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. 2019 Nov 19;11(1):82–94. doi: 10.1111/1759-7714.13236

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© 2019 The Authors. Thoracic Cancer published by China Lung Oncology Group and John Wiley & Sons Australia, Ltd

This is an open access article under the terms of the http://creativecommons.org/licenses/by-nc/4.0/ License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited and is not used for commercial purposes.

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Knockdown of miR‐148a‐3p inverted functional effects from TUG1 deletion in ESCC in vitro. sh‐NC, sh‐TUG1, sh‐TUG1 + inhibitor‐NC, sh‐TUG1 + miR‐148a‐3p inhibitor was transfected into ESCC cells for subsequent experiment, separately. (a,b) QRT‐PCR was used to confirm the level of miR‐148a‐3p. (c,d) Cell viability was analyzed by MTT assay at stated times (0 hours, 24 hours, 48 hours, 72 hours) in EC9706 and OE19 cells. () Control, () sh‐NC, () sh‐TUG1, () sh‐TUG1 + inhibitor‐NC, and () sh‐TUG1 + miR‐148a‐3p inhibitor. (e) Flow cytometry was conducted to analyze cell apoptosis rate. (f,g) Cell migration and invasion were evaluated by transwell assay. (h,i) The EMT‐related protein levels of N‐cadherin, E‐cadherin, Vimentin, and Snail were explored by western blot. *P < 0.05.

Inline graphic — Knockdown of miR‐148a‐3p inverted functional effects from TUG1 deletion in ESCC in vitro. sh‐NC, sh‐TUG1, sh‐TUG1 + inhibitor‐NC, sh‐TUG1 + miR‐148a‐3p inhibitor was transfected into ESCC cells for subsequent experiment, separately. (a,b) QRT‐PCR was used to confirm the level of miR‐148a‐3p. (c,d) Cell viability was analyzed by MTT assay at stated times (0 hours, 24 hours, 48 hours, 72 hours) in EC9706 and OE19 cells. () Control, () sh‐NC, () sh‐TUG1, () sh‐TUG1 + inhibitor‐NC, and () sh‐TUG1 + miR‐148a‐3p inhibitor. (e) Flow cytometry was conducted to analyze cell apoptosis rate. (f,g) Cell migration and invasion were evaluated by transwell assay. (h,i) The EMT‐related protein levels of N‐cadherin, E‐cadherin, Vimentin, and Snail were explored by western blot. *P < 0.05.