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. 2024 Feb 23;25(1):2315651. doi: 10.1080/15384047.2024.2315651

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© 2024 The Author(s). Published with license by Taylor & Francis Group, LLC.

This is an Open Access article distributed under the terms of the Creative Commons Attribution-NonCommercial License (http://creativecommons.org/licenses/by-nc/4.0/), which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited. The terms on which this article has been published allow the posting of the Accepted Manuscript in a repository by the author(s) or with their consent.

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Figure 4. — miR-10b-5p facilitates the proliferation, migration, and invasion of PLC cells through SLC38A2 downregulation. (a) The target mRnas of miR-10b-5p. (b) Sequences of the predicted binding sites between miR-10b-5p and the 3′-UTR of SLC38A2 gene. (c) Boxplots of SLC38A2 expression in tissues. (d) Dual-luciferase reporter assay was conducted to identify direct interaction between miR-10b-5p and SLC38A2 mRNA. (E) RT-qPCR analysis of SLC38A2 expression in tissues. (f) RT-qPCR analysis of miR-10b-5p (left) and SLC38A2 (right) expression in HepG2 cells transfected with mimics NC, miR-10b-5p mimics, oe-NC, or oe-SLC38A2. (g) WB analysis of SLC38A2 protein levels in HepG2 cells. The band intensity was assessed (right). (h) CCK-8 assay of HepG2 cells. (i) Transwell migration assay of HepG2 cells. (j) Transwell invasion assay of HepG2 cells. (k) Flow cytometric analysis of apoptosis in HepG2 cells. *p < .05, ***p < .001; ns, no significant difference; #p < .05.