lncRNA GHET1 knockdown suppresses breast cancer activity in vitro and in vivo

Area of Science:

• Oncology
• Molecular Biology
• Genetics

Background:

• Long non-coding RNA gastric carcinoma high-expressed transcript 1 (lncRNA GHET1) is frequently overexpressed in various cancers.
• lncRNA GHET1's role in breast cancer progression, particularly its interaction with epidermal growth factor receptor (EGFR) signaling, requires further elucidation.

Purpose of the Study:

• To investigate the effect of lncRNA GHET1 inhibition on MCF-7 breast cancer cell proliferation, metastasis, and apoptosis.
• To determine if lncRNA GHET1 modulates epidermal growth factor receptor (EGFR) expression and downstream signaling pathways in breast cancer.

Main Methods:

• In vitro studies involved lncRNA GHET1 knockdown in MCF-7 cells to assess effects on cell cycle, proliferation, migration, invasion, and apoptosis.
• Western blotting was used to analyze the expression levels of EGFR and related proteins.
• In vivo experiments utilized a GHET1 inhibitor in mice to evaluate its impact on tumor growth.

Main Results:

• lncRNA GHET1 knockdown significantly inhibited MCF-7 cell proliferation, migration, and invasion while enhancing apoptosis by arresting cells in the G1 phase.
• Knockdown of lncRNA GHET1 led to a reduction in EGFR expression and associated downstream proteins.
• In vivo administration of a GHET1 inhibitor effectively suppressed tumor growth in mice.

Conclusions:

• lncRNA GHET1 inhibition directly suppresses EGFR expression, thereby inhibiting the PI3K/AKT/Cyclin D1/MMP2/9 pathway.
• This mechanism underlies the suppression of breast cancer cell proliferation, migration, and invasion.
• Targeting lncRNA GHET1 presents a promising therapeutic strategy for suppressing breast cancer growth and metastasis.