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. 2019 Dec 25;12(1):65. doi: 10.3390/cancers12010065

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© 2019 by the authors.

Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/).

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Silencing of OPA3 expression decreases cell proliferation and epithelial–mesenchymal transition (EMT): (a,b) Cell proliferation in Panc-1 OPA3-shRNA cells was analyzed by clonogenic assay and quantified. (c) Cell proliferation in Panc-1 OPA3-shRNA cells was analyzed by cell counting. (d,e) Apoptosis in Panc-1 OPA-shRNA cells was analyzed by flow cytometry and quantified by Annexin-V positivity. (f) Expressions of EMT-related proteins in Panc-1 OPA3-shRNA cells were analyzed by immunoblotting. (g) Representative scheme depicting the role of OPA3 expression induced by oncogenic signaling in pancreatic cancer cells. Statistics: data are mean ± S.E.M. (n = 3); one-way ANOVA followed by Dunnett post hoc test (compared to “shCTL”) for (b) and (e) and two-way ANOVA for (c). * p < 0.05, ** p < 0.01, and *** p < 0.001. Abbreviations: 7-AAD: 7-aminoactinomycin D, K-ras: Kirsten RAS GTPase, NDUFAF1: NADH dehydrogenase 1 alpha subcomplex assembly factor 1, OPA3: optic atrophy protein 3, shCTL: control shRNA, and shOPA3: shRNA against human OPA3.