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. 2023 Oct 17;16:203. doi: 10.1186/s13048-023-01266-3

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© The Author(s) 2023

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data.

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Fig. 5 — The verification of hub genes by qRT‒PCR. The identified ten hub genes were downregulated significantly in human granulosa cells from bPOI patients compared to control patients (n = 12 in each group, *p < 0.05, **p < 0.01, ***p < 0.001, ****p < 0.0001, Mann–Whitney U-test). bPOI: biochemical premature ovarian insufficiency; CON: control; UBE2C: ubiquitin conjugating enzyme E2 C; PBK: PDZ binding kinase; BUB1: BUB1 mitotic checkpoint serine/threonine kinase; CDC20: cell division cycle 20; CENPA: centromere protein A; NUSAP1: nucleolar and spindle associated protein 1; CCNB2: cyclin B2; TOP2A: DNA topoisomerase II alpha; AURKB: aurora kinase B; FOXM1: forkhead box M1