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Nanoparticle-Mediated Small RNA Deliveries for Molecular Therapies
Published in D. Sakthi Kumar, Aswathy Ravindran Girija, Bionanotechnology in Cancer, 2023
Ramasamy Paulmurugan, Uday Kumar Sukumar, Tarik F. Massoud
Babar et al. reported the synthesis of anti-miR-155 encapsulated PLGA nanoparticles using a double emulsion solvent evaporation method [122]. PLGA nanoparticles’ surfaces were modified with cell penetrating peptides (CPP) after loading with anti-miR-155, which upon delivery reduced the growth of pre-B-cell tumors in vivo in mice and appeared as an encouraging therapeutic option for lymphoma and leukemia [122]. The miRNA-10b positively controls breast cancer cell migration and invasion through inhibition of HOXD10 target synthesis, and directly inhibits breast cancer metastasis. Anti-miRNA-10b-loaded poly-L-lysine (PLL-anti-miR-10b) nanoparticles, when administered to MDA-MB-231 breast cancer cells, strongly inhibit the invasive property of cells [123]. The miR-21 is an important player in a majority of cancers. Anti-miR-21 and 5-FU-loaded poly(amidoamine) dendrimer nanoparticles significantly enhanced the cytotoxicity of 5-FU and strongly increased the apoptosis of U251 GBM cells, and the migration ability of tumor cells was significantly decreased [124].
Inhibition of microRNA-10b-5p up-regulates HOXD10 to attenuate Alzheimer’s disease in rats via the Rho/ROCK signalling pathway
Published in Journal of Drug Targeting, 2021
Zhongfan Ruan, Yan Li, Rongzhang He, Xuewei Li
MicroRNAs (miRNAs) have been identified in AD, such as miR-128 [4], miR-10a [5] and miR-29a [6]. MiR-10b is a member of the miR-10 family [7] and it has been reported that miR-10b-5p was implicated in Huntington’s disease [8] and glioma [7], while its role in AD has seldom been studied. Belonging to HOX gene family, HOXD10 is involved in cell differentiation and morphogenesis in embryonic development [9]. Moreover, HOXD10 has been revealed to participate in the processes of glioblastoma [10] and motoneuron defferentiation [11], but the effect of HOXD10 on AD remains to be further investigated. The binding relationship between miR-10b and HOXD10 has been revealed by many previous studies [12–14]. In addition, the Rho/ROCK signalling pathway is an essential signal transduction system within the central nervous system, and is broadly implicated in cell migration, development, differentiation and growth [15]. As reported, the Rho/ROCK signalling pathway was able to inhibit neuronal degeneration [16] and promote neural regeneration [17], and was also involved in the progression of AD [18]. We aimed to evaluate the effects of miR-10b-5p on AD development by targeting HOXD10 with the involvement of the Rho/ROCK signalling pathway. We hypothesised that the inhibited miR-10b-5p may improve ethology and pathology in rat AD models by regulating HOXD10 and the Rho/ROCK pathway
MicroRNA-10b controls the metastasis and proliferation of colorectal cancer cells by regulating Krüppel-like factor 4
Published in Artificial Cells, Nanomedicine, and Biotechnology, 2019
Yue Xie, Jing Zhao, Yanling Liang, Min Chen, Yihong Luo, Xiaobing Cui, Bo Jiang, Liang Peng, Xinying Wang
MicroRNAs (miRNAs), a newly discovered class of non-protein-coding small RNAs, had been shown to play critical roles in physiological and pathological conditions, such as cell differentiation, proliferation, and more recently apoptosis [2,3]. Moreover, the aberrant expression of miRNAs had been linked to several human cancers. Increasing evidence had uncovered their functions as oncogenes and tumour suppressor genes [4]. Recent work had revealed that a large set of miRNAs were overexpressed in human tumours as compared to normal tissues [5,6]. Certain miRNAs that function as oncogenes had been shown to promote carcinogenesis by targeting tumour suppressors, cell cycle regulators and proapoptotic genes, such as miR-543 [5,6]. Among all miRNAs, miR-10b was the first to be associated with metastasis of breast cancer, because it regulated extracellular matrix remodeling by targeting HOXD10 (Homeobox D10) in breast cancer cells [7]. On the other hand, miR-10b could suppress migration of breast cancer cells by silencing TIAM1 (T-cell lymphoma invasion and metastasis [8]. Furthermore, miR-10b also inhibited the expression of neurofibromin and subsequently inactivates the RAS signalling pathway [9]. Together, miR-10b acted as an oncogene to regulate the function of cancer cells by targeting different genes in various cancers.
lncRNA MALAT1 binds chromatin remodeling subunit BRG1 to epigenetically promote inflammation-related hepatocellular carcinoma progression
Published in OncoImmunology, 2019
Mingyan Huang, Huamin Wang, Xiang Hu, Xuetao Cao
Considering the specific cancer expression signature, multiple oncogenic lncRNAs hold the potential as clinical therapeutic targets. lncRNA candidates with an oncogenic activity could be targeted by RNA interference (RNAi) or RNAi-like molecules as a potential approach for a reduction of their abundance and thus a diminution of their functional activity. The same effect could be achieved by the binding of short RNA sequences (antagolincs)50 to the lncRNA-protein interfaces, disrupting the interaction. Systematic treatment of tumor-bearing mice with short RNA sequences (antagomirs) targeting miRNA has been proved to be efficient. In vivo treatment with antagomirs targeting miR-10b inhibits tumor metastasis by increasing the expression of its target, a tumor suppressor gene HOXD10.51 Moreover, double-stranded DNA plasmids inducing toxic responses could also been used in the lncRNA targets therapies. BC-819, a double-stranded DNA plasmid carrying the gene for the a subunit of diphtheria toxin under the control of lncRNA H19 regulatory sequences, has been clinically used in vivo to knockdown H19 in different cancers, and has shown promising therapeutic benefit for the cancer patients.52,53 Our in vivo injection of MALAT1 ASO has successfully decreased the expression of MALAT1 and suppressed HCC progression, which suggested targeting MALAT1 in HCC patients is a potential and promising clinical therapy.