Table 2.
SOS2 gene silencing strategies in different tumor cell types. List of genetically-based strategies to downregulate SOS2 gene in the indicated tumor cell lines. Resulting phenotypic consequences of SOS2 disruption are shown in the corresponding column.
| SOS2 Disrution Strategy | Tumor Cell Line | Phenotypic Effect | Reference |
|---|---|---|---|
| miR-148a | BJAB and DG-75 and U2932 (B cell lymphoma and Burkitt lymphoma) | Reduction of ERK activation | [68] |
| miR-148a-3p | A549, HCC827 (lung cancer) | Reduction of proliferation and EM transition | [69] |
| miR-193a-3p | HEK293, SKOV3, and OVCA433 (ovarian cancer) | Suppression of MAPK–ERK signal transmission | [70] |
| SOS2 KO mice | MEFs expressing mutant RAS isoforms: HRASG12V, NRASG12V, or KRASG12V | Impairment of RTK-dependent AKT phosphorylation Dispensable for RTK-dependent ERK activation |
[31] |
| CRISPR/Cas9 | H358 NSCLC cells (lung cancer) | Revert the transformed phenotype of KRAS mutant cells. SOS2 participates in anchorage-independent, but not in anchorage-dependent, growth. |
[31,32] |
| CRISPR/Cas9 | H23 NSCLC cells (lung cancer) | SOS2 participates in anchorage-independent growth. Reduce cell viability. |
[32] |
| CRISPR/Cas9 | SW620 (colorrectal cancer) | SOS2 participates in anchorage-independent growth. | [32] |
| CRISPR/Cas9 | NCI-H1299 NSCLC cells (lung cancer) | SOS2 participates in anchorage-independent growth. | [32] |
| CRISPR/Cas9 | YAPC cells (pancreatic cancer) | Revert the transformed phenotype of KRAS oncogenic cells. | [31] |