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Exosome-mediated lnc-ABCA12-3 promotes proliferation and glycolysis but inhibits apoptosis by regulating the toll-like receptor 4/nuclear factor kappa-B signaling pathway in esophageal squamous cell carcinoma

  • Junliang Ma (Department of Thoracic Surgery, Affiliated Hospital of Zunyi Medical University) ;
  • Yijun Luo (Department of Thoracic Surgery, Affiliated Hospital of Zunyi Medical University) ;
  • Yingjie Liu (Department of Cardiovascular Surgery, Affiliated Hospital of Zuinyi Medical University) ;
  • Cheng Chen (Department of Thoracic Surgery, Affiliated Hospital of Zunyi Medical University) ;
  • Anping Chen (Department of Thoracic Surgery, Affiliated Hospital of Zunyi Medical University) ;
  • Lubiao Liang (Department of Thoracic Surgery, Affiliated Hospital of Zunyi Medical University) ;
  • Wenxiang Wang (The Second Department of Thoracic Surgery, Hunan Cancer Hospital and The Affiliated Cancer Hospital of Xiangya School of Medicine, Central South University) ;
  • Yongxiang Song (Department of Thoracic Surgery, Affiliated Hospital of Zunyi Medical University)
  • Received : 2022.08.16
  • Accepted : 2022.11.03
  • Published : 2023.01.01

Abstract

Esophageal squamous cell carcinoma (ESCC) is a kind of malignant tumor with high incidence and mortality in the digestive system. The aim of this study is to explore the function of lnc-ABCA12-3 in the development of ESCC and its unique mechanisms. RT-PCR was applied to detect gene transcription levels in tissues or cell lines like TE-1, EC9706, and HEEC cells. Western blot was conducted to identify protein expression levels of mitochondrial apoptosis and toll-like receptor 4 (TLR4)/nuclear factor kappa-B (NF-κB) signaling pathway. CCK-8 and EdU assays were carried out to measure cell proliferation, and cell apoptosis was examined by flow cytometry. ELISA was used for checking the changes in glycolysis-related indicators. Lnc-ABCA12-3 was highly expressed in ESCC tissues and cells, which preferred it to be a candidate target. The TE-1 and EC9706 cells proliferation and glycolysis were obviously inhibited with the downregulation of lnc-ABCA12-3, while apoptosis was promoted. TLR4 activator could largely reverse the apoptosis acceleration and relieved the proliferation and glycolysis suppression caused by lnc-ABCA12-3 downregulation. Moreover, the effect of lnc-ABCA12-3 on ESCC cells was actualized by activating the TLR4/NF-κB signaling pathway under the mediation of exosome. Taken together, the lnc-ABCA12-3 could promote the proliferation and glycolysis of ESCC, while repressing its apoptosis probably by regulating the TLR4/NF-κB signaling pathway under the mediation of exosome.

Keywords

Acknowledgement

This work is supported by The Science and Technology Foundation of Guizhou Province (Qian Ke He J-ZK [2021] General 465), Doctor start-up Fund of Zunyi Medical University (Yuan Zi [2020] No. 08), Health Commission of Guizhou Province (gzwjkj2020-1-108).

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