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跨膜内质网蛋白3（TMED3）通过叉头框蛋白O1a（FOXO1a）和叉头框蛋白O3a（FOXO3a）磷酸化促进前列腺癌。

TMED3 promotes prostate cancer via FOXO1a and FOXO3a phosphorylation.

作者信息

Wei Xiuwang, Liang Jianbo, Huang Huanwen, Yang Daming, Wang Xinxin, Wang Xiujia, Chen Changsheng, Li Kaiqiang, Pang Taisen, Hu Bin, Wu Fengning

机构信息

Department of Urology, The People's Hospital of Guangxi Zhuang Autonomous Region, Nanning, 530000, China.

Department of Rehabilitation, The People's Hospital of Guangxi Zhuang Autonomous Region, Nanning, 530000, China.

出版信息

Oncol Res. 2024 Dec 20;33(1):161-169. doi: 10.32604/or.2024.048054. eCollection 2025.

DOI:10.32604/or.2024.048054
PMID:39735675
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11671412/
Abstract

BACKGROUND

Transmembrane emp24 trafficking protein 3 (TMED3) is associated with the development of several tumors; however, whether TMED3 regulates the progression of prostate cancer remains unclear.

MATERIALS AND METHODS

Short hairpin RNA was performed to repress TMED3 in prostate cancer cells (DU145 cells) and in a prostate cancer mice model to determine its function in prostate cancer and .

RESULTS

In the present study, we found that TMED3 was highly expressed in prostate cancer cells. , shTMED3 treatment suppressed the proliferation, invasion, and migration and promoted the apoptosis of DU145 cells. Additionally, the Kyoto Encyclopedia of Genes and Genomes pathway enrichment analysis showed a strong correlation between TMED3 and forkhead box O transcription factor (FOXO) pathway. Furthermore, TMED3 inhibition efficiently decreased FOXO1a and FOXO3a phosphorylation. , TMED3 downregulation suppressed the apoptosis, growth, and metastasis of prostate cancer cells via FOXO1a and FOXO3a.

CONCLUSION

The present findings show that TMED3 participates in the regulation of prostate cancer progression via FOXO1a and FOXO3a phosphorylation, thereby revealing a novel mechanism underlying prostate cancer development and suggesting that TMED3 inhibition may serve as a novel strategy for prostate cancer treatment.

摘要

背景

跨膜emp24转运蛋白3（TMED3）与多种肿瘤的发生发展相关；然而，TMED3是否调节前列腺癌的进展仍不清楚。

材料与方法

采用短发夹RNA在前列腺癌细胞（DU145细胞）和前列腺癌小鼠模型中抑制TMED3，以确定其在前列腺癌中的作用。

结果

在本研究中，我们发现TMED3在前列腺癌细胞中高表达。shTMED3处理抑制了DU145细胞的增殖、侵袭和迁移，并促进了其凋亡。此外，京都基因与基因组百科全书通路富集分析显示TMED3与叉头框O转录因子（FOXO）通路之间存在强相关性。此外，抑制TMED3可有效降低FOXO1a和FOXO3a的磷酸化水平。因此，TMED3的下调通过FOXO1a和FOXO3a抑制了前列腺癌细胞的凋亡、生长和转移。

结论

本研究结果表明，TMED3通过FOXO1a和FOXO3a磷酸化参与前列腺癌进展的调控，从而揭示了前列腺癌发生发展的新机制，并提示抑制TMED3可能成为前列腺癌治疗的新策略。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5764/11671412/ebb06ab92313/OncolRes-33-48054-f006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5764/11671412/a1c8e0dae923/OncolRes-33-48054-f001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5764/11671412/b3a48899d057/OncolRes-33-48054-f002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5764/11671412/85c5906614c8/OncolRes-33-48054-f003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5764/11671412/6697ac160d0f/OncolRes-33-48054-f004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5764/11671412/ebe4a85258ae/OncolRes-33-48054-f005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5764/11671412/ebb06ab92313/OncolRes-33-48054-f006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5764/11671412/a1c8e0dae923/OncolRes-33-48054-f001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5764/11671412/b3a48899d057/OncolRes-33-48054-f002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5764/11671412/85c5906614c8/OncolRes-33-48054-f003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5764/11671412/6697ac160d0f/OncolRes-33-48054-f004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5764/11671412/ebe4a85258ae/OncolRes-33-48054-f005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5764/11671412/ebb06ab92313/OncolRes-33-48054-f006.jpg

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本文引用的文献

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MicroRNAs-associated with FOXO3 in cellular senescence and other stress responses.与 FOXO3 相关的 microRNAs 在细胞衰老和其他应激反应中的作用。
Biogerontology. 2024 Feb;25(1):23-51. doi: 10.1007/s10522-023-10059-6. Epub 2023 Aug 30.
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Inhibiting MicroRNA-141-3p Improves Musculoskeletal Health in Aged Mice.抑制 microRNA-141-3p 可改善老年小鼠的骨骼肌健康。
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TMED3 promotes the development of malignant melanoma by targeting CDCA8 and regulating PI3K/Akt pathway.
跨膜蛋白3（TMED3）通过靶向细胞分裂周期相关蛋白8（CDCA8）并调节磷脂酰肌醇-3激酶/蛋白激酶B（PI3K/Akt）信号通路促进恶性黑色素瘤的发展。
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Impaired autophagy-accelerated senescence of alveolar type II epithelial cells drives pulmonary fibrosis induced by single-walled carbon nanotubes.自噬受损加速肺泡 II 型上皮细胞衰老导致单壁碳纳米管诱导的肺纤维化。
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TMED3 exerts a protumor function in non-small cell lung cancer by enhancing the Wnt/β-catenin pathway via regulation of AKT.TMED3 通过调节 AKT 增强 Wnt/β-连环蛋白通路在非小细胞肺癌中发挥促肿瘤功能。
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