长链非编码RNA ABHD11-AS1促进胃癌细胞糖酵解以加速肿瘤进展
[Long non-coding RNA ABHD11-AS1 promotes glycolysis in gastric cancer cells to accelerate tumor progression].
作者信息
Feng W, Lai Y, Wang J, Xu P
机构信息
Songjiang Hospital Affiliated to Shanghai Jiaotong University School of Medicine (Preparatory Stage), Shanghai 201600, China.
出版信息
Nan Fang Yi Ke Da Xue Xue Bao. 2023 Sep 20;43(9):1485-1492. doi: 10.12122/j.issn.1673-4254.2023.09.05.
OBJECTIVE
To explore the role of long non-coding RNA ABHD11-AS1 in regulation of glycolysis in gastric cancer cells and its molecular mechanism.
METHODS
The null plasmid pcDNA-Vector and the overexpression plasmid pcDNA-ABHD11-AS1 were transfected into human gastric cancer cell lines MKN45 and MGC803 with low ABHD11-AS1 expression, and the changes in cell proliferation, colony formation, migration and invasion were examined using CCK-8 assay, colony formation assay and Transwell assay. Glucose uptake and lactate production of the cells were detected to assess the changes in glycolytic activity. The LncMAP database was used to identify potential transcription factors regulated by ABHD11-AS1, and the candidate transcription factor was determined by literature review, and the result was verified using Western blotting.
RESULTS
Transfection with pcDNA-ABHD11-AS1 significantly increased ABHD11-AS1 expression in MGC803 and MKN45 cells, which exhibited obviously accelerated cell proliferation (<0.05), increased colony formation rate and enhanced cell migration and invasion abilities (<0.01). ABHD11-AS1 overexpression obviously promoted glycolysis in MGC803 and MKN45 cells (<0.05). Analysis of the database suggested that ABHD11-AS1 may regulate the classical glycolysis-related gene - in gastric cancer cells. Western blotting demonstrated that the expression of c-Myc increased significantly after upregulating ABHD11-AS1 in gastric cancer cells.
CONCLUSION
ABHD11-AS1 promotes glycolysis in gastric cancer cells by upregulating c-Myc to accelerate gastric cancer progression.
目的
探讨长链非编码RNA ABHD11-AS1在胃癌细胞糖酵解调控中的作用及其分子机制。
方法
将空载质粒pcDNA-Vector和过表达质粒pcDNA-ABHD11-AS1转染至ABHD11-AS1表达较低的人胃癌细胞系MKN45和MGC803中，采用CCK-8法、集落形成试验和Transwell试验检测细胞增殖、集落形成、迁移和侵袭的变化。检测细胞的葡萄糖摄取和乳酸生成，以评估糖酵解活性的变化。利用LncMAP数据库鉴定受ABHD11-AS1调控的潜在转录因子，通过文献综述确定候选转录因子，并采用蛋白质免疫印迹法进行验证。
结果
pcDNA-ABHD11-AS1转染显著增加了MGC803和MKN45细胞中ABHD11-AS1的表达，细胞增殖明显加快（<0.05），集落形成率增加，细胞迁移和侵袭能力增强（<0.01）。ABHD11-AS1过表达明显促进了MGC803和MKN45细胞的糖酵解（<0.05）。数据库分析表明，ABHD11-AS1可能调控胃癌细胞中经典的糖酵解相关基因。蛋白质免疫印迹法表明，上调胃癌细胞中ABHD11-AS1后，c-Myc的表达显著增加。
结论
ABHD11-AS1通过上调c-Myc促进胃癌细胞的糖酵解，从而加速胃癌进展。
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