The objectives of the present study are to explore role of pyruvate kinase isoenzyme type M2 (PKM2) in progression of Kazakh's esophageal squamous cell carcinoma (ESCC) in Xinjiang, China, and to clarify mechanism of PKM2 in malignant phenotype. PKM2 expression was examined using immunohistochemistry (IHC) in 101 matched pairs of ESCC and normal adjacent tissues (NATs) and using enzyme-linked immunosorbent assay (ELISA) in 35 serum samples of Kazakh's ESCC and 8 serum samples of healthy subjects. To investigate mechanism, small interfering RNA (siRNA)-PKM2 was transfected into ESCC cells. Cell migration and invasion were evaluated by wound healing and Transwell assays. Apoptosis and cell cycle were analyzed by flow cytometry (FCM). PKM2 expression was significantly higher in ESCC tissues (77.2 %, 78/101) compared with matched NAT (P = 0.003) and also higher in serum samples of Kazakh's ESCC patients (78.84 ng/mL) compared with healthy subjects (13.55 ng/mL) (P = 0.001). Patients with overexpression of PKM2 had a poor prognosis (P = 0.032). After knockdown of PKM2, cell proliferation, migration, and invasion were significantly reduced (P = 0.001), apoptosis increased (P = 0.001), and cell cycle was arrested at G1 phase. PKM2 overexpression was significantly correlated with the worse outcome of Kazakh's ESCC. Furthermore, PKM2 was involved in progression of ESCC by promoting proliferation and suppressing apoptosis, accelerating invasion, and influencing cell cycle. PKM2 could be a potential biomarker for molecular classification of ESCC.

译文

:本研究的目的是探讨M2型丙酮酸激酶同工酶(PKM2)在中国新疆哈萨克族食管鳞状细胞癌(ESCC)进展中的作用,并阐明PKM2在恶性表型中的作用机制。使用免疫组化(IHC)在101对匹配的ESCC和正常相邻组织(NAT)中检测PKM2的表达,并使用酶联免疫吸附测定(ELISA)在35个哈萨克人ESCC血清样品和8个健康受试者血清样品中检测PKM2的表达。为了研究机制,将小干扰RNA(siRNA)-PKM2转染到ESCC细胞中。通过伤口愈合和Transwell测定法评估细胞迁移和侵袭。通过流式细胞仪(FCM)分析细胞凋亡和细胞周期。与匹配的NAT(P = 0.003)相比,ESCC组织中的PKM2表达显着更高(77.2%,78/101),与健康受试者(13.55 ng / mL)相比,哈萨克斯坦ESCC患者的血清样品中的PKM2表达也更高(78.84 ng / mL)。 )(P = 0.001)。 PKM2过表达的患者预后较差(P = 0.032)。敲除PKM2后,细胞增殖,迁移和侵袭显着降低(P = 0.001),细胞凋亡增加(P = 0.001),细胞周期被阻滞在G1期。 PKM2的过表达与哈萨克斯坦ESCC的不良结局显着相关。此外,PKM2通过促进增殖和抑制凋亡,加速侵袭并影响细胞周期而参与ESCC的发展。 PKM2可能是ESCC分子分类的潜在生物标志物。

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