Pyruvate kinase M2 contributes to cell growth in gastric cancer via aerobic glycolysis
Pyruvate kinase M2 contributes to cell growth in gastric cancer via aerobic glycolysis
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丙酮酸激酶 M2 通过有氧糖酵解促进胃癌细胞生长
DOI：
10.1016/j.prp.2019.04.001
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发表时间：
2019-01-01
影响因子：
2.8
通讯作者：
Lu, Youyong
中科院分区：
文献类型：
--
作者：
Li, He;Xu, Huiyu;Lu, Youyong
丙酮酸激酶M2(PKM2)是促进有氧糖酵解的关键酶。本研究探讨PKM2在胃癌(GC)肿瘤生长和维持中的作用。组织学染色检测PKM2在胃癌组织中的表达。用聚合酶链式反应和免疫印迹法检测胃癌细胞中PKM2的表达。敲除PKM2以检测肿瘤的生物学行为、糖代谢和细胞凋亡。胃癌组织中PKM2表达上调(65%，34/52)，而癌旁正常组织中表达上调(27%，10/37)。此外，PKM2基因敲除抑制了BGC823 GC细胞的增殖，且PKM2水平升高与GC患者的生存不良有关。此外，PKM2的敲除通过诱导细胞凋亡改变了BGC823细胞的生物学行为。综上所述，本研究结果表明，抑制PKM2可能成为胃癌治疗的一种新策略。
Pyruvate kinase M2 (PKM2) serves as a key enzyme that promotes aerobic glycolysis. This study investigated the function of PKM2 in tumor growth and maintenance in gastric cancer (GC). Histological staining was applied to detect PKM2 expression in GC tissues. PCR and western blotting were used to measure PKM2 expression in GC cells. PKM2 was knocked down to examine the biological behavior of tumors, glycometabolism, and apoptosis. PKM2 was upregulated in GC tissues (65%, 34/52) compared with that in adjacent normal tissues (27%, 10/37). Moreover, PKM2 knockdown inhibited proliferation of BGC823 GC cells, and elevated PKM2 levels were associated with poor survival of GC patients. Furthermore, knockdown of PKM2 altered the biological behavior of BGC823 cells through induction of apoptosis. In conclusion, the results of this study indicated that inhibition of PKM2 could represent a novel strategy for gastric cancer treatment.