Department of Bio‑material Research, National Marine Biodiversity Institute of Korea, Seocheon 33662, Republic of Korea.
Department of Biological Application & Technology, National Marine Biodiversity Institute of Korea, Seocheon 33662, Republic of Korea.
Int J Oncol. 2025 Jan;66(1). doi: 10.3892/ijo.2024.5711. Epub 2024 Nov 29.
Developing novel anti‑angiogenic agents with minimal toxicity is notably challenging for cancer therapeutics. The discovery and development of peptides, whether derived from natural sources or synthesized, has potential for developing anti‑angiogenic agents characterized by their ability to penetrate cancer cells, high specificity and low toxicity. The present study identified a ‑derived anticancer and anti‑angiogenesis marine‑derived peptide 06 (MP06). A 22‑amino acid peptide was synthesized and conjugated with fluorescein isothiocyanate (FITC‑MP06) for intracellular localization in H1299 non‑small cell lung cancer cells. Regulatory effects of this peptide on the viability, migration and self‑renewal of lung cancer cells was assessed. Furthermore, anti‑angiogenic effect of MP06 was investigated by monitoring vascular tube formation in human umbilical vein endothelial cells and a zebrafish model. Aquaporin (AQP)3, a membrane channel in various tissues, is involved in regulating stemness, epithelial‑mesenchymal transition (EMT) and angiogenesis. MP06 downregulated AQP3 expression. Consistently, AQP3 knockdown by RNA silencing downregulated its gene expression, leading to a decrease in stemness, EMT and angiogenesis properties in H1299 cells. MP06 could thus serve as a novel therapeutic target with anticancer and angiogenesis properties for non‑small cell lung cancer.
开发具有最小毒性的新型抗血管生成药物对于癌症治疗极具挑战性。无论是源自天然来源还是合成的肽的发现和开发都具有开发抗血管生成药物的潜力,其特点是能够穿透癌细胞、具有高度特异性和低毒性。本研究鉴定了一种源自抗癌和抗血管生成的海洋衍生肽 06(MP06)。合成了一个由 22 个氨基酸组成的肽,并将其与异硫氰酸荧光素(FITC-MP06)缀合,以实现 H1299 非小细胞肺癌细胞内的定位。评估了该肽对肺癌细胞活力、迁移和自我更新的调节作用。此外,通过监测人脐静脉内皮细胞和斑马鱼模型中的血管管形成来研究 MP06 的抗血管生成作用。水通道蛋白(AQP)3 是各种组织中的膜通道,参与调节干性、上皮-间充质转化(EMT)和血管生成。MP06 下调了 AQP3 的表达。一致地,通过 RNA 沉默敲低 AQP3 表达,导致 H1299 细胞中的干性、EMT 和血管生成特性降低。因此,MP06 可作为一种具有抗癌和血管生成特性的新型治疗靶点,用于非小细胞肺癌。