AI Article Synopsis

  • - The study investigates the role of Octamer transcription factor 1 (OCT1) in breast cancer, particularly in estrogen receptor (ER)-positive cases, finding that high levels of OCT1 are linked to shorter disease-free survival.
  • - OCT1 knockdown reduces cell growth in MCF-7 breast cancer cells, while overexpression increases proliferation, indicating its significant influence on cancer cell behavior.
  • - The research identifies NCAPH as a new target gene of OCT1, and both OCT1 and NCAPH are associated with poor prognostic outcomes, suggesting they could serve as therapeutic targets for ER-positive breast cancer patients.

Article Abstract

Octamer transcription factor 1 (OCT1) is a transcriptional factor reported to be a poor prognostic factor in various cancers. However, the clinical value of OCT1 in breast cancer is not fully understood. In the present study, an immunohistochemical study of OCT1 protein was performed using estrogen receptor (ER)-positive breast cancer tissues from 108 patients. Positive OCT1 immunoreactivity (IR) was associated with the shorter disease-free survival (DFS) of patients ( = 0.019). Knockdown of OCT1 inhibited cell proliferation in MCF-7 breast cancer cells as well as its derivative long-term estrogen-deprived (LTED) cells. On the other hand, the overexpression of OCT1 promoted cell proliferation in MCF-7 cells. Using microarray analysis, we identified the non-structural maintenance of chromosomes condensin I complex subunit H (NCAPH) as a novel OCT1-taget gene in MCF-7 cells. Immunohistochemical analysis showed that IR was significantly positively associated with OCT1 IR ( < 0.001) and that positive IR was significantly related to the poor DFS rate of patients ( = 0.041). The knockdown of inhibited cell proliferation in MCF-7 and LTED cells. These results demonstrate that OCT1 and its target gene are poor prognostic factors and potential therapeutic targets for patients with ER-positive breast cancer.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8584020PMC
http://dx.doi.org/10.3390/ijms222111505DOI Listing

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