Ginsenoside Rk1 inhibits HeLa cell proliferation through an endoplasmic reticulum signaling pathway

Area of Science:

• Oncology
• Pharmacology
• Cell Biology

Background:

• Rising cervical cancer incidence in younger populations linked to work-life balance changes.
• Ginsenoside Rk1, a ginseng saponin, exhibits anti-cancer properties against various human cancer cells.
• The effect of ginsenoside Rk1 on HeLa cervical cancer cell proliferation remained unexplored.

Purpose of the Study:

• To investigate the inhibitory effects of ginsenoside Rk1 on HeLa cell proliferation.
• To elucidate the underlying molecular mechanisms of ginsenoside Rk1's action on HeLa cells.

Main Methods:

• HeLa cells were treated with varying doses of ginsenoside Rk1.
• Cell cycle progression, apoptosis, autophagy, and endoplasmic reticulum protein processing were analyzed.
• Quantitative PCR and Western blotting were used to assess specific gene and protein expression levels (YOD1, HSPA4L, DNAJC3, HSP90AA1).

Main Results:

• Ginsenoside Rk1 caused dose-dependent cell cycle arrest at G0/G1 phase, inhibiting proliferation.
• Apoptosis was induced via activation of caspase 3, PARP, and caspase 6.
• Autophagy signaling pathway was promoted (increased LC3B), while endoplasmic reticulum protein processing was downregulated.
• Expression of YOD1, HSPA4L, DNAJC3, and HSP90AA1 was significantly reduced, with YOD1 showing the most pronounced inhibition.

Conclusions:

• Ginsenoside Rk1 exerts toxicity in HeLa cells by inhibiting endoplasmic reticulum protein synthesis and enhancing apoptosis.
• The downregulation of YOD1 suggests its potential as a therapeutic target for cervical cancer treatment.