Enterococcus faecalis (E. faecalis) is an important commensal microbiota member of the human gastrointestinal tract. It has been shown in many studies that infection rates with E. faecalis in gastric cancer significantly increase. It has been scientifically proven that some infections develop during the progression of cancer, but it is still unclear whether this infection factor is beneficial (reduction in metastasis) or harmful (increase in proliferation, invasion, stem cell-like phenotype) of the host. These opposed data can significantly contribute to the understanding of cancer progress when analyzed in detail. The gene expression data were retrieved from Array Express (E-MEXP-3496). Variance, t test and linear regression analysis, hierarchical clustering, network, and pathway analysis were performed. In this study, we identified altered genes involved in E. faecalis infection in the gastric cell line MKN74 and the relevant pathways to understand whether the infection slows down cancer progression. Twelve genes corresponding 15 probe sets were downregulated following the live infection of gastric cancer cells with E. faecalis. We identified a network between these genes and pathways they belong to. Pathway analysis showed that these genes are mostly associated with cancer cell proliferation. NDC80, NCAPG, CENPA, KIF23, BUB1B, BUB1, CASC5, KIF2C, CENPF, SPC25, SMC4, and KIF20A genes were found to be associated with gastric cancer pathogenesis. Almost all of these genes are effective in the proliferation of cancer cells, especially during the infection process. Therefore, it is hypothesized that downregulation of these genes may affect gastric cancer pathogenesis by reducing cell proliferation. And, it is predicted that E. faecalis infection may be an important factor for gastric cancer.

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评估粪肠球菌感染对胃癌细胞系MKN74的遗传影响

粪肠球菌（E. faecalis）是人类胃肠道的重要共生菌群成员。在许多研究中已经表明，粪肠球菌在胃癌中的感染率显着提高。科学地证明，某些感染是在癌症发展过程中发展的，但仍不清楚该感染因子对宿主是有益的（减少转移）还是有害的（增加增殖，侵袭，干细胞样表型）。当进行详细分析时，这些相反的数据可以极大地有助于理解癌症的进展。从Array Express（E-MEXP-3496）检索基因表达数据。进行了方差，t检验和线性回归分析，层次聚类，网络和路径分析。在这个研究中，我们在胃细胞系MKN74中鉴定了与粪肠球菌感染有关的已改变基因，并了解了相关途径以了解感染是否减慢了癌症的进展。粪肠球菌感染胃癌细胞后，对应于15个探针组的12个基因被下调。我们在这些基因和它们所属的途径之间确定了一个网络。途径分析表明，这些基因主要与癌细胞增殖有关。发现NDC80，NCAPG，CENPA，KIF23，BUB1B，BUB1，CASC5，KIF2C，CENPF，SPC25，SMC4和KIF20A基因与胃癌的发病机制有关。这些基因几乎都对癌细胞的增殖有效，尤其是在感染过程中。因此，据推测，这些基因的下调可能通过减少细胞增殖而影响胃癌的发病机理。并且，预计粪肠球菌感染可能是胃癌的重要因素。