Open Access

The AMPK‑mTOR axis requires increased MALAT1 expression for promoting granulosa cell proliferation in endometriosis

Retraction in: /10.3892/etm.2024.12528

  • Authors:
    • Xuejie Liu
    • Ping Zhang
    • Yanmin Li
    • Na Zhao
    • Haiyan Han
  • View Affiliations

  • Published online on: November 6, 2020     https://doi.org/10.3892/etm.2020.9453
  • Article Number: 21
  • Copyright: © Liu et al. This is an open access article distributed under the terms of Creative Commons Attribution License.

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Abstract

Endometriosis is a common reproductive disorder in women, with a global prevalence of 10‑15%. Long noncoding RNAs (lncRNAs) are critical to gene transcription, cell cycle modulation and immune response. The lncRNA metastasis‑associated lung adenocarcinoma transcript 1 (MALAT1) reportedly mediates autophagy of endometrial stromal cells in endometriosis. The present study aimed to evaluate the role and mechanism of MALAT1 in granulosa cells (GCs) in endometriosis. Consequently, MALAT1 expression was upregulated in GCs obtained from patients with endometriosis and in the steroidogenic human granulosa‑like tumor cell line KGN. However, MALAT1 knockdown consequently decreased the proliferation and viability of these cells, as determined by MTT and 5‑ethynyl‑2'‑deoxyuridine staining assays. Both Annexin V‑fluorescein isothiocyanate/propidium iodide flow cytometry and western blotting performed to detect proapoptotic factors indicated that MALAT1 depletion might promote KGN cell apoptosis. Furthermore, MALAT1 knockdown increased GC autophagy, as evidenced by microtubule‑associated protein 1A/1B‑light chain 3 (LC3) cleavage upregulation and p62 degradation. In addition, although 5'-AMP‑activated protein kinase (AMPK) mRNA expression and protein levels decreased in GCs obtained from patients with endometriosis and KGN cells, MALAT1 knockdown restored AMPK levels. However, addition of BML‑275 (MALAT1 inhibitor) to MALAT1‑knockdown KGN cells recovered their viability and proliferative capacity and simultaneously reduced their apoptotic and autophagic capacity. Therefore, MALAT1 may regulate GC proliferation via AMPK‑mTOR‑mediated cell apoptosis and autophagy.
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January-2021
Volume 21 Issue 1

Print ISSN: 1792-0981
Online ISSN:1792-1015

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Spandidos Publications style
Liu X, Zhang P, Li Y, Zhao N and Han H: The AMPK‑mTOR axis requires increased MALAT1 expression for promoting granulosa cell proliferation in endometriosis Retraction in /10.3892/etm.2024.12528. Exp Ther Med 21: 21, 2021.
APA
Liu, X., Zhang, P., Li, Y., Zhao, N., & Han, H. (2021). The AMPK‑mTOR axis requires increased MALAT1 expression for promoting granulosa cell proliferation in endometriosis Retraction in /10.3892/etm.2024.12528. Experimental and Therapeutic Medicine, 21, 21. https://doi.org/10.3892/etm.2020.9453
MLA
Liu, X., Zhang, P., Li, Y., Zhao, N., Han, H."The AMPK‑mTOR axis requires increased MALAT1 expression for promoting granulosa cell proliferation in endometriosis Retraction in /10.3892/etm.2024.12528". Experimental and Therapeutic Medicine 21.1 (2021): 21.
Chicago
Liu, X., Zhang, P., Li, Y., Zhao, N., Han, H."The AMPK‑mTOR axis requires increased MALAT1 expression for promoting granulosa cell proliferation in endometriosis Retraction in /10.3892/etm.2024.12528". Experimental and Therapeutic Medicine 21, no. 1 (2021): 21. https://doi.org/10.3892/etm.2020.9453