Network pharmacology and UHPLC-HRMS reveal the mechanism of QSFZYL and BMSCs overexpressing IFN-γ against lung adenocarcinoma

TL;DR

This study explores how a traditional Chinese medicine, QSFZYL, combined with IFN-γ, may help treat lung adenocarcinoma by affecting immune response and cancer pathways.

Contribution

The novel contribution is identifying QSFZYL's mechanism in LUAD via network pharmacology and UHPLC-HRMS, combined with IFN-γ's role in suppressing tumor growth.

Findings

QSFZYL combined with IFN-γ significantly inhibited LUAD growth and promoted CD3 and CD8 T cell infiltration.

The JAK2/STAT3 signaling pathway and PD-L1 expression were downregulated by the treatment.

26 differential components in QSFZYL were identified, including astragalus lysine alkaloids and flavonoids.

Abstract

Lung cancer is a significant public health concern in China, posing a serious threat to the population. The QiShenFuZhengYiLiu (QSFZYL) is commonly prescribed as a complementary treatment for cancer patients, although its anticancer mechanism remains unclear. The purpose of this study was to explore the therapeutic mechanisms of QSFZYL in lung adenocarcinoma (LUAD).

The mechanism of QSFZYL for treating LUAD was analyzed using comprehensive network pharmacology and UHPLC-HRMS, combined with experimental validation (in vivo).

Network pharmacology analysis suggested that the therapeutic effects of QSFZYL on LUAD may involve the JAK/STAT signaling pathway. UHPLC-HRMS identified 26 differential components, with representative compounds including astragalus lysine alkaloids, monoterpenoids, isoflavonoids, and flavonoids. In vivo experiments demonstrated that QSFZYL combined with IFN-γ significantly inhibited LUAD growth and promoted infiltration of CD3 and CD8 T cell, and downregulated JAK2, STAT3, and PD-L1 expression, promoted apoptosis.

QSFZY combined with IFN-γ overexpressing BMSCs effectively inhibit LUAD progression. The primary mechanisms include the suppression of cancer cell growth, promotion of apoptosis and infiltration of CD3 and CD8 T cells, and inhibition of the JAK2/STAT3 signaling pathway, and downregulated PD-L1 expression.

Figures