Gene expression profile analysis of ENO1 knockdown in gastric cancer cell line MGC‑803

Abstract

Gastric cancer (GC) is the third leading cause of cancer-associated mortality. In a previous study, we identified that α-enolase (ENO1) promoted cell migration in GC, but the underlying molecular mechanisms remain to be fully elucidated. In the present study, small interfering RNAs were identified to interfere with ENO1 expression. The cDNA expression profiling was performed using an Affymetrix mRNA array platform to identify genes that may be associated with ENO1 in human GC cell line MGC-803. The differentially expressed genes (DEGs) were identified using the reverse transcription-quantitative polymerase chain reaction, followed by a series of bioinformatic analyses. As a result, there were 448 DEGs, among which 183 (40.85%) were downregulated. The most significant functional terms for the DEGs were the nuclear lumen for cell components (P=2.83×10−4), transcription for biological processes (P=3.7×10−7) and transcription factor activity for molecular functions (P=1.16×104). In total, six significant pathways were enriched, including the most common cancer-associated forkhead box O signaling pathway (P=0.0077), microRNAs in cancer (P=0.0183) and the cAMP signaling pathway (P=0.0415). Furthermore, a network analysis identified three hub genes (HUWE1, PPP1CB and HSPA4), which were all involved in tumor metastasis. Taken together, the DEGs, significant pathways and hub genes identified in the present study shed some light on the molecular mechanisms of ENO1 involved in the pathogenesis of GC.

Cyclin-Dependent Kinase 1 (CDK1) is Co-Expressed with CDCA5: Their Functions in Gastric Cancer Cell Line MGC-803

“…Human GC cell line MGC-803 [ 20 ] was obtained from the Cell Bank of Sun Yat-Sen University (Guangzhou, China) and cultured in RPMI-1640 medium (Gibco BRL, Grand Island, NY, USA) supplement with 10% fetal bovine serum (FBS, Gibco BRL, Grand Island, NY, USA). The cells were incubated at 37°C with 5% CO 2 .…”

Alpha-Enolase: Emerging Tumor-Associated Antigen, Cancer Biomarker, and Oncotherapeutic Target

“…These functions can be inhibited in cancer cells by ENO1 depletion ( Georges et al, 2011 ; Song et al, 2014 ; Fu et al, 2015 ; Zhu et al, 2015 ; Capello et al, 2016 ; Principe et al, 2017 ; Qian et al, 2017 ; Zhan et al, 2017 ; Qiao et al, 2018a , 2019 ; Ji et al, 2019 ; Sun et al, 2019 ; Wang et al, 2019 ; Xu et al, 2019 ; Santana-Rivera et al, 2020 ), or targeting with antibodies ( Hsiao et al, 2013 ; Principe et al, 2015 ), microRNA (miR) ( Liu et al, 2018 ), or long non-coding RNAs (lncRNAs) ( Yu et al, 2018 ). ENO1 also regulates oncogenic signaling pathways, including PI3K/Akt ( Fu et al, 2015 ; Sun et al, 2019 ; Chen et al, 2020 ; Zang et al, 2020 ), v/β-3 integrin ( Principe et al, 2017 ), β-catenin ( Ji et al, 2019 ), transforming growth factor beta ( Xu et al, 2019 ), AMPK/mTOR ( Zhan et al, 2017 ; Dai et al, 2018 ), and others ( Huang et al, 2019 ).…”

α-Enolase Lies Downstream of mTOR/HIF1α and Promotes Thyroid Carcinoma Progression by Regulating CST1

“…Ectopic ENO1 overexpression promoted tumor formation and tumor chemoresistance (Tu et al, 2010;Song et al, 2014;Fu et al, 2015;Principe et al, 2017;Qian et al, 2017;Zhan et al, 2017;Sun et al, 2019;Chen et al, 2020). Conversely, ENO1 silencing in tumor cells significantly decreased malignant biological behavior (Fu et al, 2015;Principe et al, 2015;Zhao et al, 2015;Capello et al, 2016;Cappello et al, 2017;Huang et al, 2019). Several lines of evidence suggest that ENO1 may be a therapeutic target for endometrial carcinoma (Principe et al, 2015;Zhao et al, 2015;Yin et al, 2018).…”