and miR-26b enhanced cancer cell invasion in PCa through direct regulation of oncogenic LARP1. Elucidation of the molecular networks regulated by tumor-suppressive miRNAs will provide insights into the molecular mechanisms of PCa oncogenesis and metastasis.

  • microRNA expression signature of oral squamous cell carcinoma functional role of microRNA 26a b in the modulation of novel cancer pathways
    British Journal of Cancer, 2015
    Co-Authors: Ichiro Fukumoto, Toyoyuki Hanazawa, Takashi Kinoshita, Naoko Kikkawa, Keiichi Koshizuka, Yusuke Goto, Rika Nishikawa, Takeshi Chiyomaru, Hideki Enokida, Masayuki Nakagawa
    Abstract:

    microRNA expression signature of oral squamous cell carcinoma: functional role of microRNA-26a/b in the modulation of novel cancer pathways

  • microRNA expression signature of oral squamous cell carcinoma: functional role of microRNA-26a/b in the modulation of novel cancer pathways.
    British journal of cancer, 2015
    Co-Authors: Ichiro Fukumoto, Toyoyuki Hanazawa, Takashi Kinoshita, Naoko Kikkawa, Keiichi Koshizuka, Yusuke Goto, Rika Nishikawa, Takeshi Chiyomaru, Hideki Enokida, Masayuki Nakagawa
    Abstract:

    microRNA expression signature of oral squamous cell carcinoma: functional role of microRNA-26a/b in the modulation of novel cancer pathways