Baraniya Divyashri, Chitrala Kumaraswamy Naidu, Al-Hebshi Nezar Noor
Oral Microbiome Research Laboratory, Maurice H. Kornberg School of Dentistry, Temple University, Philadelphia, USA.
Fels Cancer Institute for Personalized Medicine, Lewis Katz School of Medicine, Temple University, Philadelphia, Pennsylvania, USA.
J Oral Microbiol. 2022 May 16;14(1):2073866. doi: 10.1080/20002297.2022.2073866. eCollection 2022.
We have recently demonstrated that health-associated oral bacteria , , and induce cytotoxicity in oral squamous cell carcinoma (OSCC) cell lines and downregulate CD36, a cancer-assocaited gene.
To explore the effect of these three species on global transcriptome of OSCC cell lines.
Gene expression of cell lines CAL27, SCC4 and SCC25 cocultured with the test species was assessed with Clariom-S Human microarray. was included as a pathogenic control. Data were analyzed using Ingenuity Pathway Analysis.
The results differed by species and cell line. Overall, the transcriptional changes by were predominantly anti-cancer including inhibition of HOTAIR regulatory pathway, JAK/Stat signaling, cyclins/cyclin-dependent kinases, and endothelin1 signaling. and resulted in a mix of pro- and anti-cancer responses including activation of acute phase response, pro-inflammatory interleukins signaling, TREM-1 signaling, and tumor microenvironment pathway; but downregulation of cell cycle by inhibition of cyclins and cyclin-dependent kinases. had a predominantly pro-cancer effect limited to SCC4, including upregulation of inflammatory pathways, phospholipases and PI3K signaling.
These findings provide a new insight into the role of commensal oral bacteria in OSCC. Animal studies are required to further explore them.
我们最近证明，与健康相关的口腔细菌、和可诱导口腔鳞状细胞癌（OSCC）细胞系产生细胞毒性，并下调一种癌症相关基因CD36。
探讨这三种细菌对OSCC细胞系整体转录组的影响。
使用Clariom-S人类微阵列评估与受试细菌共培养的CAL27、SCC4和SCC25细胞系的基因表达。将作为致病对照。使用Ingenuity通路分析对数据进行分析。
结果因细菌种类和细胞系而异。总体而言，引起的转录变化主要是抗癌作用，包括抑制HOTAIR调控通路、JAK/Stat信号传导、细胞周期蛋白/细胞周期蛋白依赖性激酶以及内皮素1信号传导。和导致了促癌和抗癌反应混合，包括急性期反应激活、促炎白细胞介素信号传导、TREM-1信号传导以及肿瘤微环境通路；但通过抑制细胞周期蛋白和细胞周期蛋白依赖性激酶来下调细胞周期。主要对SCC4产生促癌作用，包括炎症通路、磷脂酶和PI3K信号传导上调。
这些发现为共生口腔细菌在OSCC中的作用提供了新的见解。需要进行动物研究以进一步探索它们。
