Small non-coding microRNAs (miRNAs) are instrumental in physiological processes, such as proliferation, cell cycle, apoptosis, and differentiation, processes which are often disrupted in diseases like cancer. miR-155 is one of the best conserved and multifunctional miRNAs, which is mainly characterized by overexpression in multiple diseases including malignant tumors. Altered expression of miR-155 is found to be associated with various physiological and pathological processes, including hematopoietic lineage differentiation, immune response, inflammation, and tumorigenesis. Furthermore, miR-155 drives therapy resistance mechanisms in various tumor types. Therefore, miR-155-mediated signaling pathways became a potential target for the molecular treatment of cancer. In this review, we summarize the current findings of miR-155 in hematopoietic lineage differentiation, the immune response, inflammation, and cancer therapy resistance. Furthermore, we discuss the potential of miR-155-based therapeutic approaches for the treatment of cancer.

miR-155 in cancer drug resistance and as target for miRNA-based therapeutics

Morin hydrate: A comprehensive review on novel natural dietary bioactive compound with versatile biological and pharmacological potential.

MicroRNAs (miRNAs) are RNA molecules at about 22 nucleotide in length that are non-coding, which regulate gene expression in the post-transcriptional level by performing degradation or blocks translation of the target mRNA. It is known that they play roles in mechanisms such as metabolic regulation, embryogenesis, organogenesis, differentiation and growth control by providing post-transcriptional regulation of gene expression. With these properties, miRNAs play important roles in the regulation of biological processes such as proliferation, differentiation, apoptosis, drug resistance mechanisms in eukaryotic cells. In addition, there are miRNAs that can be used for cancer therapy. Tumor cells and tumor microenvironment have different miRNA expression profiles. Some miRNAs are known to play a role in the onset and progression of the tumor. miRNAs with oncogenic or tumor suppressive activity specific to different cancer types are still being investigated. This review summarizes the role of miRNAs in tumorigenesis, therapeutic strategies in human cancer and current studies.

/pdf/therapeutic-micrornas-in-human-cancer-3gwycal5ok.pdf

Therapeutic microRNAs in human cancer.

Prostate cancer (PCa) is a multifactorial disease with an unclear etiology. Due to its high prevalence, long latency, and slow progression, PCa is an ideal target for chemoprevention strategies. Many research studies have highlighted the positive effects of natural flavonoids on chronic diseases, including PCa. Different classes of dietary flavonoids exhibit anti-oxidative, anti-inflammatory, anti-mutagenic, anti-aging, cardioprotective, anti-viral/bacterial and anti-carcinogenic properties. We overviewed the most recent evidence of the antitumoral effects exerted by dietary flavonoids, with a special focus on their epigenetic action in PCa. Epigenetic alterations have been identified as key initiating events in several kinds of cancer. Many dietary flavonoids have been found to reverse DNA aberrations that promote neoplastic transformation, particularly for PCa. The epigenetic targets of the actions of flavonoids include oncogenes and tumor suppressor genes, indirectly controlled through the regulation of epigenetic enzymes such as DNA methyltransferase (DNMT), histone acetyltransferase (HAT), and histone deacetylase (HDAC). In addition, flavonoids were found capable of restoring miRNA and lncRNA expression that is altered during diseases. The optimization of the use of flavonoids as natural epigenetic modulators for chemoprevention and as a possible treatment of PCa and other kinds of cancers could represent a promising and valid strategy to inhibit carcinogenesis and fight cancer.

Flavonoids as Epigenetic Modulators for Prostate Cancer Prevention.

Paclitaxel and docetaxel resistance in prostate cancer: Molecular mechanisms and possible therapeutic strategies.

// Bin Li 1 , Xunbo Jin 1 , Huilin Meng 1 , Bo Hu 1 , Tao Zhang 1 , Jiang Yu 1 , Shaoan Chen 1 , Xudong Guo 1 , Weiguo Wang 2 , Wei Jiang 3 and Jin Wang 4, 5 1 Minimally Invasive Urology Center, Shandong Provincial Hospital Affiliated to Shandong University, Jinan 250021, Shandong, China 2 Department of Urology, Jining No1 People’s Hospital, Jining 272011, Shandong, China 3 Department of Urology, Dongying People’s Hospital, Dongying 257091, Shandong, China 4 Department of Urology, Shandong Provincial Qianfoshan Hospital Affiliated to Shandong University, Jinan 250014, Shandong, China 5 School of Basic Medical Sciences, Shandong University, Jinan 250012, Shandong, China Correspondence to: Jin Wang, email: wjinsdu@163com Keywords: prostate cancer, morin, paclitaxel-resistance, microRNA (miR)-155, GATA binding protein 3 (GATA3) Received: February 28, 2017     Accepted: April 21, 2017     Published: May 24, 2017 ABSTRACT Paclitaxel is a first-line microtubule-stabilizing drug in treating prostate cancer However, most patients develop resistance and experience relapse Morin (3,5,7,20,40-pentahydroxyflavone) is an anti-tumor flavonoid in a numerous types of cancer cells including breast, ovarian and lung cancers We therefore researched the effects of morin as an adjuvant to paclitaxel in in treating DU145 and PC-3 cells in vitro and DU145 derived prostate cancers in nude mice models The chemosensitivities of these cells to the treatments of morin and paclitaxel were tested through viability assays utilizing cell counting kit 8 (CCK-8) and apoptosis assays through flow cytometry analyses MicroRNA (miRNA) microarray was employed to determine the changes in miRNA profile of morin treated DU145 cells The results from microarrays were further certified by quantitative real-time reverse transcription-PCR (qRT-PCR) The underlying targets of miR-155 were verified using luciferase assays followed by Western blot assays In the results, morin was capable of repressing the cell viabilities in the paclitaxel-treated cells MiR-155might be an effective target that can be down-regulated in morin-treated cells We also discovered that GATA binding protein 3 (GATA3) was directly repressed by miR-155, and the treatment of morin reversed the expression of GATA3 In conclusion, morin might be a potential adjuvant of paclitaxel in treating prostate cancer through regulating miR-155/GATA3 axis

/pdf/morin-promotes-prostate-cancer-cells-chemosensitivity-to-2cgsrcvbl5.pdf

Morin promotes prostate cancer cells chemosensitivity to paclitaxel through miR-155/GATA3 axis.

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Morin promotes prostate cancer cells chemosensitivity to paclitaxel through miR-155/GATA3 axis.