MiR-361-5p acts as a tumor suppressor in prostate cancer by targeting signal transducer and activator of transcription-6(STAT6)

Liu, Dachuang; Tao, Tao; Xu, Bingying; Chen, Shuqiu; Liu, Chunhui; Zhang, Lei; Lǚ, Kai; Huang, Yeqing; Jiang, Liang; Zhang, Xiaowen; Huang, Xiaoming; Zhang, Lihua; Han, Conghui; Chen, Ming

doi:10.1016/j.bbrc.2014.01.140

Cited by 84 publications

(76 citation statements)

References 23 publications

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“…The aberrant expression of miRNAs is closely associated with the proliferation, cell cycle, apoptosis, differentiation, migration, metabolism and prognosis of various types of cancers, including PCa (3)(4)(5)(6). miR-195 is a member of the miR-15/16 family, which consists of a group of miRNAs (miR-195, miR-15a, miR-15b, miR-16-1 and miR-16-2) that share a similar seed sequence (7).…”

Section: Introductionmentioning

confidence: 99%

Downregulation of miR-195 promotes prostate cancer progression by targeting HMGA1

et al. 2016

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Abstract. Aberrant deregulation of is associated with tumorigenesis and the development of cancer. However, its expression and function in prostate cancer (PCa) remain to be elucidated. In the present study, we found that miR-195 expression levels were decreased in human PCa samples and were correlated with patient prognosis. miR-195 overexpression inhibited cell proliferation, cell cycle progression and tumorigenesis via directly targeting HMGA1. Downregulation of HMGA1 expression had an effect similar to miR-195 in the PCa cells. In clinical specimens, HMGA1 was overexpressed in castration-resistant prostate cancer when compared with its levels in benign prostate hyperplasia and androgen-dependent prostate cancer, and its expression levels were inversely correlated with overall survival and biochemical relapse-free survival. In summary, our study suggests that miR-195 functions as a tumor-suppressor gene by downregulating HMGA1 and can be used as a potential target in the treatment of PCa.

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Section: Introductionmentioning

confidence: 99%

Downregulation of miR-195 promotes prostate cancer progression by targeting HMGA1

et al. 2016

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“…Previous studies have indicated that miR-361-5p acts as a tumor suppressor in several cancers. In castration-resistant prostate cancer, miR-361-5p was demonstrated to be down-regulated through STAT/Bcl-xL pathway, suppressing cell proliferation and triggering apoptosis (16). While in colorectal carcinoma and gastric cancer, miR-361-5p also functions as a tumor-suppressive miRNA through binding to SND1 directly (15).…”

Section: Discussionmentioning

confidence: 99%

“…It has been demonstrated to be down-regulated in colorectal carcinoma and gastric cancer, suggesting that miR-361-5p functioned as a tumor-suppressive miRNA (15). Decreased miR-361-5p expression has also been observed in castration-resistant prostate cancer as well (16). However, a contradictory report identified that miR-361-5p acted as an oncogene in cervical cancer progression by enhancing cell proliferation and invasion (17).…”

Section: Original Articlementioning

confidence: 99%

Positive expression of miR-361-5p indicates better prognosis for breast cancer patients

et al. 2016

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Background: MicroRNA-361-5p (miR-361-5p) has been reported to be tumor suppressor in colorectal, gastric and prostate cancer, but as an oncogene in cervical cancer. No previous research has focused on the expression of miR-361-5p and its exact prognostic role in breast cancer (BC). with negative miR-361-5p expression (P=0.002). Moreover, the prognostic value of miR-361-5p was most significant among patients with triple-negative breast cancer (TNBC) for DFS (P=0.004).Conclusions: These results indicated that miR-361-5p expression is an independent predictive factor for better prognosis in BC.

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“…Previous studies have showed that miR-361 has important role in various cancerous diseases, such as prostate cancer, 38 cervical cancer 39 and cutaneous squamous cell carcinoma. 40 However, no report shows that miR-361 is involved in the regulation of cardiac diseases.…”

Section: Phb1mentioning

confidence: 99%

miR-361-regulated prohibitin inhibits mitochondrial fission and apoptosis and protects heart from ischemia injury

Wang

Liu

et al. 2014

Cell Death Differ

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Cardiovascular disease remains the leading cause of morbidity and mortality worldwide. Emerging evidences suggest that the abnormal mitochondrial fission participates in pathogenesis of cardiac diseases, including myocardial infarction (MI) and heart failure. However, the molecular components regulating mitochondrial network in the heart remain largely unidentified. Here we report that miR-361 and prohibitin 1 (PHB1) constitute an axis that regulates mitochondrial fission and apoptosis. The results show that PHB1 attenuates mitochondrial fission and apoptosis in response to hydrogen peroxide treatment in cardiomyocytes. Cardiac-specific PHB1 transgenic mice show reduced mitochondrial fission and myocardial infarction sizes after myocardial infarction surgery. MiR-361 is responsible for the dysfunction of PHB1 and suppresses the translation of PHB1. Knockdown of miR-361 reduces mitochondrial fission and apoptosis in vivo and in vitro. MiR-361 cardiac-specific transgenic mice represent elevated mitochondrial fission and myocardial infarction sizes upon myocardial ischemia injury. This study identifies a novel signaling pathway composed of miR-361 and PHB1 that regulates mitochondrial fission program and apoptosis. This discovery will shed new light on the therapy of myocardial infarction and heart failure. The heart drives the blood flow in the body and it has a large requirement of energy. Mitochondria meet the high energy demand of the heart by consistently providing large amounts of ATP through oxidative phosphorylation. Thus, mitochondrial malfunction is tightly related to cardiac diseases and contributes to cardiomyocyte injury, cardiomyopathy and heart failure. Mitochondria morphology is also associated with the function. Mitochondria constantly undergo fission and fusion. Fission leads to the formation of small round mitochondria and promotes cell apoptosis, 1-7 whereas fusion results in mitochondria elongation and have a protective role in cardiomyocytes maintenance. 8 The above findings strongly suggest that mitochondrial fission and fusion machinery is important for cardiac function. In addition, unveiling the mechanism of mitochondrial network regulation will provide a novel therapeutic strategy for heart failure.The mitochondrial prohibitin complex is a macromolecular structure at the inner mitochondrial membrane that is composed of prohibitin 1 (PHB1) and prohibitin 2 subunits. 9These two proteins comprise an evolutionary conserved and ubiquitously expressed family of membrane proteins and are implicated in several important cellular processes such as mitochondrial biogenesis and function, cell proliferation, replicative senescence, and cell death.10,11 The first mammalian PHB1 was identified as a potential tumor suppressor with anti-proliferative activity.12 Recent findings suggest that PHB1 has an important role in regulating mitochondrial morphology.Loss of PHB1 results in accumulation of fragmented mitochondria in MEFs and HeLa cells.13,14 However, it is not yet clear whether PHB1 participates in ...

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MiR-361-5p acts as a tumor suppressor in prostate cancer by targeting signal transducer and activator of transcription-6(STAT6)

Cited by 84 publications

References 23 publications

Downregulation of miR-195 promotes prostate cancer progression by targeting HMGA1

Downregulation of miR-195 promotes prostate cancer progression by targeting HMGA1

Positive expression of miR-361-5p indicates better prognosis for breast cancer patients

miR-361-regulated prohibitin inhibits mitochondrial fission and apoptosis and protects heart from ischemia injury

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