Scamp1, Secretory Carrier-associated Membrane Protein 1, is the most widely expressed member of the SCAMP family. It is involved in endocytosis, with its NPF repeats in the N-terminal region binding to EH domain proteins like intersectin 1 and gamma-synergin, potentially mediating the budding of transport vesicles from the plasma membrane and trans-Golgi complex [4]. It may participate in endocytosis by recruiting clathrin coats to these membranes.

In cancer research, Scamp1 knockdown has shown significant impacts. In gastric cancer, it drives hyper-proliferation, as its knockdown suppresses GC cell proliferation in vitro and in vivo, and attenuates the Akt/MAPK/Stat signaling pathway [1]. In pancreatic β-cells, Scamp1 knockdown leads to insulin hypersecretion, and expression of a non-palmitoylated Scamp1 mutant in APT1-deficient cells rescues insulin hypersecretion and apoptosis [2]. In osteosarcoma, lncRNA Scamp1 promotes cell viability and invasion via the miR-26a-5p/ZEB2 axis [3]. In pediatric renal cell carcinoma, lncRNA Scamp1 promotes tumorigenesis under oxidative stress through miR-429 and its downstream targets ZEB1 and JUN [5]. In breast cancer, silencing Scamp1-TV2 inhibits cell proliferation, migration, and invasion, and promotes apoptosis by interacting with PUM2 to facilitate INSM1 mRNA degradation [6]. In glioma, knockdown of lncRNA Scamp1 suppresses malignant behaviors via the miR-499a-5p/LMX1A/NLRC5 pathway [7]. In ovarian cancer, lncRNA Scamp1 promotes cell invasion and angiogenesis through the miR-137/CXCL12 axis [8].

In conclusion, Scamp1 is crucial for endocytosis. Its role in various cancers, as revealed through loss-of-function experiments, indicates its potential as a therapeutic target. Understanding Scamp1's function in different disease conditions can help develop new strategies for cancer treatment and management.