ArticleThe Kaohsiung journal of medical sciences2022
ASPM facilitates colorectal cancer cells migration and invasion by enhancing β-catenin expression and nuclear translocation.
Article in The Kaohsiung journal of medical sciences, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 18 citations in OpenAlex.
- A core stemness-associated module reveals PLK1, NUF2, KIF23, CDCA8, TOP2A, CENPF, AURKA, and ASPM as key genes in rectal cancer.European journal of medical research · 2025Article
- Microtubule Minus-End Binding Proteins in Cancer: Advances.Diagnostics (Basel, Switzerland) · 2025Review
- USP4-mediated CENPF deubiquitylation regulated tumor metastasis in colorectal cancer.Cell death & disease · 2025Article
- Microbial metabolite trimethylamine-N-oxide induces intestinal carcinogenesis through inhibiting farnesoid X receptor signaling.Cellular oncology (Dordrecht, Netherlands) · 2024Article
- Exhaustive identification of genome-wide binding events of transcriptional regulators.Nucleic acids research · 2024Article
- Identification of Hub Genes for Psoriasis and Cancer by Bioinformatic Analysis.BioMed research international · 2024Article
- Oncogenic ASPM Is a Regulatory Hub of Developmental and Stemness Signaling in Cancers.Cancer research · 2023Article
- ASPM promotes ATR-CHK1 activation and stabilizes stalled replication forks in response to replication stress.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- ASPM facilitates colorectal cancer cells migration and invasion by enhancing β-catenin expression and nuclear translocation.The Kaohsiung journal of medical sciences · 2022Article
- LSM12 facilitates the progression of colorectal cancer by activating the WNT/CTNNB1 signaling pathway.Oncology research · 2022Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
Increased abnormal spindle-like microcephaly (ASPM) expression has been linked to clinical stage and poor prognosis in cancers, but the molecular mechanisms by which ASPM promotes cell metastasis in colorectal cancer (CRC) has not been identified. This study showed that the abilities of cell migration, invasion, and epithelial-mesenchymal transition (EMT) were attenuated in ASPM-deficient CRC cell lines. Furthermore, we reported that attenuation of ASPM expression inhibited CRC cell metastasis in vivo. Additionally, the expression of ASPM was positively correlated with β-catenin level in CRC tissues. Mechanistically, ASPM can upregulate β-catenin transcription by stimulating the β-catenin promoter and enhancing the nuclear translocation of β-catenin in CRC cells, which leads to the activation of the Wnt/β-catenin pathway. Finally, we showed that ASPM effectively induced CRC cell migration and invasion in a β-catenin-dependent manner.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.