ANKHD1 contributes to the malignant phenotype of triple‐negative breast cancer cells

Ankyrin repeat and KH domain‐containing protein 1, ANKHD1, has been identified as a regulator of signaling pathways and cellular processes of relevance in carcinogenesis. However, the role of ANKHD1 in breast cancer remains unclear. The aim of the present study was to characterize the expression pat...

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Published inCell biology international Vol. 46; no. 9; pp. 1433 - 1446
Main Authors Almeida, Bruna O., Almeida, Larissa C., Costa‐Lotufo, Leticia V., Machado‐Neto, João A.
Format Journal Article
LanguageEnglish
Published London Wiley Subscription Services, Inc 01.09.2022
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Summary:Ankyrin repeat and KH domain‐containing protein 1, ANKHD1, has been identified as a regulator of signaling pathways and cellular processes of relevance in carcinogenesis. However, the role of ANKHD1 in breast cancer remains unclear. The aim of the present study was to characterize the expression pattern and involvement of ANKHD1 in the malignant phenotype of breast cancer cell lines and to investigate the clinical relevance of ANKHD1 in a breast cancer context. Gene and protein expressions were assessed in the cell lines by quantitative reverse transcription PCR and Western blot analysis, respectively, and ANKHD1 silencing through siRNA transfection was conducted for further in vitro functional assays. The expression of ANKHD1 was identified in non‐tumorigenic breast epithelium and breast cancer cell lines, but differences in cellular localization were found among the neoplasia subtypes. ANKHD1 silencing reduced the viability, clonogenicity, and migration of triple‐negative breast cancer (TNBC) cells. Bioinformatics analyses demonstrated that patients with triple‐negative basal‐like 2 and mesenchymal breast cancer subtypes had high ANKHD1 expression associated with poor recurrence‐free survival. Therefore, these data indicate that ANKHD1 relevance in breast cancer varies among its subtypes, indicating the importance of ANKHD1 in TNBC.
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ISSN:1065-6995
1095-8355
DOI:10.1002/cbin.11844