Treating cancer with microRNA replacement therapy: A literature review

Hosseinahli, Nayer; Aghapour, Mahyar; Duijf, Pascal H.G.; Baradaran, Behzad

doi:10.1002/jcp.26514

Cited by 258 publications

(194 citation statements)

References 140 publications

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“…[32][33][34] Strategies for prohibiting different types of human malignancy using miRNAs have been proposed in several literatures. [35][36][37] Thus, the functional roles of miRNAs in the growth mechanism of OS should be investigated which might be useful in finding novel therapeutic strategies for treating patients with OS. We are the first to detect the expression of miR-761 in OS and analyze its clinical significance in patients with OS.…”

Section: Discussionmentioning

confidence: 99%

<p>MicroRNA-761 targets FGFR1 to suppress the malignancy of osteosarcoma by deactivating PI3K/Akt pathway</p>

Wang

et al. 2019

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Purpose: has been reported to be deregulated in many types of human cancers and play important roles in cancer genesis and progression. However, the biological roles of miR-761 in osteosarcoma (OS) and the underlying mechanisms remain largely unknown. Methods: The expression of miR-761 in OS tissues and cell lines was analyzed using RT-qPCR. A series of gain-of-function tests were performed, and status of malignancy was evaluated on basis of proliferation, migration, invasion, and apoptosis using different assays to determine the regulatory roles of miR-761 in OS cells in vivo and in vitro. Notably, the mechanisms underlying the action of miR-761 in the pathogenesis of OS were investigated using bioinformatic analysis, luciferase reporter assay, RT-qPCR and Western blotting. Results: The results showed that miR-761 expression was decreased in OS tissues and cell lines and is closely correlated with clinical stage and distant metastasis in OS patients. Patients with OS having low miR-761 expression showed worse prognosis compared to OS patients with high miR-761 expression. Restoring the miR-761 expression level decreased OS cell proliferation, migration, and invasion in vitro; promoted cell apoptosis in vitro; and impaired tumor growth in vivo. In addition, fibroblast growth factor receptor 1 (FGFR1) was found as a direct target gene of miR-761 in OS cells. Furthermore, silencing FGFR1 expression stimulated the tumor-suppressing roles of miR-761 upregulation in OS cells, whereas the activity of miR-761 overexpression in OS cells was abolished by the restoration of FGFR1 expression. Moreover, restoration of miR-761 expression deactivated the PI3K/ Akt pathway in vitro and in vivo. Conclusion: These results suggest that miR-761 plays anti-cancer roles in OS by directly targeting FGFR1 and deactivating the PI3K/Akt pathway. The newly identified miR-761/ FGFR1/PI3K/Akt pathway partially illustrates the mechanism of OS pathogenesis and presents a novel candidate therapeutic target for antitumor therapy.

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Section: Discussionmentioning

confidence: 99%

<p>MicroRNA-761 targets FGFR1 to suppress the malignancy of osteosarcoma by deactivating PI3K/Akt pathway</p>

Wang

et al. 2019

OTT

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“…Moreover, other studies are required to explore the influence of gene polymorphisms as well as microRNAs on α7nAChR function and of α7nAChR activation HAJIASGHARZADEH ET AL. | 14673 or inhibition on lung cancer development, which represents valuable approaches in the understanding of lung tumorigenesis with potential clinical applications (Hosseinahli, Aghapour, Duijf, & Baradaran, 2018;Zarredar, Ansarin, Baradaran, Shekari, et al, 2018b).…”

Section: Discussionmentioning

confidence: 99%

Alpha7 nicotinic acetylcholine receptors in lung inflammation and carcinogenesis: Friends or foes?

Hajiasgharzadeh

Sadigh-Eteghad

Mansoori

et al. 2019

Journal Cellular Physiology

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The lung tissue expresses the cholinergic system including nicotinic acetylcholine receptors (nAChRs) which included in many physiologic and pathologic processes. Mounting evidence revealed that these receptors have important roles in lung carcinogenesis via modulating either stimulatory or inhibitory signaling pathways. Among different members of nicotinic receptors family, alpha7‐subtype of nAChR (α7nAChR) is a critical mediator involved in both inflammatory responses and cancers. Several studies have shown that this receptor is the most powerful regulator of responses that stimulate lung cancer processes such as proliferation, angiogenesis, metastasis, and inhibition of apoptosis. Moreover, aside from its roles in the regulation of cancer pathways, there is growing evidence indicating that α7nAChR has profound impacts on lung inflammation through the cholinergic anti‐inflammatory pathway. Regarding such diverse effects as well as the critical roles of nicotine as an activator of α7nAChR on lung cancer pathogenesis, its modulation has emerged as a promising target for drug developments. In this review, we aim to highlight the detrimental as well as the possible beneficial influences of α7nAChR downstream signaling cascades in the control of lung inflammation and cancer‐associated properties. Consequently, by considering the significant global burden of lung cancer, delineating the complex influences of α7 receptors would be of great interest in designing novel anticancer and anti‐inflammatory strategies for the patients suffering from lung cancer.

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“…In mouse models using colon CSCs, this miR‐15a mimic decreased tumor development, thus having therapeutic potential (Fesler et al, ). These examples, along with recent technical advances in the field of miRNA replacement therapy (Hosseinahli et al, ) demonstrate that miRNA mimics and lentiviral miRNAs have a high potential to effectively restore tumor suppressor miRNAs, modify “stem cell gene” expression in CSCs and reduce tumor development.…”

Section: Diagnosis Prognosis and Therapeutic Implicationsmentioning

confidence: 99%

microRNAs in cancer stem cells: Biology, pathways, and therapeutic opportunities

Asadzadeh

Mansoori

Mohammadi

et al. 2018

Journal Cellular Physiology

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Cancer stem cells (CSCs) are a small subpopulation of tumor cells that have been identified in most types of cancer. Features that distinguish them from the bulk of tumor cells include their pluripotency, self‐renewal capacity, low proliferation rate, and tumor‐initiating ability. CSCs are highly malignant, as they confer drug resistance and facilitate tumor progression, relapse, and metastasis. The molecular mechanisms underlying CSC biology are now beginning to be understood. In this context, microRNAs (miRNAs) occupy a prominent place. These endogenous, small noncoding RNA molecules control gene expression at the posttranscriptional level. This study reviews our current understanding of how the misexpression of tumor suppressor and oncogenic miRNAs in CSCs sustain their abundance and malignant properties. We discuss how they partly do so by acting on major CSC signaling pathways, including the Wnt, Notch, Hedgehog, and BMI‐1 pathways. Our current knowledge of miRNA functions in CSCs may now be used for cancer diagnostic and prognostic purposes. In addition, when combined with recent technical advances in the in vivo delivery of miRNAs, we are now in an excellent position to develop strategies that harness miRNA interference and replacement technologies for the therapeutic targeting of CSCs.

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Treating cancer with microRNA replacement therapy: A literature review

Cited by 258 publications

References 140 publications

<p>MicroRNA-761 targets FGFR1 to suppress the malignancy of osteosarcoma by deactivating PI3K/Akt pathway</p>

<p>MicroRNA-761 targets FGFR1 to suppress the malignancy of osteosarcoma by deactivating PI3K/Akt pathway</p>

Alpha7 nicotinic acetylcholine receptors in lung inflammation and carcinogenesis: Friends or foes?

microRNAs in cancer stem cells: Biology, pathways, and therapeutic opportunities

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