Effect of simvastatin and microRNA-21 inhibitor on metastasis and progression of human salivary adenoid cystic carcinoma

Wang, Chao; Li, Ting; Fang, Yan; Cai, Wei; Zheng, Jiwei; Jiang, Xingyu; Sun, Jing

doi:10.1016/j.biopha.2018.05.157

Cited by 29 publications

(27 citation statements)

References 40 publications

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“…It is possible that miR-21i could effectively inhibit the expression of oncogenic miR-21 receptors and thereby sensitizing the action of SMV. Consistently, Wang et al have reported that a combination of SMV and miR-21i was effective in inhibiting the cell migration/invasion, cell proliferation and induced cell apoptosis in salivary adenoid cystic carcinoma (SACC) (Wang et al, 2018). Similarly, Li et al reported that miR-21 was the key factor involved in the migration and invasion of pancreatic cancer cells and authors have showed that the knockdown of miR-2 by transfection miR-21i antisense oligonucleotide (ASO) significantly suppressed the migration of cancer cells and significantly inhibited the cell proliferation (Li et al, 2017).…”

Section: Discussionmentioning

confidence: 72%

MicroRNA-21 inhibitor (miR-21i) and Simvastatin-loaded poly (D,L-lactide-co-glycolide)/polyethylenimine (PLGA/PEI) nanoparticles for synergistic anticancer effect in Gastric Cancers

Liu

Yang

Zhang

et al. 2020

Preprint

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In this study, we have successfully developed a simvastatin (SMV) and miR-21i-loaded poly (D,L-lactide-co-glycolide)/polyethylenimine (PLGA/PEI) nanoparticles (NP) to enhance the therapeutic efficacy in gastric cancers. The nanoparticles were characterized for in vitro physicochemical and biological assays and pharmacokinetic study was performed in rats. CLSM/FACS results clearly showed the ability of SMV/miR-21i-loaded PLGA/PEI NP (PPN-S21i) to deliver the combinational therapeutics of SMV and miR-21i to the cancer cells. Combination of SMV+miR-21i showed significantly lower cell viability compared to that of free SMV. Our results clearly highlight the importance of simultaneous interaction of SMV+miR-21i and that it could significantly decrease the cell proliferation in BGC-823, SGC-7901 and HGC-27 gastric cancer cells while it was significantly less cytotoxic to normal gastric mucosa cells (GES-1). Cell apoptosis of SMV+miR-21i was significantly higher compared to that of individual drug or miRNA. Finally, pharmacokinetic analysis revealed that PPN-S21i significantly prolonged the blood circulation time of SMV compared to that of free SMV indicating the potential of carrier system. Overall, results clearly indicate that the combination of SMV+miR-21i (gene + drug therapy) might provide a valuable strategy for the clinical management of gastric cancers.

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Section: Discussionmentioning

confidence: 72%

MicroRNA-21 inhibitor (miR-21i) and Simvastatin-loaded poly (D,L-lactide-co-glycolide)/polyethylenimine (PLGA/PEI) nanoparticles for synergistic anticancer effect in Gastric Cancers

Liu

Yang

Zhang

et al. 2020

Preprint

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“…Tumor doubling time increased by more than 5-fold (from 2.45 to 12.77 days) for tumor cells treated with miR-21-miRNase prior to transplantation, as compared to control groups without treatment or treated with a sham (luc-POC) or the hairpin oligonucleotide (h-ODN). The biological effects induced by this miRNase are comparable or superior to those of available miR-21 oligonucleotide inhibitors (Dong et al, 2012; Wagenaar et al, 2015; Wu et al, 2016; Wang et al, 2018; Zhou et al, 2018).…”

Section: Discussionmentioning

confidence: 78%

Catalytic Knockdown of miR-21 by Artificial Ribonuclease: Biological Performance in Tumor Model

et al. 2019

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Control of the expression of oncogenic small non-coding RNAs, notably microRNAs (miRNAs), is an attractive therapeutic approach. We report a design platform for catalytic knockdown of miRNA targets with artificial, sequence-specific ribonucleases. miRNases comprise a peptide [(LeuArg) 2 Gly] 2 capable of RNA cleavage conjugated to the miRNA-targeted oligodeoxyribonucleotide, which becomes nuclease-resistant within the conjugate design, without resort to chemically modified nucleotides. Our data presented here showed for the first time a truly catalytic character of our miR-21-miRNase and its ability to cleave miR-21 in a multiple catalytic turnover mode. We demonstrate that miRNase targeted to miR-21 (miR-21-miRNase) knocked down malignant behavior of tumor cells, including induction of apoptosis, inhibition of cell invasiveness, and retardation of tumor growth, which persisted on transplantation into mice of tumor cells treated once with miR-21-miRNase. Crucially, we discover that the high biological activity of miR-21-miRNase can be directly related not only to its truly catalytic sequence-specific cleavage of miRNA but also to its ability to recruit the non-sequence specific RNase H found in most cells to elevate catalytic turnover further. miR-21-miRNase worked synergistically even with low levels of RNase H. Estimated degradation in the presence of RNase H exceeded 10 3 miRNA target molecules per hour for each miR-21-miRNase molecule, which provides the potency to minimize delivery requirements to a few molecules per cell. In contrast to the comparatively high doses required for the simple steric block of antisense oligonucleotides, truly catalytic inactivation of miRNA offers more effective, irreversible, and persistent suppression of many copy target sequences. miRNase design can be readily adapted to target other pathogenic microRNAs overexpressed in many disease states.

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“…It also induces cholangiocarcinoma cancer cell death by disrupting the colocalization of Rac1/lipid rafts, depressing Rac1 activity, and suppressing the expression of ATP-binding cassettes (ABCA1 and ABCG1) [ 65 , 66 ]. The anti-cancer effect of simvastatin in salivary adenoid cystic carcinoma (SACC) is further enhanced by the inhibition of microRNA-21, as it is highly expressed in tumors and promotes tumor development [ 67 ]. A clinical study conducted in Taiwan National Health Insurance Research Database (NHIRD) in a cohort of 15,264 hyperlipidemic prostate cancer patients shows that the mortality rate was decreased in patients receiving simvastatin or lovastatin [ 68 ].…”

Section: Statin As a Single Agent In The Suppression Of Cancer Cell Proliferation And The Induction Of Apoptosismentioning

confidence: 99%

Statin as a Potential Chemotherapeutic Agent: Current Updates as a Monotherapy, Combination Therapy, and Treatment for Anti-Cancer Drug Resistance

Pun

Jeong

2021

Pharmaceuticals

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Cancer is incurable because progressive phenotypic and genotypic changes in cancer cells lead to resistance and recurrence. This indicates the need for the development of new drugs or alternative therapeutic strategies. The impediments associated with new drug discovery have necessitated drug repurposing (i.e., the use of old drugs for new therapeutic indications), which is an economical, safe, and efficacious approach as it is emerged from clinical drug development or may even be marketed with a well-established safety profile and optimal dosing. Statins are inhibitors of HMG-CoA reductase in cholesterol biosynthesis and are used in the treatment of hypercholesterolemia, atherosclerosis, and obesity. As cholesterol is linked to the initiation and progression of cancer, statins have been extensively used in cancer therapy with a concept of drug repurposing. Many studies including in vitro and in vivo have shown that statin has been used as monotherapy to inhibit cancer cell proliferation and induce apoptosis. Moreover, it has been used as a combination therapy to mediate synergistic action to overcome anti-cancer drug resistance as well. In this review, the recent explorations are done in vitro, in vivo, and clinical trials to address the action of statin either single or in combination with anti-cancer drugs to improve the chemotherapy of the cancers were discussed. Here, we discussed the emergence of statin as a lipid-lowering drug; its use to inhibit cancer cell proliferation and induction of apoptosis as a monotherapy; and its use in combination with anti-cancer drugs for its synergistic action to overcome anti-cancer drug resistance. Furthermore, we discuss the clinical trials of statins and the current possibilities and limitations of preclinical and clinical investigations.

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Effect of simvastatin and microRNA-21 inhibitor on metastasis and progression of human salivary adenoid cystic carcinoma

Cited by 29 publications

References 40 publications

MicroRNA-21 inhibitor (miR-21i) and Simvastatin-loaded poly (D,L-lactide-co-glycolide)/polyethylenimine (PLGA/PEI) nanoparticles for synergistic anticancer effect in Gastric Cancers

MicroRNA-21 inhibitor (miR-21i) and Simvastatin-loaded poly (D,L-lactide-co-glycolide)/polyethylenimine (PLGA/PEI) nanoparticles for synergistic anticancer effect in Gastric Cancers

Catalytic Knockdown of miR-21 by Artificial Ribonuclease: Biological Performance in Tumor Model

Statin as a Potential Chemotherapeutic Agent: Current Updates as a Monotherapy, Combination Therapy, and Treatment for Anti-Cancer Drug Resistance

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