Human bone marrow mesenchymal stem cell‐derived extracellular vesicles impede the progression of cervical cancer via the miR‐144‐3p/CEP55 pathway. Issue 4 (8th January 2021)

• Record Type: Journal Article
• Authors: Meng, Qin; Zhang, Baofang; Zhang, Yingming; Wang, Shuyan; Zhu, Xiaohui
• Is Part Of: Journal of cellular and molecular medicine. Volume 25:Issue 4(2021)
• Page Start: 1867
• Page End: 1883
• Publication Date: 2021-01-08
• Subjects: centrosomal protein -- 55 Kd -- cervical cancer -- extracellular vesicles -- human bone marrow mesenchymal stem cells -- microRNA‐144‐3p; Cytology; Medicine; Molecular Biology; Cytologie -- Périodiques; Médecine -- Périodiques; Biologie moléculaire -- Périodiques; Cytology -- Periodicals; Medicine -- Periodicals; Molecular biology -- Periodicals; 611.01805
• DOI: 10.1111/jcmm.15573
• Languages: English
• ISSNs: 1582-1838

Abstract

Abstract: Cervical cancer is the most common gynaecological malignancy, with a high incidence rate and mortality rate in middle‐aged women. Human bone marrow mesenchymal stem cells (hBMSCs) have been implicated in the initiation and subsequent development of cancer, along with the involvement of extracellular vesicles (EVs) mediating intracellular communication by delivering microRNAs (miRNAs or miRs). This study is aimed at investigating the physiological mechanisms by which EVs‐encapsulated miR‐144‐3p derived from hBMSCs might mediate the progression of cervical cancer. The expression profiles of centrosomal protein, 55 Kd (CEP55) and miR‐144‐3p in cervical cancer cell lines and tissues, were quantified by RT‐qPCR and Western blot analysis. The binding affinity between miR‐144‐3p and CEP55 was identified using in silico analysis and luciferase activity determination. Cervical cancer cells were co‐cultured with EVs derived from hBMSCs that were treated with either miR‐144‐3p mimic or miR‐144‐3p inhibitor. Cervical cancer cell proliferation, invasion, migration and apoptosis were detected in vitro. The effects of hBMSCs‐miR‐144‐3p on tumour growth were also investigated in vivo. miR‐144‐3p was down‐regulated, whereas CEP55 was up‐regulated in cervical cancer cell lines and tissues. CEP55 was targeted by miR‐144‐3p, which suppressed cervical cancer cell proliferation, invasion and migration and promoted apoptosis via CEP55. Furthermore, similar results were obtained by hBMSCs‐derived EVs carrying miR‐144‐3p. In vivo assays confirmed the tumour‐suppressive effects of miR‐144‐3p in hBMSCs‐derived EVs on cervical cancer. Collectively, hBMSCs‐derived EVs‐loaded miR‐144‐3p impedes the development and progression of cervical cancer through target inhibition of CEP55, therefore providing us with a potential therapeutic target for treating cervical cancer.