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PCSK9 promotes tumor cell proliferation and migration by facilitating CCL25 secretion in esophageal squamous cell carcinoma

  • Authors:
    • Haijun Wang
    • Qiang Guo
    • Mingbo Wang
    • Changjiang Liu
    • Ziqiang Tian
  • View Affiliations / Copyright

    Affiliations: Department of Thoracic Surgery, The Fourth Hospital of Hebei Medical University, Shijiazhuang, Hebei 050010, P.R. China
    Copyright: © Wang et al. This is an open access article distributed under the terms of Creative Commons Attribution License.
  • Article Number: 500
    |
    Published online on: October 4, 2023
       https://doi.org/10.3892/ol.2023.14086
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Abstract

Proprotein convertase subtilisin/kexin type 9 (PCSK9) serves an important role in maintaining plasma cholesterol levels, and fatty acid metabolism is involved in the progression of various types of cancer. In the present study, the role of PCSK9 in the development of esophageal squamous cell carcinoma (ESCC) was investigated. PCSK9 expression was compared between ESCC and normal esophageal epithelial tissues using reverse transcription‑quantitative PCR. In addition, the association between PCSK9 expression and clinical staging and prognosis was assessed by immunohistochemistry. The effects of PCSK9 overexpression or knockdown on cell proliferation was evaluated using Cell Counting Kit‑8 and colony formation assays. The invasion and migration of cancer cells was assessed using wound healing and Transwell assays. Western blotting was performed to evaluate changes in the expression levels of epithelial‑mesenchymal transition (EMT)‑related proteins. ELISA was performed to detect the effects of PCSK9 on chemokine (C‑C motif) ligand 25 (CCL25) secretion. The results revealed that PCSK9 was highly expressed in ESCC tissues compared with that in normal esophageal tissues, and the high expression of PCSK9 was associated with a poor prognosis. Furthermore, PCSK9 could promote the proliferation, migration and invasion of ESCC cells in vitro. Mechanistically, PCSK9 could promote EMT by secreting CCL25. In conclusion, patients with ESCC may benefit from a novel therapeutic strategy based on these findings.
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Copy and paste a formatted citation
Spandidos Publications style
Wang H, Guo Q, Wang M, Liu C and Tian Z: PCSK9 promotes tumor cell proliferation and migration by facilitating CCL25 secretion in esophageal squamous cell carcinoma. Oncol Lett 26: 500, 2023.
APA
Wang, H., Guo, Q., Wang, M., Liu, C., & Tian, Z. (2023). PCSK9 promotes tumor cell proliferation and migration by facilitating CCL25 secretion in esophageal squamous cell carcinoma. Oncology Letters, 26, 500. https://doi.org/10.3892/ol.2023.14086
MLA
Wang, H., Guo, Q., Wang, M., Liu, C., Tian, Z."PCSK9 promotes tumor cell proliferation and migration by facilitating CCL25 secretion in esophageal squamous cell carcinoma". Oncology Letters 26.5 (2023): 500.
Chicago
Wang, H., Guo, Q., Wang, M., Liu, C., Tian, Z."PCSK9 promotes tumor cell proliferation and migration by facilitating CCL25 secretion in esophageal squamous cell carcinoma". Oncology Letters 26, no. 5 (2023): 500. https://doi.org/10.3892/ol.2023.14086
Copy and paste a formatted citation
x
Spandidos Publications style
Wang H, Guo Q, Wang M, Liu C and Tian Z: PCSK9 promotes tumor cell proliferation and migration by facilitating CCL25 secretion in esophageal squamous cell carcinoma. Oncol Lett 26: 500, 2023.
APA
Wang, H., Guo, Q., Wang, M., Liu, C., & Tian, Z. (2023). PCSK9 promotes tumor cell proliferation and migration by facilitating CCL25 secretion in esophageal squamous cell carcinoma. Oncology Letters, 26, 500. https://doi.org/10.3892/ol.2023.14086
MLA
Wang, H., Guo, Q., Wang, M., Liu, C., Tian, Z."PCSK9 promotes tumor cell proliferation and migration by facilitating CCL25 secretion in esophageal squamous cell carcinoma". Oncology Letters 26.5 (2023): 500.
Chicago
Wang, H., Guo, Q., Wang, M., Liu, C., Tian, Z."PCSK9 promotes tumor cell proliferation and migration by facilitating CCL25 secretion in esophageal squamous cell carcinoma". Oncology Letters 26, no. 5 (2023): 500. https://doi.org/10.3892/ol.2023.14086
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