title: miR-106a* inhibits the proliferation of esophageal carcinoma cells by targeting CDK2-associated Cullin 1 (CACUL1).
abstract: Previous studies suggest that aberrant microRNA expression is common in plenty of cancers. The expression of miR-106a* was decreased in follicular lymphoma, but the expression and functions of miR-106a* in esophageal carcinoma (EC) remain unclear. In this study, we explored the expression and anti-oncogenic roles of miR-106a* in human EC. The expression of miR-106a* is significantly decreased in EC tissues and EC cell lines. Overexpression of miR-106a* suppressed EC cell proliferation, clonogenicity, G1/S transition, and induced apoptosis in vitro, but inhibition of miR-106a* facilitated cell proliferation, clonogenicity, G1/S transition. Luciferase reporter assay results showed that CDK2-associated Cullin 1 (CACUL1) was a direct target of miR-106a* in EC cells. Moreover, silencing CACUL1 resulted in the same biologic effects of miR-106a* overexpression in EC cells, which included suppressed EC cell proliferation, clonogenicity, and blocked G1/S transition through CDK2 pathway by inhibiting cell cycle regulators (Cyclin A, Cyclin E). Our data indicate that miR-106a* might play an anti-oncogenic role in EC by regulating CACUL1 expression, which suggest miR-106a* as a new potential diagnostic and therapeutic target for EC.
authors: Xi&apos;an Jiaotong University Department of Radiation Oncology, the First Affiliated Hospital of Medical Colledge, Shaanxi Xi&apos;an China.
authors: H L
authors: HL
authors: Ma
authors: Xi&apos;an Jiaotong University Department of Thoracic Surgery, the First Affiliated Hospital of Medical Colledge Shaanxi Xi&apos;an China.
authors: X P
authors: XP
authors: Wen
authors: Xi&apos;an Jiaotong University Department of Radiation Oncology, the First Affiliated Hospital of Medical Colledge, Shaanxi Xi&apos;an China.
authors: X Z
authors: XZ
authors: Zhang
authors: Xi&apos;an Jiaotong University Department of Radiation Oncology, the First Affiliated Hospital of Medical Colledge, Shaanxi Xi&apos;an China.
authors: X L
authors: XL
authors: Wang
authors: Xi&apos;an Jiaotong University Department of Radiation Oncology, the First Affiliated Hospital of Medical Colledge, Shaanxi Xi&apos;an China.
authors: D L
authors: DL
authors: Zhao
authors: Xi&apos;an Jiaotong University Department of Radiation Oncology, the First Affiliated Hospital of Medical Colledge, Shaanxi Xi&apos;an China.
authors: S M
authors: SM
authors: Che
authors: Xi&apos;an Jiaotong University Department of Oncology Surgery, the First Affiliated Hospital of Medical Colledge Shaanxi Xi&apos;an China dangchengxue2014&commat;126.com.
authors: C X
authors: CX
authors: Dang
mesh_terms: D017209:Apoptosis / Q000235:genetics; D045744:Cell Line, Tumor; D049109:Cell Proliferation / Q000235:genetics*; D044842:Cullin Proteins / Q000096:biosynthesis / Q000235:genetics*; D019925:Cyclin A / Q000378:metabolism; D019927:Cyclin E / Q000378:metabolism; D004938:Esophageal Neoplasms / Q000235:genetics* / Q000473:pathology; D006801:Humans; D035683:MicroRNAs / Q000037:antagonists & inhibitors / Q000096:biosynthesis / Q000235:genetics*; D034622:RNA Interference; D034741:RNA, Small Interfering / Q000235:genetics; D059807:S Phase Cell Cycle Checkpoints / Q000235:genetics
chemical_list: C546534:CACUL1 protein, human; D044842:Cullin Proteins; D019925:Cyclin A; D019927:Cyclin E; C542541:MIRN106 microRNA, human; D035683:MicroRNAs; D034741:RNA, Small Interfering