Abstract
MicroRNAs (miRNAs) important for posttranscriptional gene expression are involved in the initiation and progression of human cancer. In this study, we reported that miR-26a was over-expressed in human EOC specimens and the expression level of extracellular miR-26a in plasma can distinguish patients from healthy controls in EOC. Ectopic expression of miR-26a in ovarian cancer (OC) cells increased cell proliferation and clonal formation. This growth promoting effect of OC cell growth was mediated by miR-26a inhibition of the posttranscription of ER-α. Furthermore, inhibition of miR-26a suppressed the tumor formation generated by injecting OC cells in nude mice. Our results suggest that aberrantly expressed miR-26a may contribute to OC development.
Highlights
ovarian cancer (OC) is the fifth most common cancer in women and the leading cause of cancer deaths from gynecological malignancy in western countries [1]
It has been observed that the expression level of miR-26a was decreased or increased in human malignancies, such as breast carcinoma [16], nasopharyngeal carcinoma [17,18], and glioblastoma [19], indicating a complicated role of miR-26a in progression of the malignancies
We examined whether miR-26a affects EOC cell growth using SKOV3 and ES2 cells as models
Summary
OC is the fifth most common cancer in women and the leading cause of cancer deaths from gynecological malignancy in western countries [1]. Recent studies have revealed critical functions of miRNAs in essential processes, including proliferation, differentiation and cell death [3]. Altered expression or mutation of miRNAs has been reported in cancer, such as lung cancer, breast cancer, leukemia and other carcinomas [4]. Over-expression of let-7 inhibited their growth by targeting Ras [5,6]. MiR-21 directly targets the tumor suppressor PTEN in hepatocellular cancer [7]. Several studies showed that miRNAs can function either as tumor suppressors (as is the case for the miR15a-miR-16-1 cluster [8]) or oncogenes (as is the case for miR-21 [9])
Sign-in/Register to view highlights & summary Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
