Radiologic factors related to double-bar insertion in minimal invasive repair of pectus excavatum

Kim, Ki Hwan; Lee, Ki Yeol; Lee, Jung Bok; Yang, Kyung Sook; Hwang, Jinwook; Je, Bo Kyung; Park, Hyung Joo

doi:10.1007/s12519-014-0522-9

Cited by 2 publications

(1 citation statement)

References 19 publications

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“…A previous study confirmed that miR-182 activates the PI3K/AKT pathway (31), whereas CADM3 inhibits activation of the PI3K/AKT signaling pathway, and CADM3 can bind to CADM4 (32). Non-overlapping expression of CADM2 and CADM3 has been detected in the developing retina, and binding of CADM2 and CADM3 to CADM1 and CADM4 in vitro may indicate the functional role of CADMs during nervous system development (33). VEGF is an angiogenic growth factor that is involved in the pathogenesis of retinal diseases, such as diabetic retinopathy (34).…”

Section: Discussionsupporting

confidence: 55%

Downregulation of microRNA‑182 inhibits cell viability, invasion and angiogenesis in retinoblastoma through inhibition of the PI3K/AKT pathway and CADM2 upregulation

Huang

Nie

et al. 2018

Int J Oncol

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Retinoblastoma (RB) is a well-vascularized tumor dependent on angiogenesis. The present study aimed to explore whether microRNA (miR)-182 regulates cell viability, invasion and angiogenesis in RB via the phosphatidylinositol-3-OH kinase (PI3K)/protein kinase B (AKT) signaling pathway and by targeting cell adhesion molecule 2 (CADM2). The expression levels of miR-182 and CADM2 were initially detected in RB tissues from patients with RB who underwent ophthalmectomy, and normal retinal tissues collected from other trauma patients who underwent eye enucleation. To determine whether CADM2 was targeted by miR-182, a dual luciferase reporter assay was conducted. Subsequently, Y79 and WERI-Rb-1 RB cells were transfected with a miR-182 mimic or miR-182 inhibitor, or small interfering RNA against CADM2, in order to investigate the effects of miR-182 on viability and invasion, which were detected using MTT and Transwell assays, respectively. In addition, to determine whether the regulatory mechanism underlying the effects of miR-182 was associated with the PI3K/AKT signaling pathway, the expression levels of associated genes were detected by reverse transcription-quantitative polymerase chain reaction and western blot analysis. A xenograft tumor model in nude mice was also established, in order to evaluate the effects of miR-182 on tumor growth and angiogenesis. The results indicated that miR-182 expression was increased and CADM2 expression was reduced in RB tissues; CADM2 was confirmed to be targeted and negatively regulated by miR-182. When the expression of miR-182 was downregulated, cell viability, invasion, tumor volume and angiogenesis were significantly decreased. Furthermore, the expression levels of PI3K/AKT signaling pathway-associated genes were increased in response to miR-182 overexpression or CADM2 silencing. Taken together, these results suggested that inhibition of miR-182 may suppress cell viability, invasion and angiogenesis in RB through inactivation of the PI3K/AKT pathway and CADM2 upregulation. This mechanism may reveal a novel potential therapeutic target.

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Section: Discussionsupporting

confidence: 55%