PM_2.5 regulates the progression of lung adenocarcinoma through the axis of HCG18, miR-195 and ATG14

Area of Science:

• Molecular Oncology
• Environmental Health Science

Background:

• HCG18 has been linked to tumor development and progression.
• Particulate matter (PM2.5) is a known environmental risk factor for various cancers.

Purpose of the Study:

• To investigate the role of HCG18 in PM2.5-induced lung adenocarcinoma.
• To elucidate the molecular mechanisms by which PM2.5 affects lung cancer cells.

Main Methods:

• Overexpression and knockout experiments were performed to analyze HCG18 function.
• The regulatory relationship between HCG18, miR-195, and ATG14 was investigated.
• Autophagy pathway activation was assessed in response to PM2.5 exposure.

Main Results:

• PM2.5 exposure was found to enhance lung adenocarcinoma cell growth by modulating HCG18 expression.
• HCG18 was shown to suppress miR-195, leading to increased ATG14 expression.
• PM2.5 exposure elevated HCG18 and ATG14 expression in lung tissues, activating autophagy.

Conclusions:

• PM2.5 promotes lung adenocarcinoma oncogenesis by upregulating HCG18, which inhibits miR-195, thereby activating ATG14-mediated autophagy.
• HCG18 acts as a key mediator in the carcinogenic effects of PM2.5 on lung adenocarcinoma.