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. 2020 May 28;9(5):54. doi: 10.1038/s41389-020-0242-z

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© The Author(s) 2020

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 6 — a Overexpression of miR-122-5p blocks the promotion of PKM2 mRNA by SOX2OT. On the contrary, knockdown of mR-122 attenuated the inhibition of PKM2 by shRNA- SOX2OT. b The change of PKM2 protein level in HCCLM3 cells after overexpression and knockdown the expression of lncRNA-SOX2OT or miR-122-5p. c The rate of glycolysis in HCCLM3 cells was enhanced by SOX2OT overexpression and this enhancement could be blocked by overexpression of miR-122-5p. On the contrary, knockdown of mR-122 attenuated the inhibition of glycolysis rate by shRNA- SOX2OT. d The value of SUV max in lncRNA-SOX2OT overexpression orthotopic nude mice liver tumor was much higher than control group. Reciprocally, the increase of SUV max value was blocked by ectopic expression of miR-122-5p. e The promoting effect of lncRNA-SOX2OT on HCC cell invasion was antagonized by miR-122-5p overexpression. One the contrary, knockdown of miR-122-5p attenuated the inhibition effect of shRNA-lncRNA-SOX2OT. f The total number of lung metastatic lesions in the lncRNA-SOX2OT over-expression lung metastasis model was much more than that of control group. However, this increase can be blocked by overexpression of miR-122-5p.