RIPK2 and lysosomal pathway: Unveiling a new mechanism for lung cancer metastasis
Year: 2024
Type: article
Abstract: • Elevated RIPK2 expression in lung cancer patients and cell lines. • RIPK2 knockdown inhibits, while RIPK2 overexpression promotes, lung cancer cell proliferation, migration, and invasion. • RIPK2 promotes lung cancer metastasis by inhibiting LAMP2 expression and suppressing the lysosomal pathway. • Overexpression of LAMP2 reverses the malignant effects of RIPK2 overexpression. This study aims to explore the role of RIPK2 in lung cancer metastasis and its potential mechanisms. The expression levels of RIPK2 in lung cancer patients and cell lines were detected by immunohistochemistry, qRT-PCR, and Western blot. RIPK2 expression was knocked down using siRNA technology, and its effects on the proliferation, migration, and invasion capabilities of lung cancer cells were assessed through CCK-8, EdU, colony formation, and Transwell assays. Furthermore, by overexpressing RIPK2 and LAMP2, the regulatory effect of RIPK2 on the lysosomal pathway and its mechanism of action in lung cancer metastasis were investigated. The results showed that the expression of RIPK2 was significantly increased in lung cancer patients and cell lines. Knockdown of RIPK2 significantly inhibited the migration, invasion, and proliferation capabilities of lung cancer cells, while overexpression of RIPK2 promoted these malignant behaviors. Further studies found that RIPK2 promoted lung cancer metastasis by inhibiting LAMP2 expression, thereby suppressing the lysosomal pathway and altering the tumor microenvironment. Additionally, overexpression of LAMP2 could reverse the promotive effects of RIPK2 overexpression on the malignant behaviors of lung cancer cells. This study reveals for the first time that RIPK2 promotes lung cancer metastasis by inhibiting LAMP2 expression, thereby suppressing the lysosomal pathway and altering the tumor microenvironment. In the future, targeted therapy against RIPK2 and LAMP2 may become an effective means to inhibit lung cancer metastasis.
Source: Translational Oncology
Institution: Hebei Medical University
Language: English
Subfield: Physiology
Domain: Life Sciences
Open Access status: gold
Estimated APC paid: $3,130
OpenAlex ID: W4404129602