Role of an autophagy/lysosome pathway in NF-κB pathway blocked pancreatic cancer Panc-1 cells

Area of Science:

• Oncology
• Cell Biology
• Molecular Biology

Background:

• Pancreatic cancer remains a significant health challenge with limited treatment options.
• The NF-κB pathway is frequently dysregulated in various cancers, including pancreatic cancer.
• Autophagy, a cellular degradation process, plays a complex role in cancer progression and treatment response.

Purpose of the Study:

• To investigate the role of the autophagy/lysosome pathway in pancreatic cancer cells with a blocked NF-κB pathway.
• To determine the effects of SN50, an inhibitor of p65 nuclear translocation, on pancreatic cancer cell line Panc-1.
• To elucidate the relationship between NF-κB inhibition, autophagy activation, and cell death in pancreatic cancer.

Main Methods:

• Cell viability was assessed using MTT assay after SN50 treatment.
• Autophagy activation was visualized using MDC staining and transmission electron microscopy (TEM).
• Expression levels of apoptosis-related protein p53 and autophagy-related proteins LC3, p62, and Beclin1 were analyzed by Western blotting and immunofluorescence.

Main Results:

• SN50 treatment significantly inhibited Panc-1 cell activity in a time-dependent manner.
• Western blotting revealed increased expression of p53, LC3, and Beclin1, and decreased expression of p62.
• MDC staining and TEM confirmed autophagy activation and observed ultrastructural changes indicative of autophagy.

Conclusions:

• Inhibition of NF-κB pathway activation by SN50 leads to autophagy activation in pancreatic cancer Panc-1 cells.
• The activated autophagy pathway contributes to autophagic cell death in these cancer cells.
• Targeting the NF-κB pathway and modulating autophagy presents a potential therapeutic strategy for pancreatic cancer.