Open Access

ARTICLE

Circ_0003855 involvement of esophageal cancer progression through miR-622/FLOT1

JINGJING TIAN^1,*, XIBAO HU², XINRONG ZHANG¹

1 Department of Gastroenterology, Tianjin Nankai Hospital, Tianjin, 300100, China
2 Department of Digestive Medicine, First Teaching Hospital of Tianjin University of Traditional Chinese Medicine, Tianjin, 300100, China

* Corresponding Author: JINGJING TIAN. Email:

(This article belongs to the Special Issue: Signaling Pathway Crosstalk in Malignant Tumors: Molecular Targets and Combinatorial Therapeutics)

Oncology Research 2024, 32(5), 925-931. https://doi.org/10.32604/or.2023.042447

Received 30 May 2023; Accepted 13 November 2023; Issue published 23 April 2024

Abstract

To confirm the relationship between Circ_0003855 and EC, we purchased the Human esophageal carcinoma cell line Eca109 and normal human esophageal epithelial cells HEEC, and the expression levels of Circ_0003855, miR-622, and FLOT1 were detected. The results show that Circ_0003855 and FLOT1 were highly expressed in Eca109 cells, while miR-622 was lowly expressed (p < 0.05). Subsequently, Circ_0003855 small interfering RNA (si-Circ_0003855) and its negative control (si-NC) were used to detect changes in cellular biological behaviors. We found that the activity of Eca109 cells was reduced after interfering with the expression of Circ_0003855, and miR-622 expression was elevated, while FLOT1 was decreased (p < 0.05). Additionally, si-Circ_0003855 and miR-622 inhibitor sequence (miR-622-inhibition) were co-transfected into cells with miR-622-inhibition alone, and untreated Eca109 cells were used as a control to detect the expression of FLOT1. Co-transfection of si-Circ_0003855 and miR-622-inhibition showed no significant difference in FLOT1 expression compared to the control cells (p > 0.05). Synthesizing the results of these experiments above, we believe that interfering with the expression of Circ_0003855 can inhibit the activity of EC cells, and its mechanism is related to miR-622 and FLOT1.

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Keywords

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