Alterations in expression of specific microRNAs by combination of 4-HPR and EGCG inhibited growth of human malignant neuroblastoma cells

Chakrabarti, Mrinmay; Khandkar, Mehrab; Banik, Naren L.; Ray, Swapan K.

doi:10.1016/j.brainres.2012.03.017

Cited by 73 publications

(48 citation statements)

References 28 publications

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“…The custom synthesized primers were procured from Eurofins MWG Operon (Huntsville, AL, USA). Total RNA was used for RT to cDNA using the specific primers following a procedure as we reported previously (Chakrabarti et al, 2012). Here, primers in RT reaction included a mixture of 10 μM each of the antisense primers for specific miRs and U6 RNA (Table 1).…”

Section: Methodsmentioning

confidence: 99%

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MiR-7-1 potentiated estrogen receptor agonists for functional neuroprotection in VSC4.1 motoneurons

2014

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Protection of motoneurons is an important goal in the treatment of spinal cord injury (SCI). We tested whether neuroprotective microRNAs (miRs) like miR-206, miR-17, miR-21, miR-7-1, and miR-106a could enhance efficacy of estrogen receptor (ER) agonists such as 1,3,5-tris (4-hydroxyphenyl)-4-propyl-1H-pyrazole (PPT, ERα agonist), Way200070 (WAY, ERβ agonist), and estrogen (EST, ERα and ERβ agonist) in preventing apoptosis in the calcium ionophore (CI) insulted VSC4.1 motoneurons. We determined that 200 nM CI induced 70% cell death. Treatment with 50 nM PPT, 100 nM WAY, and 150 nM EST induced overexpression of ERα, ERβ, and both receptors, respectively, at mRNA and protein levels. Treatment with ER agonists significantly upregulated miR-206, miR-17, and miR-7-1 in the CI insulted VSC4.1 motoneurons. Transfection with miR-206, miR-17, or miR-7-1 mimic potentiated WAY or EST to inhibit apoptosis in the CI insulted VSC4.1 motoneurons. Overexpression of miR-7-1 maximally increased efficacy of WAY and EST for down regulation of pro-apoptotic Bax and upregulation of anti-apoptotic Bcl-2. A search using miRDB indicated that miR-7-1 could inhibit expression of L-type Ca2+ channel protein alpha 1C (CPα1C). miR-7-1 overexpression and WAY or EST treatment down regulated CPα1C but upregulated p-Akt to trigger cell survival signaling. The same therapeutic strategy increased expression of the Ca2+/calmodulin-dependent protein kinase II beta (CaMKIIβ) and the phosphorylated cAMP response element binding protein (p-CREB) so as to promote Bcl-2 transcription. Whole cell membrane potential and mitochondrial membrane potential studies indicated that miR-7-1 highly potentiated EST to preserve functionality in the CI insulted VSC4.1 motoneurons. In conclusion, our data indicated that miR-7-1 most significantly potentiated efficacy of EST for functional neuroprotection and this therapeutic strategy could be used in the future to attenuate apoptosis of motoneurons in SCI.

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Section: Methodsmentioning

confidence: 99%

“…The levels of expression of specific miRs were determined using real-time qRT-PCR, as we described previously (Chakrabarti et al, 2012), with several modifications. All PCR reagents were used from the SYBR green core reagent kit (Applied Biosystems, Foster City, CA, USA).…”

Section: Methodsmentioning

confidence: 99%

MiR-7-1 potentiated estrogen receptor agonists for functional neuroprotection in VSC4.1 motoneurons

2014

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“…EGCG antagonizes androgen action and down-regulates miR-21 and upregulates tumor suppressor miR-330 in prostate tumors of mice [679]. EGCG has also been shown to decrease expression of oncomirs (miR-92, miR-93, and miR-106b) and increase the expression of tumor suppressor miRs (miR-7-1, miR-34a, and miR-99a) in neuroblastoma cells [680]. …”

Section: Microrna (Mir)mentioning

confidence: 99%

A multi-targeted approach to suppress tumor-promoting inflammation

Samadi

Bilsland

Georgakilas

et al. 2015

Seminars in Cancer Biology

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Cancers harbor significant genetic heterogeneity and patterns of relapse following many therapies are due to evolved resistance to treatment. While efforts have been made to combine targeted therapies, significant levels of toxicity have stymied efforts to effectively treat cancer with multi-drug combinations using currently approved therapeutics. We discuss the relationship between tumor-promoting inflammation and cancer as part of a larger effort to develop a broad-spectrum therapeutic approach aimed at a wide range of targets to address this heterogeneity. Specifically, macrophage migration inhibitory factor, cyclooxygenase-2, transcription factor nuclear factor-kappaB, tumor necrosis factor alpha, inducible nitric oxide synthase, protein kinase B, and CXC chemokines are reviewed as important antiinflammatory targets while curcumin, resveratrol, epigallocatechin gallate, genistein, lycopene, and anthocyanins are reviewed as low-cost, low toxicity means by which these targets might all be reached simultaneously. Future translational work will need to assess the resulting synergies of rationally designed antiinflammatory mixtures (employing low-toxicity constituents), and then combine this with similar approaches targeting the most important pathways across the range of cancer hallmark phenotypes.

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“…It has been noted that EGCG treatment inhibits the expression of androgen-induced miR-21 in prostate cancer cells [129]. Other reports also indicate that EGCG increases the expression of let-7 and miR-34a in human hepatocellular carcinoma cells and neuroblastoma cells [130, 131]. However, the decreased expression of miR-200a is observed in EGCG-treated HepG2 cells by microarray analysis [131].…”

Section: The Role Of Naturally Occurring Agents (Nutraceuticals) Imentioning

confidence: 99%

Targeting CSC-Related miRNAs for Cancer Therapy by Natural Agents

Bao

Ahmad

et al. 2012

CDT

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The theory of cancer stem cells (CSCs) has provided evidence on fundamental clinical implications because of the involvement of CSCs in cell migration, invasion, metastasis, and treatment resistance, which leads to the poor clinical outcome of cancer patients. Therefore, targeting CSCs will provide a novel therapeutic strategy for the treatment and/or prevention of tumors. However, the regulation of CSCs and its signaling pathways during tumorigenesis are not well understood. MicroRNAs (miRNAs) have been proved to act as key regulators of the post-transcriptional regulation of genes, which involve in a wide array of biological processes including tumorigenesis. The altered expressions of miRNAs are associated with poor clinical outcome of patients diagnosed with a variety of tumors. Therefore, emerging evidence strongly suggest that miRMAs play critical roles in tumor development and progression. Emerging evidence also suggest that miRNAs participate in the regulation of tumor cell growth, migration, invasion, angiogenesis, drug resistance, and metastasis. Moreover, miRNAs such as let-7, miR-21, miR-22, miR-34, miR-101, miR-146a, and miR-200 have been found to be associated with CSC phenotype and function mediated through targeting oncogenic signaling pathways. In this article, we will discuss the role of miRNAs in the regulation of CSC phenotype and function during tumor development and progression. We will also discuss the potential role of naturally occurring agents (nutraceuticals) as potent anti-tumor agents that are believed to function by targeting CSC-related miRNAs.

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Alterations in expression of specific microRNAs by combination of 4-HPR and EGCG inhibited growth of human malignant neuroblastoma cells

Cited by 73 publications

References 28 publications

MiR-7-1 potentiated estrogen receptor agonists for functional neuroprotection in VSC4.1 motoneurons

MiR-7-1 potentiated estrogen receptor agonists for functional neuroprotection in VSC4.1 motoneurons

A multi-targeted approach to suppress tumor-promoting inflammation

Targeting CSC-Related miRNAs for Cancer Therapy by Natural Agents

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