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. 2023 Jan 29;45(2):1073–1085. doi: 10.3390/cimb45020071

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© 2023 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 (https://creativecommons.org/licenses/by/4.0/).

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NEAT1v1 activates the AKT pathway through SOD2, thereby conferring sorafenib and lenvatinib resistance in liver cancer cells, which are concomitantly sensitized to capivasertib. This result suggests that NEAT1v1 switches the growth modality of liver cancer cells from MEK/ERK-dependent to AKT-dependent mode via SOD2. Consistently, NEAT1 or SOD2 knockdown results in MEK/ERK activation, thereby sensitizing liver cancer cells to sorafenib and lenvatinib and conferring capivasertib resistance. NEAT1v1 or SOD2 knockdown also exacerbates ER stress; however, AKT is suppressed in an ER stress-independent manner.