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二甲双胍通过调控 miR-378a-3p/VEGFA/RGC-32 轴抑制胰腺癌的进展。

Metformin Inhibits the Progression of Pancreatic Cancer Through Regulating miR-378a-3p/VEGFA/RGC-32 Axis.

机构信息

Department of Gastroenterology, The First Affiliated Hospital, Jiangxi Medical College, Nanchang University, Nanchang, China.

Department of Medical Cosmetology, The Second Affiliated Hospital, Jiangxi Medical College, Nanchang University, Nanchang, China.

出版信息

Cancer Med. 2024 Dec;13(23):e70446. doi: 10.1002/cam4.70446.

DOI:10.1002/cam4.70446
PMID:39606802
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11602749/
Abstract

BACKGROUND

Pancreatic cancer (PC) is a major contributor to global cancer-related mortality. While the inhibitory effect of metformin (Met) on PC has been reported, the underlying mechanism remains elusive.

METHODS

We established BxPC-3 cell models with miR-378a-3p and VEGFA knockdown. The expression of miR-378a-3p, VEGFA, and RGC-32 in PC and normal tissues was analyzed using GEPIA, TCGA databases. Cell proliferation, invasion, migration, and apoptosis were assessed through CCK8, Transwell, wound healing, and flow cytometry.

RESULTS

Significantly lower expression of miR-378a-3p was observed in PC tissues and cells. Knockdown of miR-378a-3p reversed the impact of Met on cell viability in PANC-1 and BxPC3. VEGFA emerged as a potential regulator in PC and a downstream target of miR-378a-3p. The interaction between VEGFA and RGC-32 played a crucial role in PC regulation. Knockdown of VEGFA substantially reversed the impact of miR-378a-3p inhibitor on tumor growth and the epithelial-mesenchymal transition (EMT) process. Moreover, knockdown of VEGFA effectively countered the influence of miR-378a-3p inhibitor on cell viability and the EMT process in BxPC3 cells.

CONCLUSIONS

Met exerted inhibitory effects on PC through the miR-378a-3p/VEGFA/RGC-32 pathway. Strategies targeting the miR-378a-3p/VEGFA/RGC-32 axis represent a novel avenue for the prevention and treatment of PC.

摘要

背景

胰腺癌（PC）是导致全球癌症相关死亡率的主要原因之一。虽然已经报道了二甲双胍（Met）对 PC 的抑制作用，但潜在的机制仍不清楚。

方法

我们建立了 miR-378a-3p 和 VEGFA 敲低的 BxPC-3 细胞模型。使用 GEPIA 和 TCGA 数据库分析了 PC 和正常组织中 miR-378a-3p、VEGFA 和 RGC-32 的表达。通过 CCK8、Transwell、划痕愈合和流式细胞术评估细胞增殖、侵袭、迁移和凋亡。

结果

PC 组织和细胞中 miR-378a-3p 的表达明显降低。miR-378a-3p 的敲低逆转了 Met 对 PANC-1 和 BxPC3 细胞活力的影响。VEGFA 是 PC 的一个潜在调节剂，也是 miR-378a-3p 的下游靶标。VEGFA 和 RGC-32 之间的相互作用在 PC 调节中起着关键作用。VEGFA 的敲低显著逆转了 miR-378a-3p 抑制剂对肿瘤生长和上皮-间充质转化（EMT）过程的影响。此外，VEGFA 的敲低有效地抵消了 miR-378a-3p 抑制剂对 BxPC3 细胞活力和 EMT 过程的影响。

结论

Met 通过 miR-378a-3p/VEGFA/RGC-32 途径对 PC 发挥抑制作用。靶向 miR-378a-3p/VEGFA/RGC-32 轴的策略为 PC 的预防和治疗提供了一种新途径。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/396e/11602749/0dd0fe1ba439/CAM4-13-e70446-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/396e/11602749/5a438f8cae1d/CAM4-13-e70446-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/396e/11602749/62bc4bb6034b/CAM4-13-e70446-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/396e/11602749/5b820855d709/CAM4-13-e70446-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/396e/11602749/8b9e338741ce/CAM4-13-e70446-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/396e/11602749/cca7c9624335/CAM4-13-e70446-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/396e/11602749/0dd0fe1ba439/CAM4-13-e70446-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/396e/11602749/5a438f8cae1d/CAM4-13-e70446-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/396e/11602749/62bc4bb6034b/CAM4-13-e70446-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/396e/11602749/5b820855d709/CAM4-13-e70446-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/396e/11602749/8b9e338741ce/CAM4-13-e70446-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/396e/11602749/cca7c9624335/CAM4-13-e70446-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/396e/11602749/0dd0fe1ba439/CAM4-13-e70446-g001.jpg

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