Mechanism of monocarboxylate transporter 1 promoting migration and invasion in pancreatic ductal adenocarcinoma

张　敏; 王琳娜; 孙　超

doi:10.19401/j.cnki.1007-3639.2019.03.005

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Mechanism of monocarboxylate transporter 1 promoting migration and invasion in pancreatic ductal adenocarcinoma

更新时间：2026-01-27

- Mechanism of monocarboxylate transporter 1 promoting migration and invasion in pancreatic ductal adenocarcinoma
- China Oncology Vol. 29, Issue 3, Pages: 183-192(2019)
- 作者机构：
  
  1. 济南市人民医院检验科,山东,济南,271100
  2. 山东省青岛疗养院检验科,山东,青岛,266071
  3. 青岛市市立医院高压氧科,山东,青岛,266071
- 作者简介：
- 基金信息：
- DOI：10.19401/j.cnki.1007-3639.2019.03.005
  CLC： R735.9
- Published Online：26 April 2019，
  
  Published：26 April 2019
- 稿件说明：
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张　敏，王琳娜，孙　超. 单羧酸转运蛋白1促进胰腺导管癌细胞浸润转移的机制研究[J]. 中国癌症杂志, 2019, 29(3): 183-192.

张　敏, 王琳娜, 孙　超. Mechanism of monocarboxylate transporter 1 promoting migration and invasion in pancreatic ductal adenocarcinoma[J]. China Oncology, 2019, 29(3): 183-192.
张　敏，王琳娜，孙　超. 单羧酸转运蛋白1促进胰腺导管癌细胞浸润转移的机制研究[J]. 中国癌症杂志, 2019, 29(3): 183-192. DOI： 10.19401/j.cnki.1007-3639.2019.03.005.

张　敏, 王琳娜, 孙　超. Mechanism of monocarboxylate transporter 1 promoting migration and invasion in pancreatic ductal adenocarcinoma[J]. China Oncology, 2019, 29(3): 183-192. DOI： 10.19401/j.cnki.1007-3639.2019.03.005.

摘要

背景与目的：单羧酸转运蛋白1（monocarboxylate transporter 1，MCT1）是细胞转运乳酸、丙酮酸等代谢产物及能量物质的一种重要蛋白质，其在胰腺导管癌中的作用及机制鲜有研究报道。该研究旨在探讨MCT1在胰腺导管癌中的表达及临床病理学意义。方法：纳入78例胰腺导管癌患者的癌组织及癌旁正常组织，运用免疫组织化学技术检测MCT1在癌组织和癌旁正常组织中的表达水平并分析其临床病理学意义。在体外细胞系水平上，我们运用胰腺癌细胞系PANC-1和Capan-1，运用细胞克隆形成实验、细胞划痕和Transwell实验分析沉默MCT1后胰腺癌细胞增殖、迁移和浸润的改变。为明确MCT1的相关作用机制，我们通过生物信息学分析，预测miR-124-3p是MCT1的潜在调控微小RNA；为了进一步验证，我们运用双荧光素酶报告实验分析miR-124-3p对MCT1的调控效果；运用实时荧光定量聚合酶链反应（real-time fluorescence quantitative polymerase chain reaction，RTFQ-PCR）分别检测51对新鲜胰腺癌组织中MCT1和miR-124-3p的基因表达并分析两者的相关性。结果：MCT1的阳性表达主要位于细胞膜和细胞质。相比癌旁正常组织，MCT1在胰腺导管癌组织中显著高表达，其表达水平与胰腺导管癌的分化程度、临床分期、淋巴结转移和不良预后具有显著相关性。在体外细胞系水平上，沉默MCT1能够显著抑制胰腺癌细胞系PANC-1和Capan-1的增殖、迁移和浸润；miR-124-3p在胰腺癌组织中显著低表达，并且与MCT1 mRNA的表达具有显著负相关性，能够负调控MCT1的蛋白表达。结论：MCT1是胰腺导管腺癌的致癌基因，miR-124-3p能够负调控MCT1的表达。

Abstract

Background and purpose: Monocarboxylate transporter 1 (MCT1) is commonly seen to be significantly overexpressed in cancer tissues that takes charge of transporting the lactate

pyruvate and their derivatives belonging to monocarboxylate in cells. However

the role of MCT1 in pancreatic ductal adenocarcinoma has rarely been described. This study aimed to investigate the expression of MCT1 and its clinicopathological significance. Methods: The tumor tissues from 78 cases of pancreatic ductal adenocarcinoma and the paired normal control tissues were collected. Immunohistochemistry was performed to detect and analyze the expression of MCT1 and its clinicopathological significance. In vitro

pancreatic ductal adenocarcinoma cell lines PANC-1 and Capan-1 were used to analyze the biological role of MCT1 in the proliferation

migration and invasion of cancer cells using clonogenic

wound-healing and Transwell assays. To explore the relevant mechanism by which MCT1 functions in pancreatic cancer cells

miR-124-3p was predicted to be a putative regulatory miRNA. To further confirm the potential regulation

luciferase reporter assay was used. Moreover

both mRNA of MCT1 and miR-124-3p were detected using real-time fluorescence quantitative polymerase chain reaction (RTFQ-PCR) in additional 51 paired cases of pancreatic ductal adenocarcinoma and their normal controls. Results: The positive expression of MCT1 was mainly located in the cell membrane and cytoplasm and remarkably up-regulated in pancreatic ductal adenocarcinoma tissues compared with paired normal control tissues. Over-expressed MCT1 significantly correlated with differentiation

clinical stage

lymph node metastasis and poor overall prognosis. In vitro

silencing of MCT1 was shown to be able to markedly suppress the proliferation

migration and invasion of PANC-1 and Capan-1 cells. miR-124-3p was identified to be able to negatively regulate MCT1 expression. Conclusion: MCT1 is an oncogene in pancreatic ductal adenocarcinoma

and miR-124-3p can negatively modulate the expression of MCT1 in pancreatic ductal adenocarcinoma.

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