title: miR-133a inhibits cervical cancer growth by targeting EGFR.
abstract: MicroRNAs (miRNAs) are small non-coding RNAs that play critical roles in cervical carcinogenesis and progression. microRNA-133a (miR-133a) has been reported to play a tumor-suppressor role in a range of cancers. However, the role and underlying molecular mechanism of miR-133a in cervical cancer have not been investigated. In the present study, we investigated the role of miR-133a in the tumorigenicity of cervical cancer cells in vivo and in vitro. The expression of miR-133a was investigated using real-time reverse transcription-polymerase chain reaction (qRT-PCR) in 30 cervical specimens and matched adjacent normal tissues and cervical cancer cell lines. We found that the expression level of miR‑133a was significantly downregulated in cervical cancer tissues and cervical cancer cell lines, and the aberrant expression of miR-133a was correlated with lymph node metastasis, histological grade and FIGO stage. The role of miR-133a in tumorigenicity of cervical cancer cells was assessed by the restoration of miR-133a. We found that restoration of miR‑133a inhibited cell proliferation, colony formation, migration and invasion, promoted cell apoptosis in vitro and suppressed tumorigenicity in vivo. The epidermal growth factor receptor (EGFR) was confirmed to be a direct target of miR-133a in cervical cancer cells using luciferase assay and western blotting. Restoration of miR-133a inhibited EGFR expression and activated the AKT and ERK signaling pathways. These results showed that miR-133a suppresses cervical cancer growth in vitro and in vivo through targeting EGFR, suggesting that miR-133a can be a potential target for the treatment of cervical cancer.
authors.affiliation: Department of Anesthesiology, The First Hospital of Jilin University, Chaoyang, Changchun, Jilin 130021, P.R. China.
authors.forename: Xuesong
authors.initials: X
authors.lastname: Song
authors.affiliation: The Experiment Center, College of Basic Medical Sciences, Jilin University, Chaoyang, Changchun, Jilin 130021, P.R. China.
authors.forename: Bo
authors.initials: B
authors.lastname: Shi
authors.affiliation: The Experiment Center, College of Basic Medical Sciences, Jilin University, Chaoyang, Changchun, Jilin 130021, P.R. China.
authors.forename: Kexin
authors.initials: K
authors.lastname: Huang
authors.affiliation: Department of Pathology, China‑Japan Union Hospital of Jilin University, Nanguan, Changchun, Jilin 130033, P.R. China.
authors.forename: Wenjie
authors.initials: W
authors.lastname: Zhang
mesh_terms: D000368:Aged; D000369:Aged, 80 and over; D000818:Animals; D045744:Cell Line, Tumor; D049109:Cell Proliferation / Q000235:genetics*; D066246:ErbB Receptors / Q000096:biosynthesis* / Q000235:genetics; D005260:Female; D015972:Gene Expression Regulation, Neoplastic; D006801:Humans; D051379:Mice; D035683:MicroRNAs / Q000096:biosynthesis* / Q000235:genetics; D008875:Middle Aged; D009361:Neoplasm Invasiveness / Q000235:genetics; D009367:Neoplasm Staging; D015398:Signal Transduction; D002583:Uterine Cervical Neoplasms / Q000235:genetics* / Q000473:pathology; D023041:Xenograft Model Antitumor Assays
chemical_list: C548234:MIRN133 microRNA, human; D035683:MicroRNAs; C512478:EGFR protein, human; D066246:ErbB Receptors