LncRNA MYLK antisense RNA 1 activates cell division cycle 42/Neutal Wiskott‐Aldrich syndrome protein pathway via microRNA‐101‐5p to accelerate epithelial‐to‐mesenchymal transition of colon cancer cells

Autor: Zhen‐Hao Quan, Fei‐Peng Xu, Zhe Huang, Ri‐Hong Chen, Qing‐Wen Xu, Lin Lin
Jazyk: angličtina
Rok vydání: 2024
Předmět:
Zdroj: Kaohsiung Journal of Medical Sciences, Vol 40, Iss 1, Pp 11-22 (2024)
Druh dokumentu: article
ISSN: 2410-8650
1607-551X
DOI: 10.1002/kjm2.12773
Popis: Abstract Long noncoding RNA MYLK antisense RNA 1 (MYLK‐AS1) is the crux in multiple diseases. Therefore, the purpose of this study was to investigate the possible mechanism of MYLK‐AS1. A total of 62 colon cancer (CC) specimens and paired adjacent normal tissues were collected, and the expression of MYLK‐AS1, microRNA (miR)‐101‐5p/cell division cycle 42 (CDC42) was detected. CC cell lines were transfected with MYLK‐AS1, miR‐101‐5p, CDC42‐related plasmids, and the biological functions and markers of epithelial‐mesenchymal transition (EMT) were analyzed. The binding relationship between MYLK‐AS1, miR‐101‐5p, and CDC42 was evaluated. In CC tissues and cell lines, MYLK‐AS1 and CDC42 were highly expressed, and miR‐101‐5p was lowly expressed. Inhibition of MYLK‐AS1 or upregulation of miR‐101‐5p can inhibit CC cell growth and EMT. miR‐101‐5p inhibited CDC42/N‐wasp axis activation in CC cells by targeting CDC42. Knockdown of CDC42 or upregulation of miR‐101‐5p partially reversed the effects caused by upregulation of MYLK‐AS1. MYLK‐AS1, which is significantly upregulated in CC, may be a molecular sponge for miR‐101‐5p, and MYLK‐AS1 promotes the activation of the CDC42/N‐wasp axis in CC cells by targeting CDC42 through miR‐101‐5p, which in turn promotes tumor development. MYLK‐AS1 may be a potential biomarker and target for CC therapy.
Databáze: Directory of Open Access Journals
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