circ-ITCH suppresses prostate cancer cell proliferation, migration and invasion in-vitro through the miR-106b-5p/SETD2 axis.

Authors

Junbin Jiang, Jianwen Wei, Feicheng Chen, Yutong Li, Longhong Ba, Bin Pan

Published in

Pakistan journal of pharmaceutical sciences. Volume 39. Issue 11. Pages 3489-3499. Nov 01, 2026.

Abstract

Prostate cancer (PCa) is one of the leading causes of male morbidity and mortality due to malignant disease throughout the world. Recently, circRNAs have been considered as important regulators in tumorigenesis related networks. Nevertheless, the biological role and expression pattern of circRNA-ITCH (circ-ITCH) in prostate cancer are still not fully understood.
The purpose of the present study was to determine circ-ITCH expression in prostate cancer tissues and cell lines and analyze its potential regulatory effects on the proliferation, apoptosis, migration and invasion of prostate cells in-vitro.
The expression of circ-ITCH was detected in 6 pairs of PC tissues and adjacent normal tissues (n = 6) as well as PC cell lines by quantitative real-time PCR. The function of circ-ITCH was assessed by gain-of-function experiments. Cell proliferation and colony-forming efficiency were assessed using Cell Counting Kit-8 and plate cloning assays, respectively. The migratory and invasive abilities were examined via Wound Healing and Transwell assay and Annexin V-FITC/propidium iodide (PI) staining was used to assess apoptosis. Bioinformatic analysis in combination with dual-luciferase reporter analysis was performed to validate the regulatory relationships between circ-ITCH, miR-106b-5p and SETD2.
Relative to the corresponding control group, circ-ITCH expression was markedly decreased in prostate cancer tissues and cell lines. In-vitro, circ-ITCH overexpression inhibited cell proliferation and clonogenicity and increased the number of apoptotic cells in prostate cancer. Moreover, circ-ITCH overexpression reduced cell migration and invasion abilities. The luciferase reporter assays confirmed that circ-ITCH was the target of miR-106b-5p and miR-106b-5p targeted SETD2. circ-ITCH upregulation was correlated with elevated SETD2 expression, which is in line with a miR-106b-5p-dependent pattern of regulation.
These findings suggest that circ-ITCH can modulate malignant cell phenotypes (proliferation, apoptosis, migration and invasion) in PCa cells in-vitro through the miR-106b-5p/SETD2 axis. There are only a limited number of tissue samples and in-vitro experimental designs in our study and more experiments will be needed to further confirm these findings and reveal the biological significance.

PMID:
42633546
Bibliographic data and abstract were imported from PubMed on 23 Aug 2026.

Read full publication at:
Please sign in to see all details.

Stats

1-terrible, 9-excellent. How would you rate this publication? Sign in in to submit your rating.

Post a comment

You need to be signed in to post comments. You can sign in here.

Comments

There are no comments yet.