ArticleCancer management and research2020
KLHL22 Regulates the EMT and Proliferation in Colorectal Cancer Cells in Part via the Wnt/β-Catenin Signaling Pathway.
Article in Cancer management and research, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 16 citations in OpenAlex.
- Colorectal Cancer Cell's Weapon: RNF32 Engages SPP1Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Identification of key biomarkers associated with necroptosis and immune infiltration in hepatitis B virus-related acute-on-chronic liver failure.Scientific reports · 2025Article
- Mechanism of KLF4 Inhibition of epithelial-mesenchymal transition in gastric cancer cells.Open life sciences · 2025Article
- COLEC10 inhibits the stemness of hepatocellular carcinoma by suppressing the activity of β-catenin signaling.Cellular oncology (Dordrecht, Netherlands) · 2024Article
- Overexpression of KLHL22 correlates with poor prognosis in patients with triple-negative breast cancer.Translational cancer research · 2024Article
- Emerging role of ubiquitination/deubiquitination modification of PD-1/PD-L1 in cancer immunotherapy.Genes & diseases · 2023Review
- Kelch-like proteins in the gastrointestinal tumors.Acta pharmacologica Sinica · 2023Review
- The roles of KLHL family members in human cancers.American journal of cancer research · 2022Review
- The Wnt Signalling Pathway: A Tailored Target in Cancer.International journal of molecular sciences · 2020Review
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Authors and funding
6 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundColorectal cancer (CRC) is one of the most common aggressive malignancies. KLHL22 functions as a tumor suppressor, and previous findings have demonstrated that KLHL22 can regulate the development of breast cancer and CRC. However, few studies have investigated the role of KLHL22 in CRC cell epithelial-to-mesenchymal transition (EMT) and proliferation. The current study aimed to detect the role of KLHL22 in CRC cell proliferation and EMT and to elucidate the probable molecular mechanisms through which KLHL22 is involved with these processes. MATERIALS AND
methodsTranswell invasion, MTT, immunohistochemistry and Western blotting assays were performed to evaluate the migration, invasion and proliferation abilities of CRC cells, and the levels of active molecules involved in the Wnt/β-catenin signaling pathway were examined through Western blotting analysis. In addition, the in vivo function of KLHL22 was assessed using a tumor xenograft model.
resultsKLHL22 expression was weaker in CRC tissues than in nonmalignant tissues and could inhibit cell invasion, migration, and proliferation in vitro. Furthermore, the regulatory effects of KLHL22 on EMT were partially attributed to the Wnt/β-catenin signaling pathway. The in vivo results also showed that KLHL22 modulated CRC tumorigenesis.
conclusionKLHL22 can regulate the activity of GSK-3β to influence the level of PI3K, and this regulation promotes EMT inhibition partially through the Wnt/β-catenin signaling pathway.
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