MIST1 regulates SNAI1 and acts through the PTEN/AKT signaling axis to promote anoikis resistance in human melanoma cells Corrigendum in /10.3892/etm.2020.9481

Lee,Yiju; Yao,Weifeng; Yang,Chunjun; Li,Yunrui; Ni,Haiyang; Wang,Lei; Ji,Bin; Gu,Yongge; Yang,Sen

doi:10.3892/etm.2018.6225

MIST1 regulates SNAI1 and acts through the PTEN/AKT signaling axis to promote anoikis resistance in human melanoma cells

Corrigendum in: /10.3892/etm.2020.9481

Authors:
- Yiju Lee
- Weifeng Yao
- Chunjun Yang
- Yunrui Li
- Haiyang Ni
- Lei Wang
- Bin Ji
- Yongge Gu
- Sen Yang
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Affiliations: Department of Dermatology, The First Affiliated Hospital of Anhui Medical University, Hefei, Anhui 230022, P.R. China, Department of Dermatology, Tianjin Academy of Traditional Chinese Medicine Affiliated Hospital, Tianjin 300120, P.R. China, School of Basic Medicine, Tianjin Medical University, Tianjin 300070, P.R. China
Published online on: May 29, 2018 https://doi.org/10.3892/etm.2018.6225
Pages: 695-703
Copyright: © Lee et al. This is an open access article distributed under the terms of Creative Commons Attribution License.

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Abstract

Cutaneous malignant melanoma (CMM) is one of the most dangerous types of skin cancer. The prognosis of CMM patients with ulcers, regional lymph node metastasis or organ metastasis is poor. In this process, resistance to anoikis is a critical step in tumor cell metastasis. Tumor cells survive in the vascular and lymphatic system through the escape of anoikis to finally form clones in the distal tissue. The present study revealed that muscle intestine and stomach expression 1 (MIST1), a secreting cell‑restricted transcription factor, was overexpressed in melanoma cells. At the same time, the expression of SNAI1 was also high. High expression of MIST1 and SNAI1 all contributed to melanoma cells bypassing anoikis. By changing the expression of MIST1, SNAI1 was indicated to be a downstream gene of MIST1. Chromatin immunoprecipitation and luciferase reporter gene technology revealed that MIST1 promoted the expression of SNAI1 by directly binding to its promoter region. Furthermore, inhibition of the phosphorylation/activity of Akt by LY294002 and knockdown of phosphatase and tensin homologue (PTEN) with simultaneous upregulation or knockdown of MIST1 revealed that SNAI1 improved the phosphorylation of Akt by inhibiting the expression of PTEN. These results suggested that MIST1 hijacked the PTEN/AKT signaling pathway through directly regulating SNAI1 and affected the anoikis resistance capacity of melanoma cells.

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