ArticleMolecular medicine reports2021
Pleckstrin 2 is a potential drug target for colorectal carcinoma with activation of APC/β‑catenin.
Article in Molecular medicine reports, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 6 citations in OpenAlex.
- Colitis-Associated Colorectal Cancer-STAT3 Inhibition as a Preventive Strategy.International journal of molecular sciences · 2026Article
- Pleckstrin-2 promotes the progression of colorectal cancer via YTHDF2-mediated TYMS mRNA stability.Cellular and molecular life sciences : CMLS · 2025Article
- Engineering and targeting potential of CAR NK cells in colorectal cancer.Chinese medical journal · 2025Review
- Identification and Validation of a Hypoxia and Glycolysis Prognostic Signatures in Lung Adenocarcinoma.Journal of Cancer · 2024Article
- Let-7b-5p inhibits colon cancer progression by prohibiting APC ubiquitination degradation and the Wnt pathway by targeting NKD1.Cancer science · 2023Article
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Authors and funding
9 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The tumor suppressor gene adenomatous polyposis coli (APC) is frequently inactivated or absent in colorectal carcinoma (CRC). Loss‑of‑function of APC promotes the expression of β‑catenin, which is critical for CRC development. Since β‑catenin acts as an important transcription factor, blockage of β‑catenin may have side effects, including impairment of tissue homeostasis and regeneration, thus limiting the application of β‑catenin inhibitors for the treatment of patients with CRC. Therefore, identifying a novel substrate of APC/β‑catenin may provide essential clues to develop effective drugs. Small interfering RNA technology and lentivirus‑mediated overexpression were performed for knockdown and overexpression of pleckstrin 2 (PLEK2) in CRC cells. Cell Counting Kit‑8 and colony formation assays, and cell cycle analysis and cell apoptosis detection were used to detect the capacity of cell proliferation, cell cycle distribution and apoptosis. The present study demonstrated that the APC/β‑catenin signaling cascade transcriptionally activated PLEK2 in CRC cells. PLEK2 expression was markedly increased in CRC tissues. There was an inverse correlation between APC and PLEK2 expression in patients with CRC.
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