Exploring targeted therapies against RFPL3 for non-small cell lung cancer with lymph node metastasis

Non-small cell lung cancer (NSCLC) is one of the leading causes of cancer-related deaths worldwide, marked by its aggressive nature and high likelihood of metastasis. The precise function of ret finger protein-like 3 (RFPL3) in NSCLC progression remains incompletely understood.

This study measured RFPL3 expression in NSCLC by immunohistochemistry, qPCR, and Western blot. RFPL3's effects on proliferation were assessed with CCK-8 and colony formation assays. Transwell and wound-healing assays evaluated its role in invasion, metastasis, and EMT. In vitro and in vivo studies determined RFPL3's mechanisms driving EMT and lymphatic metastasis.

RFPL3 was overexpressed in NSCLC tissues, correlating with lymphatic metastasis and poor prognosis, establishing it as a distinct prognostic risk factor. Knockdown reduced NSCLC cell proliferation, invasion, and metastasis, while overexpression enhanced these malignant phenotypes. RFPL3 increased EMT-related protein expression by western blot, promoting tumor cell metastasis. In vivo, RFPL3 overexpression accelerated tumor growth and lymphatic metastasis in mice.

This study revealed the critical role of RFPL3 in NSCLC, suggesting that RFPL3 might serve as both a biomarker and a therapeutic target for this type of cancer, which provides new insight for improving patient prognoses.