口腔癌细胞通过外体 miR-21/RMND5A 途径与内皮细胞进行通信
Yu-Qi Sun1, Bing Wang1, Lin-Wei Zheng1
1The State Key Laboratory Breeding Base of Basic Science of Stomatology (Hubei-MOST) & Key Laboratory of Oral Biomedicine Ministry of Education, School & Hospital of Stomatology, Wuhan University, No. 237 Luoyu Road, Wuhan, 430079, China.
BMC oral health
|January 16, 2024
概括
口腔状细胞癌 (OSCC) 细胞通过通过外体miR-21通过内皮细胞抑制RMND5A表达来促进血管生成. 这种miR-21/RMND5A通路为OSCC治疗提供了潜在的治疗点.
科学领域:
- 在瘤学瘤学.
- 细胞生物学 细胞生物学
- 分子生物学分子生物学
背景情况:
- 对于介质核分裂5同位素A (RMND5A) 需要一种与癌症预后不佳相关的全方位素E3联酶.
- 在内皮细胞中RMND5A的特定作用及其在口腔状细胞癌 (OSCC) 血管生成中的参与仍然在很大程度上未被探索.
研究的目的:
- 研究RMND5A在人类静脉内皮细胞 (HUVEC) 的功能.
- 阐明OSCC细胞和涉及RMND5A和外体微RNA的内皮细胞之间的交叉.
- 通过了解血管生成机制来确定OSCC治疗的潜在治疗点.
主要方法:
- 在使用lentiviral感染的HUVEC中RMND5A的过度表达.
- 使用MTT,伤口愈合和管形成试验评估HUVEC的扩散,迁移和管形成.
- 信号通路 (ERK,NF-κB) 的分析和通过条件介质和瘤细胞衍生外体的细胞间通信的调查.
主要成果:
- 过度表达RMND5A通过抑制ERK和NF-κB激活,显著抑制了HUVEC的增殖,迁移和管形成.
- 发现OSCC细胞通过外体miR-21.1通过内皮细胞抑制RMND5A的表达.
- 该研究表明,OSCC细胞通过外体miR-21/RMND5A通路激活内皮细胞,促进血管生成.
结论:
- OSCC细胞利用外体miR-21降低内皮细胞中的RMND5A的调节,从而促进血管生成.
- 已确定的外体miR-21/RMND5A通路代表了一种驱动OSCC血管生成的新机制.
- 准这种途径可能为治疗口腔状细胞癌提供新的治疗策略.
更多相关视频
相关概念视频
MicroRNAs
3.0K
MicroRNA (miRNA) are short, regulatory RNA transcribed from introns (non-coding regions of a gene) or intergenic regions (stretches of DNA present between genes). Several processing steps are required to form biologically active, mature miRNA. The initial transcript, called primary miRNA (pri-mRNA), base-pairs with itself, forming a stem-loop structure. Within the nucleus, an endonuclease enzyme, called Drosha, shortens the stem-loop structure into hairpin-shaped pre-miRNA. After the pre-miRNA...
3.0K
Rous Sarcoma Virus (RSV) and Cancer
5.1K
Rous Sarcoma virus or RSV was discovered by F. Peyton Rous in the year 1911 as a filterable transmissible agent that could cause tumors in chickens. He won a Nobel Prize for this discovery in 1966. His experiments clearly demonstrated that some cancers could be caused by infectious agents and led to the discovery of many more cancer-causing viruses in animals as well as humans.
RSV is a retrovirus that contains two copies of a plus-strand RNA genome. Its genome consists of four main open...
RSV is a retrovirus that contains two copies of a plus-strand RNA genome. Its genome consists of four main open...
5.1K
The Tumor Microenvironment
6.6K
Every normal cell or tissue is embedded in a complex local environment called stroma, consisting of different cell types, a basal membrane, and blood vessels. As normal cells mutate and develop into cancer cells, their local environment also changes to allow cancer progression. The tumor microenvironment (TME) consists of a complex cellular matrix of stromal cells and the developing tumor. The cross-talk between cancer cells and surrounding stromal cells is critical to disrupt normal tissue...
6.6K
Non-Canonical Wnt Signaling Pathways
7.3K
Wnt is a zygotic effect gene that is expressed during very early embryonic development. It regulates various processes in animals starting from early development through the adult stage, such as organogenesis in the embryo and maintenance of neuronal and blood stem cells. Wnt proteins can induce a wide variety of intracellular pathways depending upon the specific abilities of different Wnt ligands to form a complex with shared and cognate receptors in the presence of different co-receptors. The...
7.3K
mTOR Signaling and Cancer Progression
3.8K
The mammalian target of rapamycin or mTOR protein was discovered in 1994 due to its direct interaction with rapamycin. The protein gets its name from a yeast homolog called TOR. The mTOR protein complex in mammalian cells plays a major role in balancing anabolic processes such as the synthesis of proteins, lipids, and nucleotides and catabolic processes, such as autophagy in response to environmental cues, such as availability of nutrients and growth factors.
The mTOR pathway or the...
The mTOR pathway or the...
3.8K
Canonical Wnt Signaling Pathway
8.8K
The gene encoding the main signaling molecules of the Wnt signaling pathways (the Wnt proteins) was discovered almost four decades ago by Nüsslein-Volhard and Wieschaus. They identified and originally named the gene "wingless" (wg) after a phenotype discovered during their landmark genetic screen in Drosophila for body pattern defects. At around the same time, another researcher named Harold Varmus found that a murine tumor virus activates the mammalian wg homolog, Int-1, which...
8.8K


