TMED5,全称为Transmembrane P24 Trafficking Protein 5,是一种定位于细胞膜上的蛋白。它属于TMED家族,该家族成员在哺乳动物中主要与内质网到高尔基体的蛋白质转运有关。TMED5在细胞内物质转运和信号传导中发挥着重要作用,特别是在膜泡运输和囊泡融合过程中。其功能异常可能与多种疾病的发生发展相关。
在肿瘤研究中,TMED5的表达异常与肿瘤的发生、发展及预后密切相关。如在卵巢癌中,TMED5的表达水平显著升高,其过表达与肿瘤的增殖、迁移、侵袭能力增强以及凋亡减少相关[1]。在肝细胞癌中,TMED5的过表达与肿瘤的恶性表型相关,包括细胞增殖、迁移、侵袭能力的增强以及凋亡的减少[2]。在宫颈癌中,TMED5的表达上调与肿瘤的恶性表型相关,包括细胞增殖、迁移、侵袭能力的增强以及核自噬的促进[3]。
此外,TMED5的表达异常还与其他多种疾病相关。如在儿童急性髓细胞性白血病中,TMED5的表达水平显著升高,其过表达与肿瘤的发生发展相关[4]。在膀胱癌中,TMED5的表达水平也显著升高,其过表达与肿瘤的恶性表型相关[5]。在多发性骨髓瘤中,TMED5基因所在的1p22.1-21.2区域是频繁发生缺失的区域,其缺失与患者的不良预后相关[6]。
综上所述,TMED5作为一种重要的膜转运蛋白,在细胞内物质转运和信号传导中发挥着重要作用。其在多种肿瘤中的表达异常与肿瘤的发生、发展及预后密切相关,可能是肿瘤治疗的新靶点。同时,TMED5的表达异常还与其他多种疾病相关,其功能机制有待进一步研究。
参考文献:
1. Liu, Chao, Zhao, Shu, Lv, Zhi Xiang, Zhao, Xiao Juan. . Promoting action of long non-coding RNA small nucleolar RNA host gene 4 in ovarian cancer. In Acta biochimica Polonica, 70, 59-68. doi:10.18388/abp.2020_6141. https://pubmed.ncbi.nlm.nih.gov/36657061/
2. Cheng, Xianyi, Deng, Xiulan, Zeng, Huiping, Li, Dezhi, Zheng, Wei V. . Silencing of TMED5 inhibits proliferation, migration and invasion, and enhances apoptosis of hepatocellular carcinoma cells. In Advances in clinical and experimental medicine : official organ Wroclaw Medical University, 32, 677-688. doi:10.17219/acem/156673. https://pubmed.ncbi.nlm.nih.gov/36530030/
3. Yang, Zhen, Sun, Qi, Guo, Junfei, Liu, Min, Tang, Hua. 2018. GRSF1-mediated MIR-G-1 promotes malignant behavior and nuclear autophagy by directly upregulating TMED5 and LMNB1 in cervical cancer cells. In Autophagy, 15, 668-685. doi:10.1080/15548627.2018.1539590. https://pubmed.ncbi.nlm.nih.gov/30394198/
4. Wang, Qing, Yue, Chao, Liu, Qin, Che, Xuchun. 2022. Exploration of differentially expressed mRNAs and miRNAs for pediatric acute myeloid leukemia. In Frontiers in genetics, 13, 865111. doi:10.3389/fgene.2022.865111. https://pubmed.ncbi.nlm.nih.gov/36160019/
5. Scaravilli, Mauro, Asero, Paola, Tammela, Teuvo L J, Visakorpi, Tapio, Saramäki, Outi R. 2014. Mapping of the chromosomal amplification 1p21-22 in bladder cancer. In BMC research notes, 7, 547. doi:10.1186/1756-0500-7-547. https://pubmed.ncbi.nlm.nih.gov/25135188/
6. Boyd, Kevin D, Ross, Fiona M, Walker, Brian A, Davies, Faith E, Morgan, Gareth J. 2011. Mapping of chromosome 1p deletions in myeloma identifies FAM46C at 1p12 and CDKN2C at 1p32.3 as being genes in regions associated with adverse survival. In Clinical cancer research : an official journal of the American Association for Cancer Research, 17, 7776-84. doi:10.1158/1078-0432.CCR-11-1791. https://pubmed.ncbi.nlm.nih.gov/21994415/