# SCAMP1 silencing inhibits proliferation by attenuating multiple pro-survival signaling pathways in gastric cancer

## TL;DR

SCAMP1 promotes gastric cancer growth by activating survival pathways, and reducing it could be a potential treatment strategy.

## Contribution

This study reveals SCAMP1's role in gastric cancer proliferation through multiple signaling pathways.

## Key findings

- SCAMP1 is overexpressed in gastric cancer and linked to worse patient outcomes.
- SCAMP1 knockdown reduces cancer cell proliferation in lab and animal models.
- SCAMP1 depletion disrupts Akt/MAPK/Stat signaling pathways in gastric cancer cells.

## Abstract

Secretory carrier-associated membrane protein 1 (SCAMP1) is the most universally expressed member of the SCAMP family, and its ability to facilitate endocytosis was demonstrated approximately two decades ago. Nevertheless, its roles in cancer biology are largely unknown, although its expression is significantly increased in most cancer types. Herein, we examined the expression of SCAMP1 in gastric cancer (GC) tissues and found that it was aberrantly increased and positively correlated with tumor size and lymph node metastasis. More importantly, increased SCAMP1 expression was associated with poor prognosis in patients with GC. Functional experiments demonstrated that SCAMP1 knockdown markedly suppressed the proliferation of GC cells in vitro and in vivo. RNA sequencing assays demonstrated that SCAMP1 knockdown altered the expression profile of GC cells, and a significant portion of the altered genes were enriched in receptor tyrosine kinases and their related downstream signaling pathways. Immunoblotting confirmed that the Akt/MAPK/Stat signaling pathway was strongly attenuated in GC cells with SCAMP1 depletion. Taken together, these results demonstrated that SCAMP1 drives hyperproliferation in GC cells, thus suggesting that further investigation into the mechanisms and translational value of SCAMP1 in treating patients with GC is warranted.