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Breast cancer (BC) cell lines are useful experimental models to understand cancer biology. Yet, their relevance to modelling cancer remains unclear. To better understand the tumour-modelling efficacy of cell lines, we performed RNA-seq analyses on a combined dataset of 2D and 3D cultures of tumourigenic MCF7 and non-tumourigenic MCF10A. To our knowledge, this was the first RNA-seq dataset comprising of 2D and 3D cultures of MCF7 and MCF10A within the same experiment, which facilitates the elucidation of differences between MCF7 and MCF10A across culture types. We compared the genes and gene sets distinguishing MCF7 from MCF10A against separate RNA-seq analyses of clinical luminal A (LumA) and normal samples from the TCGA-BRCA dataset. Among the 1031 cancer-related genes distinguishing LumA from normal samples, only 5.1% and 15.7% of these genes also distinguished MCF7 from MCF10A in 2D and 3D cultures respectively, suggesting that different genes drive cancer-related differences in cell lines compared to clinical BC. Unlike LumA tumours which showed increased nuclear division-related gene expression compared to normal tissue, nuclear division-related gene expression in MCF7 was similar to MCF10A. Moreover, although LumA tumours had similar cell adhesion-related gene expression compared to normal tissues, MCF7 showed reduced cell adhesion-related gene expression compared to MCF10A. These findings suggest that MCF7 and MCF10A cell lines were limited in their ability to model cancer-related processes in clinical LumA tumours.

Hepatocellular carcinoma is the cancer with the highest incidence among liver cancers and how to treat this cancer effectively is still a difficult problem we must face. We selected meiotic nuclear divisions 1 (MND1) as the study object by combining data from The Cancer Genome Atlas (TCGA) database with prognostic survival analysis. We validated the value of MND1 in evaluating the prognosis of hepatocellular carcinoma through a diagnostic and prognostic model. At the same time, cellular experiments were used to demonstrate the effect of MND1 on hepatocellular carcinoma proliferation and migration. We used short hairpin RNA (shRNA) to knock down MND1 in Hun7 and HCCLM3 cell lines. Through 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) and colony formation assays, we found that knocking down MND1 reduced the proliferation of cells. Through wound healing and Transwell assays, we found that knocking down MND1 reduced cell migration and invasion. Moreover, we found that MND1 can promote the proliferation, migration, and invasion of Hep3B cells by overexpressing MND1. Therefore, in general, MND1 is expected to be a gene that can effectively diagnose and treat hepatocellular carcinoma.