Abstract:Objective: To explore the effect of miR-30a-5p on apoptosis and glycolysis in gastric cancer (GC) cells by targeting up-regulated gene 4 (URGCP), and to elucidate its potential regulatory mechanisms. Methods: Quantificational real-time polymerase chain reaction (RT-PCR) was used to detect the expression of miR-30a-5p and URGCP in normal gastric epithelial cells (GES-1) and GC cells (AGS, HGC-27 and SGC-7901). HGC-27 cells were used in subsequent experiments and cells were randomly divided into six groups, namely, control group, miR-NC group (transfected with miR-NC), miR-30a-5p mimic group (transfected with miR-30a-5p mimic), pcDNA-NC group (transfected with pcDNA-NC), pcDNA-URGCP group (transfected with pcDNA-URGCP), and pcDNA-URGCP+miR-30a-5p mimic group (transfected with pcDNA-URGCP and miR-30a-5p mimic). CCK-8 assay was used to detect the proliferation activity. Flow cytometry was used to detect the apoptosis. ATP and lactate detection kit were used to detect the production of ATP and lactate. In addition, the luciferase reporter assay was used to verify the targeting relationship between miR-30a-5p and URGCP. Results: Compared with normal gastric epithelial cells (GES-1), the expression of miR-30a-5p in GC cells (AGS, HGC-27 and SGC-7901) was decreased significantly (P<0.01), while the expression of URGCP showed the opposite trend. Then, compared with miR-NC group, the proliferation ability of GC cells in miR-30a-5p mimic group was decreased (P<0.01), the level of apoptosis was increased (P<0.01), and the production of ATP and lactate was decreased (P<0.01). Additionally, miR-30a-5p could directly target URGCP, and there is a negative correlation between the expression of miR-30a-5p and URGCP. Finally, compared with pcDNA-NC group, the proliferation ability of GC cells in pcDNA-URGCP group was increased (P<0.01), the level of apoptosis was decreased (P<0.01), and the production of ATP and lactate was increased (P<0.01). However, these activity changes could be reversed by miR-30a-5p overexpression. Conclusion: MiR-30a-5p inhibited the growth and glycolysis in GC cells by targeting URGCP, indicating that miR-30a-5p/URGCP axis may be a new target for the treatment of GC in the future.
杨勐. miR-30a-5p靶向URGCP调控胃癌细胞凋亡和糖酵解的机制研究[J]. 河北医学, 2022, 28(6): 887-891.
YANG Meng. MiR-30a-5p Regulates Apoptosis and Glycolysis in Gastric Cancer Cells via Targeting URGCP. HeBei Med, 2022, 28(6): 887-891.
[1] Bray F,Ferlay J,Soerjomataram I,et al.Global cancer statistics 2018:GLOBOCAN estimates of incidence and mortality worldwide for 36 cancers in 185 countries[J].Cancer Journal for Clinicians,2018,68(6):394-424. [2] Zhou Q,Wang X,Yu Z,et al.Transducin (β)-like 1 X-linked receptor 1 promotes gastric cancer progression via the ERK1/2 pathway[J].Oncogene,2017,36(13):1873-1886. [3] Mo YY.MicroRNA regulatory networks and human disease[J].Cellular and Molecular Life Sciences,2012,69(21):3529-3531. [4] Mousa H,Yuan M,Zhang X,et al.MicroRNA-4316 inhibits gastric cancer proliferation and migration via directly targeting VEGF-A[J].Cancer Cell International,2020,20(1):1-12. [5] Wang Z,Yao L,Li Y,et al.miR-337-3p inhibits gastric tumor metastasis by targeting ARHGAP10[J].Molecular Medicine Reports,2020,21(2):705-719. [6] Yao W,Guo P,Mu Q,et al.Exosome-derived Circ-PVT1 contributes to cisplatin resistance by regulating autophagy,invasion,and apoptosis via miR-30a-5p/YAP1 axis in gastric cancer cells[J].Cancer Biotherapy & Radiopharmaceuticals,2021,36(4):347-359. [7] Cai J,Li R,Xu X,et al.URGCP promotes non-small cell lung cancer invasiveness by activating the NF-κB-MMP-9 pathway[J].Oncotarget,2015,6(34):36489. [8] Zhu J,Zeng Y,Xu C,et al.Expression profile analysis of microRNAs and downregulated miR-486-5p and miR-30a-5p in non-small cell lung cancer[J].Oncology reports,2015,34(4):1779-1786. [9] Wang K,Jia Z,Zou J,et al.Analysis of hsa-miR-30a-5p expression in human gliomas[J].Pathology & Oncology Research,2013,19(3):405-411. [10] Jia Z,Wang K,Wang G,et al.MiR-30a-5p antisense oligonucleotide suppresses glioma cell growth by targeting SEPT7[J].PloS One,2013,8(1):e55008.