miR181b is induced by the chemopreventive polyphenol curcumin and inhibits breast cancer metastasis via down‐regulation of the inflammatory cytokines CXCL1 and ‐2

Kronski, Emanuel; Fiori, Micol Eleonora; Barbieri, Ottavia; Astigiano, Simonetta; Mirisola, Valentina; Killian, Peter H.; Bruno, Antonino; Pagani, Arianna; Rovera, Francesca; Pfeffer, Ulrich; Sommerhoff, Christian P.; Noonan, Douglas M.; Nerlich, Andreas G.; Fontana, Laura; Bachmeier, Beatrice E.

doi:10.1016/j.molonc.2014.01.005

Cited by 161 publications

(112 citation statements)

References 55 publications

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“…Furthermore, it was mirrored that decreased miR‐181b restrained vascular remodelling by activating TGF‐β/pSmadD2/3 pathway,40 and addition of angiotensin II into cardiac fibroblasts could significantly down‐regulate miR‐181b expression 41. In addition, it has been illuminated that miR‐181b might suppress breast cancer cells’ capacity of metastasis by targeting CXCL1 and CXCL2, a couple of inflammatory cytokines 42, 43, 44. He et al45 arrived at conclusions that miR‐181b was highly expressed with prostate cancer tissues and cell line (ie.…”

Section: Discussionmentioning

confidence: 99%

The interplay of LncRNA ANRIL and miR‐181b on the inflammation‐relevant coronary artery disease through mediating NF‐κB signalling pathway

Guo

Tang

et al. 2018

J Cellular Molecular Medi

103

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This study was designed to investigate whether ANRIL affected the aetiology of coronary artery disease (CAD) by acting on downstream miR‐181b and NF‐κB signalling. Altogether 327 CAD patients diagnosed by angiography were included, and mice models of CAD were established. Human coronary endothelial cells (HCAECs) and human umbilical vein endothelial cells (HUVECs) were also purchased. In addition, shRNA‐ANRIL, shRNA‐NC, pcDNA3.1‐ANRIL, miR‐181b mimic, miR‐181b inhibitor and miR‐NC were transfected into the cells. The lipopolysaccharides (LPS) and pyrrolidine dithiocarbamate (PDTC) were also added to activate or deactivate NF‐κB signalling. Both highly expressed ANRIL and lowly expressed miR‐181b were associated with CAD population aged over 60 years old, with smoking history, with hypertension and hyperlipidemia, with CHOL H 4.34 mmol/L, TG ≥ 1.93 mmol/L and Hcy ≥ 16.8 μmol/L (all P < 0.05). Besides, IL‐6, IL‐8, NF‐κB, TNF‐α, iNOS, ICAM‐1, VCAM‐1 and COX‐2 expressions observed within AD mice models were all beyond those within NC and sham‐operated groups (P < 0.05). Also VEGF and HSP 70 were highly expressed within AD mice models than within NC and sham‐operated mice (P < 0.05). Transfection of either pcDNA‐ANRIL or miR‐181b inhibitor could significantly fortify HCAECs’ viability and put on their survival rate. At the meantime, the inflammatory factors and vascular‐protective parameters were released to a greater level (P < 0.05). Finally, highly expressed ANRIL also notably bring down miR‐181b expression and raise p50/p65 expressions within HCAECs (P < 0.05). The joint role of ANRIL, miR‐181b and NF‐κB signalling could aid in further treating and diagnosing CAD.

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Section: Discussionmentioning

confidence: 99%

The interplay of LncRNA ANRIL and miR‐181b on the inflammation‐relevant coronary artery disease through mediating NF‐κB signalling pathway

Guo

Tang

et al. 2018

J Cellular Molecular Medi

103

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“…Kronski et al found that miR181b-mediated CXCL1 and -2 expression through direct binding to 3'UTR that mediated curcuminrelated down-regulation of CXCL1 and -2 in breast cancer cells (MDA-MB-231) (53). They also suggested that miR181b induces apoptosis and inhibits the expression of MMPs in vitro, thus inhibiting invasion of cancer cells.…”

Section: Curcumin Regulates Micrornas (Mirnas) Expressionmentioning

confidence: 99%

“…Therefore, miRNAs regulate cellular proliferation, differentiation and apoptosis, closely associated with cancer (51-53). miRNAs regulate several proteins' expressions by binding to mRNA three prime untranslated region (3'UTR), which then degrades mRNA or inhibits mRNA translation (53). miRNAs have a dual effect in cancers, either acting as tumor promoters or tumor suppressors (53).…”

Section: Curcumin Regulates Micrornas (Mirnas) Expressionmentioning

confidence: 99%

“…miRNAs regulate several proteins' expressions by binding to mRNA three prime untranslated region (3'UTR), which then degrades mRNA or inhibits mRNA translation (53). miRNAs have a dual effect in cancers, either acting as tumor promoters or tumor suppressors (53). miR-21 is upregulated in almost all cancers, including breast, lung, colon, liver and prostate (51,52).…”

Section: Curcumin Regulates Micrornas (Mirnas) Expressionmentioning

confidence: 99%

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Molecular Mechanisms of Anti-metastatic Activity of Curcumin

Deng

Verron

Rohanizadeh

2016

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Abstract. Cancer is the leading cause of death worldwide. Although cancer occurs as a localized disease, its morbidity and mortality rates remain high due to the ability of cancer cells to break-off from the primary tumor and spread to distant organs. Currently, chemotherapy is the main treatment for cancer; however, the increase in proportion of drug-resistant cancer cells and unpleasant side-effects of chemotherapy are still the major challenges in cancer therapy. Curcumin is a natural polyphenol compound and the main bioactive constituent of Indian spice turmeric, widely used in Indian and Chinese medicines. Curcumin has well-known therapeutic actions, including antiinflammatory, anti-microbial, anti-oxidant and anti-cancer properties. Curcumin induces cancer cell apoptosis through regulating various signaling pathways and arresting tumor cell cycle. Curcumin's therapeutic/ preventative actions on metastatic cancers have not been yet fully understood and studied. The present review explores the potential anti-metastatic mechanisms of curcumin, including inhibition of transcription factors and their signaling pathways (e.g., inflammatory cytokines (e.g., CXCL1, CXCL2, multiple proteases (e.g., uPA, MMPs), multiple protein kinases (e.g., MAPKs, FAK), regulation of miRNAs (e.g., miR21, miR181b) and heat shock proteins (HLJ1). In addition, possible synergistic actions of combination therapy of curcumin with current chemotherapies are discussed in this review.Despite all recent advances in oncology, cancer is still one of the deadliest diseases around the world (1). Cancer occurs as a localized disease but can spread to distant organs through migration, invasion and metastasis (2). Metastatic cancer is one of the major causes of death in cancer patients. Metastasis is a complex process involving multiple steps: (i) local migration through degrading basement membrane and extracellular matrix (ECM), (ii) intravasation into blood and/or lymphatic vessels, (iii) circulating to the target organ site, (iv) extravasation into target organ tissue and, finally, (v) multiplication in the target organ (2, 3). These steps are mediated by various factors, including growth factors, proteolysis degradation of extracellular matrix, cell-cell adhesion, cytoskeleton remodeling and changes of genes' expressions (2, 3). Metastasis is a non-random process that means each metastatic cancer type has its own preferred site of metastasis. For example, breast cancer cells preferentially metastasize to regional lymph nodes, liver, lungs and bone (4). Nowadays, there are different therapeutic approaches available for patients with metastatic cancers, including surgery, radiotherapy and chemotherapy. Chemotherapy remains the main treatment modality for cancer patients because of its ability of preventing invasion and metastasis. However, the morbidity and mortality rates in patients with metastatic cancer still remain high since current chemotherapy agents fail to selectively and effectively kill cancer cells without destroying normal ce...

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“…They reported that miR-22 was upregulated upon curcumin treatment, and the predicted targets were ERα and transcription factor Sp1, while miR-196, an oncogenic miRNA in gastric cancers, was significantly downregulated after curcumin treatment [61] . Curcumin has been shown to downregulate putative oncogenic miRNAs, such as miR-21 [62,63] , while it upregulates key tumor-suppressor miRNAs, including miR-200 family, let-7 family, miR-185b, and miR-22 [64,65,66] . More recently, Toden and colleagues reported that curcumin chemosensitizes colorectal cancer cells to 5-fluorouracil (5FU) by suppression of epithelial-mesenchymal transition (EMT) through upregulation of EMT-suppressive miRNAs in 5-fluorouracil resistant (5FUR) cell lines.…”

Section: Curcuminmentioning

confidence: 99%

Modulation of miRNAs by Natural Agents: Nature’s way of dealing with cancer

Masika

Zhao

Hescheler

et al. 2015

RNA Dis

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Accumulating lines of evidence have revealed that microRNAs (miRNAs) play critical roles in many biological processes, such as carcinogenesis, angiogenesis, programmed cell death, cell proliferation, invasion, migration, and differentiation. They act either as tumor suppressors or oncogenes, and alteration in their expression patterns has been linked to onset, progression and chemoresistance of various cancers. Moreover, miRNAs are also crucial for the regulation of cancer stem cells (CSCs) self-renewal and proliferation as well as control of Epithelial-to-Mesenchymal Transition (EMT) of cancer cells. Therefore, exploitation of miRNAs as targets for cancer prevention and therapy could be a promising approach. Several experimental and epidemiologic studies have shown that dietary intake of natural agents such as baicalin, ginsenoside, curcumin, resveratrol, genistein, epigallocatechin-3-gallate (EGCG), indole-3-carbinol, 3,3΄-diindolylmethane (DIM) including antioxidants among others is inversely associated with the risk for cancer, demonstrating the inhibitory effects of natural agents on carcinogenesis. Additionally, the anticancer agents from natural agents have been found to inhibit the development and progression of cancer through the regulation of various cancer processes such as apoptosis, cell cycle regulation, differentiation, inflammation, angiogenesis, and metastasis. Importantly, natural agents could significantly impact the expression of tumor-suppressor and oncogenic miRNAs, regulate cellular signaling networks, inhibit cancer cell growth and cancer stem cell self-renewal. This is important for the normalization of altered cellular signaling mechanisms in cancer cells. This postulates a much broader use of natural agents in the prevention and/or treatment of various cancers in combination with conventional chemotherapeutics. However, more in vitro mechanistic experiments, in vivo animal studies, and clinical trials are warranted to realize the true value of natural agents in the prevention and/or treatment of cancer. Herein, we provide an overview of natural agents' modulation of miRNA expression as well as highlight the significance of these observations as potential new strategies in cancer therapies. This review will help us to understand how miRNAs are regulated by natural agents and also help in the development of effective and secure natural agents for therapeutic purposes.

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miR181b is induced by the chemopreventive polyphenol curcumin and inhibits breast cancer metastasis via down‐regulation of the inflammatory cytokines CXCL1 and ‐2

Cited by 161 publications

References 55 publications

The interplay of LncRNA ANRIL and miR‐181b on the inflammation‐relevant coronary artery disease through mediating NF‐κB signalling pathway

The interplay of LncRNA ANRIL and miR‐181b on the inflammation‐relevant coronary artery disease through mediating NF‐κB signalling pathway

Molecular Mechanisms of Anti-metastatic Activity of Curcumin

Modulation of miRNAs by Natural Agents: Nature’s way of dealing with cancer

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