Targeted Expression of miR-34a Using the T-VISA System Suppresses Breast Cancer Cell Growth and Invasion

Deng

Clinical Cancer Research

et al. 2013

Self Cite

149

122

Section: Introductionmentioning

confidence: 99%

miR-200b and miR-200c as Prognostic Factors and Mediators of Gastric Cancer Cell Progression

Deng

Clinical Cancer Research

et al. 2013

Self Cite

149

122

Journal of Lipid Research

“…An alternative strategy involves the expression of a shRNA or pri-miR mimic from a plasmid or viral construct that provides a more stable expression of the mature microRNA ( 124 ). MicroRNA-34a exogenously expressed in cultured breast cancer cells was reported to reduce tumor cell proliferation, migration, and invasion ( 139 ), and an adenoviral vector expressing shRNAs against microRNA-221 and -222 has been described in cultured glioblastoma cells (GBM) ( 140 ).…”

Section: Micrornas Disrupting Lipid Homeostasis In Cancermentioning

confidence: 99%

“…Lipidand polymer-based carriers have been tested for siRNA/ shRNA delivery in preclinical studies ( 141 ). Liposomemediated delivery of a plasmid encoding microRNA-34a reduced several microRNA-34a target genes in cultured breast cancer cells ( 139 ), and liposome-formulated microRNA-34a is being tested in a phase I clinical trial in patients with primary or metastatic liver cancer (http:// clinicaltrials.gov/ct2/show/NCT01829971).…”

Section: Micrornas Disrupting Lipid Homeostasis In Cancermentioning

confidence: 99%

Microtargeting cancer metabolism: opening new therapeutic windows based on lipid metabolism

Cedrón

Molina

2016

and fl exibility to adapt to the microenvironment (oxygen, pH, and nutrient availability) ( 2-4 ).MicroRNAs are small single-stranded noncoding RNAs (19-25 nucleotides) that posttranscriptionally repress the expression of mRNAs implicated in nearly all cellular processes, such as cell cycle, apoptosis, autophagy, stemness, differentiation, angiogenesis, infl ammation, drug resistance, stress response, transformation, and migration. MicroRNAs are frequently deregulated in cancer and so they are important biomarkers for diagnosis and prognosis of the cellular outcome ( 5,6 ) Importantly, individual microRNAs, combinations of microRNAs, or even artifi cial microRNAs can specifi cally be designed to affect entire biological pathways ( 7,8 ), and this makes them good candidates for therapeutic intervention compared with classical single target approaches.In this review, we briefl y describe the altered cancer cell metabolism, and then we discuss the use of microRNAs as modulators of specifi c metabolic pathways in cancer (summarized in Fig. 1 ). We note the promising potentiallity of microRNAs for therapeutic intervention toward the altered lipid metabolism in cancer (summarized in Fig. 2 ). In an attempt to open new therapeutic windows, we emphasize two exciting scenarios for microRNA-mediated intervention that need to be further explored: 1 ) the cooperation between FA biosynthesis (lipogenesis) and FA oxidation (FAO) as a survival mechanism in cancer; and 2 ) the regulation of the intracellular lipid content in the Abstract Metabolic reprogramming has emerged as a hallmark of cancer. MicroRNAs are noncoding RNAs that posttranscriptionally repress the expression of target mRNAs implicated in multiple physiological processes, including apoptosis, differentiation, and cancer. MicroRNAs can affect entire biological pathways, making them good candidates for therapeutic intervention compared with classical single target approaches. Moreover, microRNAs may become more relevant in the fi ne-tuning adaptation to stress situations, such as oncogenic events, hypoxia, nutrient deprivation, and oxidative stress. Furthermore, artifi cial microRNAs can be designed to modulate the expression of multiple targets of a specifi c pathway. In this review, we describe the metabolic reprogramming associated to cancer, with a special interest in the altered lipid metabolism. Next, we describe specifi c features of microRNAs that make them relevant to target cancer cell metabolism. Finally, in an attempt to open new therapeutic windows, we emphasize two exciting scenarios for microRNA-mediated intervention that need to be further explored: 1 ) the cooperation between FA biosynthesis (lipogenesis) and FA oxidation as complementary partners for the survival of cancer cells; and 2 ) the regulation of the intracellular lipid content modulating both lipid storage into lipid droplets, and lipid mobilization through lipolysis and/or lipophagy. metabolism is interrupted, they may rely on glucose-dependent anaplerosis of the TCA cycle ( 11 ). This...

“…5 Identified causes of recurrence are cancer stem cell (CSC) 6,7 , epithelial-mesenchymal transition (EMT) 8 , β 1-integrin 9 , notch signaling 10, wnt signaling, 11,12 hedgehog signaling 13,14 and miRNA. 15,16 CSCs are group of cancer cells capable of self-renewing and producing heterogeneous lineages of cancer cells. 17 A number of cell surface markers such as CD44…”

Section: Introductionmentioning

confidence: 99%

Inhibitory Effect of D-chiro-inositol on Both Growth and Recurrence of Breast Tumor from MDA-MB-231 Cancer Cells

et al. 2017

-D-chiro-inositol (DCI) is a secondary messenger in insulin signal transduction. It is produced in vivo from myo-inositol via action of epimerase. In this study, we evaluated antitumor activity of DCI against human breast cancer both in vitro and in vivo. In order to determine the inhibitory effects of DCI on growth of human breast cancer cells (MDA-MB-231), two different assessment methods were implemented: MTT assay and mouse xenograft assay. MTT assay demonstrated downturn in cell proliferation by DCI treatment (1, 5, 10, 20 and 40 mM) groups by 18.3% (p < 0.05), 17.2% (p < 0.05), 17.5% (p < 0.05), 18.4% (p < 0.05), and 24.9% (p < 0.01), respectively. Also, inhibition of tumor growth was investigated in mouse xenograft model. DCI was administered orally at the dose of 500 mg/kg and 1000 mg/kg body weight to treat nude mouse for 45 consecutive days. On the 45th day, tumor growth of DCI (500 mg/kg and 1000 mg/kg) groups was suppressed by 22.1% and 67.6% as mean tumor volumes were 9313.8 ± 474.1 mm 3 and 3879.1 ± 1044.1 mm 3 , respectively. Furthermore, breast cancer stem cell (CSC) phenotype (CD44 + /CD24 − ) was measured using flow cytometry. On the 46th day, CSC ratios of DCI (500 mg/kg) and co-treatment with doxorubicin (4 mg/kg) and DCI (500 mg/kg) group decreased by 24.7% and 53.9% (p < 0.01), respectively. Finally, from tumor recurrence assay, delay of 5 days in the cotreatment group compared to doxorubicin (4 mg/kg) alone group was observed. Based on these findings, we propose that DCI holds potential as an anti-cancer drug for treatment of breast cancer.