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Updated: Mar 22, 2026

siRNA Electroporation to Modulate Autophagy in Herpes Simplex Virus Type 1-Infected Monocyte-Derived Dendritic Cells
Published on: October 28, 2019
G protein γ subunit 7 induces autophagy and inhibits cell division
Juanjuan Liu1,2, Xinmiao Ji1, Zhiyuan Li1
1High Magnetic Field Laboratory, Chinese Academy of Sciences, Hefei, Anhui, 230031, P. R. China.
Abstract:
GNG7 (G protein γ subunit 7), a subunit of heterotrimeric G protein, is ubiquitously expressed in multiple tissues but is down-regulated in various cancers. Its expression could reduce tumor volume in mice but the mechanism was not clear. Here we show that GNG7 overexpression inhibits cell proliferation and increases cell death. GNG7 level is cell cycle-dependent and it regulates actin cytoskeleton and cell division. In addition, GNG7 is an autophagy inducer, which is the first reported Gγ protein involved in autophagy. GNG7 knockdown reduces Rapamycin and starvation-induced autophagy. Further analysis reveals that GNG7 inhibits MTOR in cells, a central regulator for autophagy and cell proliferation. In conclusion, GNG7 inhibits MTOR pathway to induce autophagy and cell death, inhibits cell division by regulating actin cytoskeleton. These combined effects lead to the antitumor capacity of GNG7.
Insights
G protein γ subunit 7 (GNG7) inhibits cancer cell proliferation and promotes cell death by inducing autophagy and regulating the cell cycle. GNG7
Area of Science:
- Molecular Biology
- Cell Biology
- Cancer Research
Background:
- G protein γ subunit 7 (GNG7) is down-regulated in various cancers.
- Previous studies suggested GNG7 expression reduces tumor volume in mice, but the underlying mechanisms were unclear.
Purpose of the Study:
- To elucidate the molecular mechanisms by which GNG7 exerts its antitumor effects.
- To investigate the role of GNG7 in cell proliferation, cell death, autophagy, and cell division.
Main Methods:
- Overexpression and knockdown of GNG7 in cancer cells.
- Cell cycle analysis.
- Actin cytoskeleton assessment.
- Autophagy induction assays (Rapamycin and starvation).
- Western blot analysis to assess MTOR pathway activity.
Main Results:
- GNG7 overexpression inhibits cell proliferation and increases cell death.
- GNG7 expression is cell cycle-dependent and regulates the actin cytoskeleton and cell division.
- GNG7 acts as an autophagy inducer, inhibiting the MTOR pathway.
- GNG7 knockdown reduces autophagy induced by Rapamycin and starvation.
Conclusions:
- GNG7 inhibits the MTOR pathway, thereby inducing autophagy and cell death.
- GNG7 regulates the actin cytoskeleton, inhibiting cell division.
- These combined actions contribute to the observed antitumor capacity of GNG7.
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